A Comprehensive Guide to AP Biology by Brian Lin

Table of Contents: About the new AP Bio test (pages 2-­3) I. Evolution (pages 4-­8) II. Biochemistry (pages 8-­16) III. Cells, Membranes, Transport (pages 16-­22) IV. DNA Replication and Cell Cycle (pages 23-­28) V. Ecology and Behavior (pages 29-­37) VI. Plants and Photosynthesis (38-­47) *Second Semester Google Doc found here.

Important disclaimers:

All diagrams are copyrighted by Pearson Education inc. and used for NONPROFIT EDUCATIONAL purposes under Section 107 for educational Fair Use.

This review guide is NOT meant for resale and should not be sold since it contains copyrighted materials from Pearson.

Units I-­VIII are kinda organized by target according to the green targets sheet and should prepare you for each test (they worked for me at least). Of course, teachers may have changed stuff so… yeah. Units IX-­XII, I just used teacher handouts and diagrams. I’ve still included friends’ notes for your convenience though.

If you want to make changes/edit/etc. check with your peers/teacher/etc. make a comment (top right hand corner next to the blue “Share” button).

If you have biology questions, DO NOT flood my FB with messages! Instead please ask your classmates, FB group, teacher, etc. FIRST before asking me online because I’m going to be insanely busy this fall with college apps/cello/cross country/NHS/school/SAT/etc. During school is completely different though, and I’ll be more than happy to explain stuff to the best of my ability if I have the time.

Q. What’s with the random Pokemon, man? A. Wynaut? Q. Seriously, why? A. So, in V. Ecology and Behavior, you learn about ‘kinesis’ in the pill

bug lab (fun fact: 2 years ago, Justin Doong came to my backyard to look for pill bugs before the school started buying them last year). Well, kinesis just happens to be a Pokemon move... hence the pictures.

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About Me... and the new AP Bio test. My name is Brian Lin, if you don’t already know me, then you sure will 70-­80 pages later. Anyways, I like playing the cello, fooling around, and complaining about things in review guides. So have fun, learn a lot, and eat a lot (the pre-­AP test breakfast is AMAZING!) However, don’t eat so much that you end up throwing up during the test and losing time (one of my friends lol).

On the AP Bio Test...

Alright, so my year (2014) got kinda screwed over... they happen to be changing the AP Bio and AP Chem tests the year we take them. Oh well... that’s life, isn’t it? Anyways, you can see for yourself how the AP Bio test went last year:

The mean went up, but the percentage of 5s went down (down down down down...). DO NOT BE WORRIED! I will explain below what happened and what you can do to be prepared!

Now here’s what the graders/College Board had to say about this (typos included):

1,200 college students were administered redesigned AP Biology exam questions this spring;; their work was scored at the AP Reading. College professors also took the full redesigned AP Biology exam themselves & evaluated each question to set the pts needed for 2,3,4,5. Most AP Biology students earned enough pts to get a 2,3,4, but very few scored well enough on the grid-­ins and free-­response to score a 5. AP Biology grid-­in questions require students to use mathematics to solve biological problems. The avg score on these was very low: 36%. Multiple-­choice: last year, students earned 63% correct on average;; this year, 61% FRQs require students to "explain," "describe," "justify" their content knowledge. Very low scores on avg.ow.ly/mmH0O. What % of AP Bio students earned 0 pts on these FRQs? Q5 (polypeptides): 45%. Q6 (organelles): 49%. Q8 (hormone-­signalling): 54%. AP Bio students performed well on Q3 (evaluating fossils of a transitional species) and Q7 (effect of alcohol on urine production). I have posted a 6-­page summary of the AP Biology exam results on the AP Biology Teacher Community. College professors attest that AP Biology cousre & exam are now the gold standard in college-­level Biology. Kudos to AP Biology teachers. Previously, the free response questions (FRQs) were only 25% of the total score. Now, the FRQs make up 50% of the total score. And if you combine that with the fact that ~50% of students got 0s on about half of their FRQs, there you go. So, my explanation for the drop in 5s is that kids in other schools (aka not Stevenson) had NO CLUE how to write FRQs. FRQ tip: Points are cumulative only! Therefore, you can have tons of incorrect stuff but they can’t take points off for that (obviously, this is different on other AP tests). “Somehow, maybe just due to the stress of the test, kids saw that message, and thought the

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proctor would tell them when to move on to the grid-­in problems. So time ran out, and they didn't do them!” -­Some teacher guy Apparently some people just didn’t do the grid-­ins because… I have no idea really. Luckily, all of us were told to work backwards on the MC, starting with the grid-­ins (and the harder normal MC) so I (at least) did not have that problem. Grid-­ins are not really that hard though. Even though you can’t guess like a MC question, there’s quite a bit of room for rounding errors and stuff. And the math is pretty easy (though tedious). Also, time was not an issue for me (that’s for me though, one of my friends had to throw up in the middle and didn’t finish…). I had enough time left after the MC to check over about half of them. On the FRQs, I was able to read through all of them (and my responses). In fact, make sure you leave plenty of space to add stuff later since you will have time to go back and stuff more key words in. Also, it’s important to realize that the test has shifted away from memorization/content-­based and more towards skill/application/understanding (for example, they will have questions where they will explain a lab/concept for you and then ask you about it). Your teachers will say corny stuff about how understanding stuff is important (the whole Big Idea thing). They’re actually right. Seriously, I thought it was really cheesy but it helped A LOT. Big disclaimer here: The AP Biology test content NO LONGER coincides (completely) with the SAT Bio test. You will have to self study around half of the material. Sucks since the College Board makes both but haven’t updated the SAT subject test. Also, there’s a lot less curve than physics, which sucks. Take SAT PHYSICS or CHEM! Please! (Plus Princeton doesn’t take Bio for engineering majors). Seriously, I regret not taking SAT Physics. Also, do not pay for test-­prep books/ tutoring unless they’re based on/have actually taken the new test. I bought the Barron’s book last year and it was a waste of money considering entire chapters were irrelevant (and useless) and covered stuff we didn’t need to know (all the while leaving other stuff out). Just ask someone who took the new test.

Reasons Why You Shouldn’t Be Scared

All three teachers are very qualified (from personal experience + friends’ experience) A lot less homework than before (notes are not mandatory-­ more college style) Teachers/we now know what to look out for (no old tests to look at) I think David Chen got like a 100% on the 1st semester final. That should inspire you. The test was ‘easier’ but the curve was a lot tougher. This should be fixed (I hope). The percentages do not reflect Stevenson! You will be fine if you work hard!

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I. Evolution 1. Evolution by Natural Selection • Okay, let’s start off with a population (bunch of same species in same place) • There’s going to be genetic variation. Why?

1. Random mutations. Point mutations (insert/delete/frameshift) 2. Crossing over and recombination (getting back together) 3. Law of Independent Assortment (Metaphase I 2 dif. orientations) 4. Random fertilization (You learn about all this stuff later, I just added it here since this is a big FRQ topic)

• These different individuals will be selected for or against by selective pressures • Any developed traits that help you survive are known as adaptations • Those that survive to reproduce will create offspring and change the allele frequency of the population in favor of the ‘fit’ allele (allele = version of a gene) • Divergent evolution branching out (becoming “more different”) • Convergent evolution evolving similarly (explains analogous structures in 5.) • Population a group of individuals of same species that can interbreed and create fertile offspring (so a herd of deer or something) • Species a group of populations whose members can interbreed and produce fertile offspring (all the deer herds in the world)

2. Hardy-­Weinberg • What’s it say? Allele frequency and genotype frequency remain constant! • But for this to apply, we’ll need 5 conditions:

1. Really big population/sample size 2. No mutations 3. Random mating 4. No natural selection 5. No migration/gene flow (ie no adding/removing organisms)

Equation 1: Q P + = 1

Equation 2: P ² 2PQ Q² 1+ + = P is the dominant allele frequency. Q is the recessive allele frequency. So if you have mice that can either have brown hair or black hair (where hair color is the gene with 2 different alleles). Then % brown (P) + % black (Q) = 100% (1). Should make sense.

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P² is the frequency in the population with homozygous dominant allele. 2PQ is the frequency in the population with heterozygous both alleles. Q² is the frequency in the population with homozygous recessive allele. Since the mice get one allele from each parent, you multiply the allele frequencies together. Since P = chance of getting the dominant allele and Q = chance of getting the recessive allele, you multiple P * P to get the chance of getting homozygous (2) dominant alleles and so on. • Genotype Set of genes it carries;; 2 alleles. • Phenotype Expressed traits;; characteristics. (Straight hair) So if brown is dominant, a brown mouse can have the genotype Bb (one brown and one black) but still have the phenotype brown since that allele takes over.

3. Microevolution • What is microevolution? Changes in allele frequencies within a population. • There are 4 main causes for microevolution:

1. Random mutations 2. Natural/Artificial Selection 3. Genetic drift 4. Gene flow

• Genetic drift is changing allele frequencies by changing the sample size

1. Bottleneck (natural disasterrandom drop in gene pool, depends on survivors) 2. Founder (random group leaves and ‘founds’ new population, depends on founders)

• Gene flow and migration is when you transfer alleles from one population to another

4. Macroevolution • What is macroevolution? Formation of a new species (speciation) • How does this happen?

1. Start off with parent species 2. Add a reproductive barrier 3. Wait some time 4. Divergent groups can’t produce fertile offspring 5. Voilà! Macroevolution

• There are two main modes of speciation • Allopatric speciation geographic/physical isolation

Examples would be mountains, long distances, oceans, etc.

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• Sympatric speciation non-­physical isolation Examples would be all the stuff in I.6: Reproductive Barriers (scroll down 1 page)

• Adaptive radiation refers to when a parent species diversifies and fills many different niches

5. Evidence for Evolution • Embryology stuff looks the same as an embryo and early stages of development • Anatomy (what stuff looks like)

Homologous structures (different function, similar anatomy) Vestigial structures (random crap left over from common ancestor, ex. tailbone) Analogous structures (NOT evidence, stuff that evolved same, bird/bug wings)

• Molecular Biology all organisms have similarities in DNA, RNA, proteins, ATP use, etc. Use bioinformatics to compare chimpanzee DNA to human DNA • Paleontology dig up stuff, do carbon dating, look at fossil records, ratio Carbon 14 to 12 • Physiology similar processes and functions in organisms (jaw bones, chloroplasts, etc.)

6. Reproductive Barriers gg Sperm ZygoteE + =

• Pre-­zygotic impede mating or hinder fertilization even if mating occurs Type 1: No mating (ie NO SEX!)

Habitat Isolation: different areas (water/land snake) Temporal Isolation: different times (winter/summer skunk) Behavioral Isolation: different courtship rituals (bird songs)

Type 2: No fertilization (sperm never meets egg)

Mechanical Isolation: the ‘parts don’t fit’ (use your imagination) Gametic Isolation: sperm cannot fertilize egg (dif. color eggs in sea urchins)

• Post-­zygotic prevent the hybrid (offspring) from developing correctly

Reduced Hybrid Viability: too weak and dies Reduced Hybrid Fertility: sterile offspring (mule) Hybrid Breakdown: hybrid’s offspring can’t survive

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7. Modes of Selection

• Directional favors one extreme • Diversifying/Disruptive favors both extremes • Stabilizing favors the middle • Frequency Dependent fitness declines if too common (ex. Google ‘scale eating fish’) • Sexual Selection organisms with best traits get to reproduce

Intrasexual: compete with same gender (ex. alpha lion) Intersexual: ‘mate choice’ (choose flashy colors of peacock, etc.)

8. Chi-­Square

² Σ X = E

(O−E)²

• X² means “chi-­squared”. DO NOT take the square root or anything. • O means observed number • E means expected number • Degrees of Freedom number of possibilities minus one (ex. rolling a die 5 degrees of freedom) • P value probability observed results are due to chance • If P < .05 results are NOT due to chance • Null hypothesis predicting that there is NO change

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9. Cladograms/Phylogenetic Trees

“Jaws, lungs, etc.” are traits that distinguish each branch. • Clade bunch of organisms evolved from same common ancestor • There are different types of clades

Monophyletic: complete, all from same common ancestor (all the animals above) Paraphyletic: incomplete, not everyone (just the chimp, mouse, and pigeon) Polyphyletic: different common ancestor (all the animals above + a plant)

II. Biochemistry 1. Bonds Note: Bonds are listed in order of strongest weakest • Intramolecular Bonds hold a single molecule together, covalent and ionic bonds • Covalent Bonds a sharing of valence electrons

Nonpolar (equal b/w two of same atom): O2, H2, etc. Polar (unequal sharing, difference in electronegativity): H2O

• Ionic Bonds giving or taking electrons Need a big difference in electronegativity (NaCl) Cation donates electron, Anion receives

• Intermolecular Bonds attraction between multiple molecules • Hydrogen Bonds attraction between positive (H) and negative (O) poles of water molecules • Van der Waals temporary dipoles from random electron movement, need to be close together So... Covalent>Ionic >>>>>>> Hydrogen>Van der Waals

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2. Why is Water so Special? • Structure polar molecule, easily forms H-­bonds, hydrophilic of course • 4 awesome properties: 1. Cohesion: Water molecules link together with H-­bonds, allows for transpiration pull in plants 2. Moderation of Temperature: High specific heat takes a lot of heat to increase temperature, evaporative cooling (sweating), regulates the Earth’s climate 3. Freezing: ice floats on water, keeps fish and stuff alive, oceans can thaw out during spring/summer 4. ‘Universal Solvent’: forms aqueous solution

3. Acids and Bases • Acid Donates H+ ions • Base Accepts H+ ions (increases OH+ concentration) • Strong acids/bases dissociates completely in water (completely falls apart)

ex. HCL H+ and Cl-­ • Weak acids/bases ionically binds and stuff, does not dissociate completely

ex. H2CO3 H+ HCO3−

Carbonic Acid Hydrogen Ion + Bicarbonate Ion Notice how you get the random clump of crap (Bicarbonate Ion)

• pH scale measures how acidic or basic a solution is • Acids pH 0-­7 • Bases pH 7-­14 • Go up 1 number multiply by 10

4. Carbon and its Isomers • Carbon has 4 valence electrons equal as likely to give or receive • Isomer same chemical formula, different physical arrangement of atoms • Structural different covalent bond arrangements, always single bonds • Geometric double bonded in center (can’t move), X/H can rotate in 3D

Cis: 1st example, Trans: 2nd example (trans = across, like trans-­continental) • Enantiomer same arrangement of atoms, but are ‘mirror images’ of each other, always in tetrahedral shape (3D), also known as “chiral compounds”

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5. Functional Groups

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(Make sure to refresh on these before the AP test/final)

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6. Macromolecules • Dehydration synthesis take out a water molecule, combine two things (anabolism) • Hydrolysis add a water molecule, break things apart (catabolism) • 4 groups of macromolecules Carbohydrates, lipids, proteins, nucleic acids

• Notice that maltose does not follow the 1:2:1 ratio as it loses 2 hydrogens and 1 oxygen in the release of a water molecule • Carbohydrates C, H, O ~ 1:2:1 ratio, sugars end in -­ose • Monomer Monosaccharides • Type of covalent bond glycosidic linkages For energy purposes:

Monosaccharides: single sugar (glucose, fructose, ribose, deoxyribose) Disaccharides: double sugar

Sucrose: glucose + lactose (sucrose table sugar) Maltose: glucose + glucose (amylase breaks down starch maltose) Lactose: glucose + galactose (sugar found in milk)

Polysaccharides: multiple sugars, used for energy storage Starch in plants (don’t move, can store energy long term as carbs) Glycogen in animals (short term storage, fat is for long term)

For structural purposes: Chitin: forms the exoskeleton of arthropods (crabs, bugs, etc.) and fungi cell walls Cellulose: plant cell walls

• Lipids insulation + long term energy storage • Monomer Fatty acids, glycerol, other stuff • Type of covalent bond Ester linkages

Saturated fats: solid at room temperature, 3 fatty acids + glycerol

Unsaturated fats: liquid at room temperature;; 3 fatty acids + glycerol

Steroids: 4 carbon ring things with functional groups Phospholipids: polar head (phosphate) and nonpolar tail

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(fatty acids) 2 fatty acids + glycerol + phosphate Phospholipid bilayer in semi-­permeable membranes

Waxes: long fatty acid + alcohol • Proteins do a ton of stuff • Monomer Amino acids (20 different) • Type of covalent bond Peptide bond • Functions:

Structure (keratin, collagen) Transport (hemoglobin) Enzymes (amylase, lipase, polymerase, etc.) Defense (antibodies, cytokines, etc.) Hormones (insulin) Motion (actin and myosin in muscles)

• 4 Levels of Protein Structure 1. Primary Structure (polypeptide chain of amino acids linked by peptide bonds) 2. Secondary Structure (folding between polypeptides, linked by Hydrogen bonds)

Forms Alpha helices and Beta pleated sheets 3. Tertiary Structure (bonds between R-­groups, forms 3D shape)

Ionic bonds/ Salt bridges from acidic (-­) and basic (+) R-­groups Hydrogen bonds (between -­COOH and -­NH2 and -­OH groups on side chains) Hydrophobic forces between non polar side groups Disulphide bridges (strong covalent bonds b/w sulfhydryl groups in thiols)

4. Quaternary Structure (not necessary, interaction between multiple subunits) • Nucleic Acids (Note: Nucleic acids may no longer be in this unit) encoding, transferring, and expressing genetic information • Monomer Nucleotides (phosphate + pentose + nitrogen base) • Type of covalent bond Phosphodiester bonds • Two types of nucleotides:

Pyrimidines: 1 carbon ring nitrogen bases (cytosine, thymine/uracil) Purines: 2 carbon rings nitrogen bases (adenine, guanine)

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7. Enzymes and Regulation • Enzymes protein catalysts;; lower the activation energy needed for a reaction to take place

Enzymes are reusable. Enzymes bind to specific substrates.

Lock and key model: specific substrate for specific enzyme, binds to active site Induced fit model: more accurate, the substrate induces (causes) the enzyme to align

with the substrate (not a perfect fit) • Denaturing temperature/salt/pH break apart bonds in secondary/tertiary structure

For example, if you have an acid such as Hydrochloric acid (HCl), it might interrupt the H-­bonds of the secondary structure, causing everything to fall apart

Also, raising the temperature can denature enzymes because of either: 1. Going beyond the optimum enzyme temperature (when enzymes are most

efficient) 2. Adding heat which raises the kinetic energy of the enzyme to the point that

bonds begin falling apart • Cofactors non-­protein helper for enzymatic reactions

Inorganic minerals (zinc, iron, copper, etc.) Organic coenzymes (vitamins, etc.)

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• Enzyme regulation in addition to active site, enzymes also have allosteric sites

III. Cells, Membranes, and Transport 1. Surface Area to Volume Ratio • The greater the SA:V ratio is more efficient because more ‘stuff’ can pass through • Smaller the cell higher the SA:V ratio better

2. Cell Organelles • Eukaryotes can have golgi apparatus, mitochondria, vacuole, chloroplast (plants only), cell wall (plants, fungi, etc.), nucleus, ribosomes, endoplasmic reticulum, cytoplasm, cytoskeleton, plasma membrane • Prokaryotes can have ribosomes, cytoplasm, nucleoid, plasma membrane, cell wall, capsule

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3. Organelle Interaction • Let’s follow a protein pathway. For our purposes, the protein has already been synthesized. The process of protein synthesis will be covered in VIII: Protein Synthesis • Proteins are synthesized in ribosomes. Free ribosomes are found floating around in the cytoplasm while bound ribosomes are stuck to the rough endoplasmic reticulum. • Rough-­ER bound ribosomes

Protein is synthesized in ribosome Enters lumen (area within the entire ER) Chaperonin (protein) folds new protein in secondary and tertiary structure Protein travels to Smooth-­ER (parts of ER without ribosomes) Buds off in a transport vesicle towards the Golgi Within the Golgi, travels in cis to trans direction At cis end, enzymes will begin modifying protein by phosphorylation or glycosylation Glycosylation adds/removes sugars. This decides where the protein will go At trans end, the finished protein will exit the Golgi in secretory vesicles If the vesicles fuse with lysosomes, the proteins will be for digestion of stuff

Protein examples: Nuclease, lipase, protease, etc. Stuff examples: Food, antigens, screwed up organelles, etc.

These vesicles can also carry the proteins out or to other organelles The proteins will leave the cell and enter the bloodstream via exocytosis Examples of RER proteins include: hormones (insulin) and digestive enzymes (lipase)

• Free ribosomes

Protein is synthesized in ribosome Receive little amount of modification (compared to RER proteins) Still fold into tertiary structure by chaperonin in the cytosol Cytosol: glycolytic enzymes, Actin for microfilaments (in cytoskeleton, muscles, etc.) Nucleus: histones, transcription factors, etc. very important! Mitochondria and Chloroplast

These organelles actually have their own genome and protein factories Still import most integral proteins (electron transport chain, etc.) from cytosol

Always inside the cell it was produced in!

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4. Prokaryotic vs. Eukaryotic Cells

• Prokaryotes include domains Archaea and Bacteria (E. coli, mold, etc.) • Eukaryotes include domain Eukarya (echinoderms, chordates, plants, etc.)

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5. The Three Domains of Life

6. Origin of Life • Abiotically synthesize small organic molecules (amino acids, hydrocarbons, etc.)

Miller-­Urey experiment “Primordial soup” of methane, ammonia, water, hydrogen, energy NO oxygen present in large amounts (not until plants spread)

• These molecule form big macromolecules (proteins, carbs, lipids, nucleic acids, etc.) • Formation of protobionts (membrane-­enclosed molecules) • RNA World

RNA can replicate, pass down inherited traits (like DNA) RNA can also act like an enzyme as a ribozyme

• Endosymbiosis membrane bound prokaryotes engulf each other, mutually beneficial More efficient (compartmentalized processes) Chloroplasts/mitochondria have own genome, proof for endosymbiosis

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7. Parts of a Plasma Membrane

• Peripheral proteins located on the hydrophilic surface of membrane, responsible for regulating cell signaling, interaction, and other events • Integral proteins embedded within membrane, serve as pumps, channels, and electron transport chains • Cholesterol located within the hydrophobic regions, maintains membrane stability when warm, maintains fluidity when cool • Glycolipids carbohydrate (glyco-­) bound directly to membrane (lipid), provides energy, cellular recognition, • Glycoproteins carbohydrate (glyco-­) bound to a membrane protein (usually peripheral), cell signaling, determine blood type, recognition of self vs. nonself lycolipids Glycoproteins GlycocalyxG + =

Immune system can recognize and attack foreign (nonself) organisms Immune system can recognize and attack cancerous cells Transplant issues

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8. Types of Passive Transport • Concentration Gradient substances, molecules, ions, etc. will naturally travel from high concentrations to low concentrations • Diffusion simply going down the concentration gradient • Osmosis the diffusion of water down its concentration gradient (from high water potential to low water potential) • Facilitated Diffusion still going down the concentration gradient, but traveling through an integral protein channel (ex. ‘leak’ channels for K+ ions)

9. Types of Active Transport • The cell spends energy (ATP) to send stuff against its concentration gradient • Proton pumps pump ions in or out of a cell in order to establish a concentration gradient • Cotransport pump H+ ions, other ions or molecules hitch a ride

10. Types of Bulk Transport • Exocytosis create a vesicle to send stuff outside of the cell • Endocytosis vesicle meets membrane and enters the cell to deliver contents

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IV. DNA Replication and Cell Cycle 1. Scientists and DNA • Griffith Experiment

1. Live smooth bacteria + mouse mouse dead 2. Live rough bacteria (no protective coat) + mouse mouse alive 3. Heat killed smooth bacteria + mouse mouse alive 4. Heat killed smooth bacteria + live rough bacteria + mouse mouse dead Genetic material for coat passed between bacteria transformation

• Avery Experiment: what is the genetic material? Same bacteria as Griffith experiment Isolate potential genetic materials (DNA, RNA, and proteins) Turns out to be DNA!

• Hershey and Chase: what is the genetic material? Bacteriophage: virus which injects its own genetic material into bacteria Protein labeled with radioactive sulfur DNA labeled with radioactive phosphorus Process: infection (phage attaches) blending (break phage off) centrifuge Results: proteins stays in phage, DNA enters the bacteria!

• Chargaff’s Rules: what is the ratio between nucleotide bases? Ratio of AT = CG = 1

• Watson and Crick: what is DNA’s structure? Rosalind Franklin: x-­ray crystallography (picture of double helix) 1953: W&C publish article in Nature magazine Double helix model

2. Nucleotides • Nucleotide phosphate + sugar + nitrogen base • Phosphate creates negatively charged ‘phosphate backbone’ • Purines double ringed bases, adenine and guanine “AG is pur 2” • Pyrimidines single ringed bases, cytosine and thymine • Hydrogen bonds (the ‘ladder rungs’) formed between 1 pyrimidine and 1 purine (bases) • Phosphodiester bonds (covalent) connect nucleotides • A&T 2 hydrogen bonds • C&G 3 hydrogen bonds (C 3rd letter of the alphabet) • Nitrogen bases are hexagonal. Sugars are pentagonal.

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• RNA is older than DNA (think RNA world thing) • RNA is multipurpose (mRNA sends messages, rRNA composes ribosomes, tRNA carries proteins, ribozymes catalyze reactions)

3. DNA Structure • OH 3’ end • Phosphate backbone is negatively charged

4. Prokaryotic vs. Eukaryotic Genomes • Prokaryotes have no nucleus or nuclear membrane

Circular ‘supercoil’ of DNA in nucleoid (like a ball of yarn)

Packed by DNA gyrase Unpacked by DNA gyrase or DNA topoisomerase

• Eukaryotes nuclear membrane During interphase, stored as loose chromatin Positively charged histone proteins + negative DNA strands nucleosome Chromosome (packaged up DNA) is packed by histones before mitosis

• Genome all the DNA present in an organism

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Prokaryotes Eukaryotes

• Single celled • Nucleoid • Simultaneous transcription and translation ofproteins • Haploid/ Monoploid (1 copy of chromosome per gene) • Contains plasmids • No telomeres (circular DNA) • Replicates via binary fission (mitosis)

• Multicellular • Nucleus (membrane-­bound) • Transcription within nucleus (DNA RNA) • Translation in cytoplasm/RER (RNA proteins) • Diploid/Polyploid (multiple copies per chromosome) • Multiple chromosomes • Has telomeres (linear DNA) • Grows and heals via mitosis (body cells) • Gametic cells (sex cells) duplicate via meiosis

5. DNA Replication

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6. DNA Replication and Repair

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7. Mitosis

• Let’s keep a chromosome count!

1. G1 phase somatic cell has 46 chromosomes in 23 pairs of 2 2. S phase 46 chromosomes with 92 sister chromatids 3. Anaphase/Telophase 2 new sets, each has 46 chromatids/chromosomes

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• This is what happens during S phase to duplicate the chromosomes:

8. Cell Cycle Regulation • Regulate cell cycle with protein kinases and cyclin • Cyclin protein that binds with cyclin-­dependent protein kinases (CDKs), which are enzymes • This complex of cyclin + CDK functions as a maturation promoting factor • The MPF activates other proteins via phosphorylation in order to push along the events of the cell cycle • G1 Checkpoint Decide if cell should 1. Divide (mitosis) 2. Rest (G0) 3. Delay (repairs) • G2 Checkpoint p53, other tumor suppressor proteins, make final check before mitosis • M Checkpoint Check that chromosomes line up properly on metaphase plate • p53 tumor suppressor protein, calls in repair cells OR calls for apoptosis (cell self-­destruction) • Proto Oncogenes normally cause and regulate

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cell division, oncogenes (mutated) are the equivalent of a “stuck accelerator”

V. Ecology 1. Ecological Levels

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2. Trophic Levels and Energy Flow

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3. Survivorship Curves

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4. Logistic and Exponential Growth Graphs

• Density-­dependent factors factors that increase as density increases

ex. Competition for food, predation, waste buildup, disease • Density-­independent factors factors whose occurrence is unrelated to density

ex. Floods, forest fire, hurricane

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5. Relationships

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6. Behavior • Operant Conditioning behavior depends on consequences (reward/punish)

ex. Don’t get straight A’s. Asian parents yell at you. • Classical Conditioning associate two things together

ex. Pavlov’s Dogs (ring bell dog salivates) • Fixed Action Pattern/ Sign Stimulus organism has to follow through with response

Receive stimulus or signal (ex. Goose sees egg-­shaped ball outside nest) Action or response (ex. Goose retrieves ball and places it into the nest) Once started, this behavior cannot stop

• Imprinting parents pass on characteristics or behavior to offspring

Can only occur within a short critical period • Taxis directional movement

Move towards a positive stimulus Move away from a negative stimulus

• Kinesis non-­directional movement

Move in random direction Movement slows down or stops once in the presence of a positive stimulus

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7. Biogeochemical Cycles

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VI. Plants and Photosynthesis 1. Photosynthetic Pigments • Each pigment has its own absorption spectrum • Having a greater variety of pigments (and wider absorption spectrum) allows plant to harvest more energy

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2. Light Dependent Reactions • Stroma the ‘cytoplasm’ of a chloroplast (fluid) • Thylakoid one of the poker chip things • Thylakoid space space inside a poker chip • Granum a stack of poker chips • Photosystem integral protein complex, conducts both light harvesting, light reaction, and electron transfer, located in the thylakoid membrane • Photosystem II discovered second, but starts first

Wavelength p680 Water is split donates electrons(2) to PSII, protons for gradient, oxygen released Released energy (electrons) travel down electron transport chain Primary electron acceptor is plastoquinone Cytochrome complex pumps H+ ions from stroma (out) to thylakoid space (in) Creates chemiosmotic (H+) gradient H+ have to leave through ATP synthase Photophosphorylation adds phosphate to ADP to make ATP

• Photosystem I discovered first, starts second Wavelength p700 Receives electrons from PSII

Released energy (electrons) travel down another electron transport chain Primary electron acceptor is ferredoxin Enzyme NADP+ reductase combines NADP+ and H+ to make NADPH

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3. Electron Flow Comparisons • In non-­cyclic / linear electron flow goal is making NADPH with some ATP along the way

Process is described in detail above Reactants: light, water Products: ATP, NADPH, O2 (waste product from splitting water)

• In cyclic electron flow goal is making ATP Only uses Photosystem I Recycles electrons Cytochrome complex, chemiosmosis, and phosphorylation work same way as above

4. 1st Law of Thermodynamics • Basically just says energy will be conserved • What does that mean for photosynthesis? Light energy (sun) Chemical energy (ATP, NADPH, and finally Glucose)

5. Paper Chromatography • You have a pigment and a solvent • Pigments that are soluble in the solvent will travel farther up the paper strip • Pigments that have lower molecular mass will also travel farther up the paper strip

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6. Calvin Cycle (Light Independent Reactions) • What was the purpose of the light reactions?

Make a little bit of ATP Make NADPH (energy ‘truck’) for the Calvin cycle

• The Calvin cycle does not require light to occur • The Calvin cycle takes place within the stroma of the chloroplast

• Carbon dioxide first enters the plant by diffusing through the stomata • 3 carbon dioxides (1C) are ‘fixed’ to 3 RuBP molecules (5C) • This is catalyzed by the enzyme rubisco and creates a 6 carbon compound, which quickly breaks into two 3-­phosphoglycerate (3C) • Next, ATP and NADPH allow for reduction to G3P (3C), which is a sugar • Once you collect 2 G3P molecules, you can form glucose and other sugars • More ATP is used to regenerate the RuBP to accommodate more carbon dioxides

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• Now that we understand what’s going on, let’s take a look at the math: 3 Carbon Dioxide + 9 ATP + 6 NADPH 1 G3P + 9 ADP + 6 NADP+ Note: Double all coefficients if you want to produce a glucose molecule

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7. C3 Plants in Hot and Dry Weather • C3 3 carbons, carbon dioxide creates a 3 carbon molecule (3-­phosphoglycerate) • C3 plants like warm moist climates. Hot and dry weather is bad.

• It’s hot and dry the plant wants to save water! • Where does the water evaporate from? Stomata (openings in the leaves) • So, C3 plants respond to hot and dry weather by closing the stomata • Unfortunately, this also traps O2 in (waste from LR) and CO2 out (what plants like) • Remember rubisco, the enzyme from before? It can also bind to O2. • Now, the plant goes through the process of photorespiration in order to get rid of the O2 • Photorespiration uses up the carbon stores of the plant, wastes energy, and doesn’t do anything • This is bad. That’s why plants in hot and dry climates have evolved ways to cope (they join support groups)

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8. C4 Plants in Hot and Dry Weather • C4 plants have evolved to spend a bit more energy to limit water loss in arid conditions • C4 4 carbon compound • There is spatial separation between mesophyll and bundle sheath cells

• Rubisco is replaced by PEP Carboxylase (only binds to carbon dioxide, not oxygen) • 3-­phosphoglycerate is replaced by Oxaloacetate (are 4 carbon compound) • This is then stored as malate / malic acid • Now we move from the mesophyll to the bundle and sheath cells for the Calvin cycle • Pyruvate is recycled while CO2 can now go into the normal Calvin cycle

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9. CAM Plants in Hot and Dry Weather • CAM plants have temporal separation time (night and day) • Same thing as C4 plants with oxaloacetate and everything, but instead of separating by cell, CAM plants separate by time

10. Roots, Stems, and Leaves • Roots

1. Absorption of water and nutrients (root hairs increase surface area for this) 2. Anchoring the plant body to the ground 3. Storage of food and nutrients as starch (carbohydrates)

• Stems Carry water and nutrients from roots (source) to destination (sink)

• Leaves

Stomata (openings) allow water to evaporate, CO2 to enter, and O2 to exit Main photosynthetic surfaces

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11. Adhesion-­Cohesion-­Transpiration Mechanism • Water Potential = Solute Potential + Pressure Potential • Pressure potential pressure exerted by the cell wall against its contents • Solute potential more solute means a lower solute potential • More solute added solute potential becomes more negative water potential also becomes more negative • Water moves from high water potential low water potential

12. Stomata and Guard Cells • What affects transpiration rates? • Humidity increased water potential outside of the stomata reduces the rate of transpiration • Wind wind removes the ‘boundary layer’ of still air immediately outside the leaf. This increases the rate of transpiration • Waxy cuticle hydrophobic, thicker cuticle reduces the rate of transpiration • Temperature warmer air holds more water, so pseudo “less humid”, so increases rate of transpiration • Light stoma open in the light so that light dependent processes can take place Thanks for reading! Once again, the second semester review guide can be found here.

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A Comprehensive Guide to AP Biology (cont’d) by Brian Lin

Table of Contents VII. Cellular Respiration (pages 2-­9) VIII. Protein Synthesis (pages 10-­16)

IX. Meiosis and Inheritance (pages 17-­19) X. Gene Expression (pages 20-­21) XI. Immune System (pages 21-­23) XII. Cell Signaling (pages 24-­31)

Alright, so I need your help here! After unit VIII, I basically stopped taking notes. First reason was because... well you know, I didn’t want to. Second reason was that my teacher gave us those Power Point print out notes (the ones with like 6 hard-­to-­read slides per page). But most importantly, and I cannot emphasize this enough, I switched over to taking my notes on my Bio diagrams, call it ‘annotating’ if you will. I am a heavily visual learner and found that I could learn just as well (with a lot less effort/work) simply by annotating diagrams, watching Wiki videos, paying attention in class, and answering other people’s questions. So if you have GOOD notes, either in print (send ‘em to me and I’ll post them here) or on paper (I have a scanner at home) I’ll be happy to share them with everyone else unless they suck. If they’re on paper and you have crappy handwriting, forget it. No one can physically read that (lookin’ at you Pulkit). Also, if you have super crappy formatting with stuff you type out (still lookin’ at you Pulkit) then forget it as well. In my opinion, notes are supposed to be super compact and concise and meant for looking at in-­between classes/during classes/etc. I don’t want you sending me paragraphs of notes... save it for English class or Facebook rants. Anyways, in order to finish up this guide, I’ve recruited the help of Chris Yao and Pulkit Kashyap... I’ve merely edited/touched up/reformatted their stuff for Units IX.-­XII. Have fun. Actually, I gave up on XII since Pulkit’s notes are impossible. So please, send me yours to replace those units!

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VII. Cellular Respiration

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Anaerobic: don’t need oxygen present to occur Takes place in the cytoplasm

Since we’re going from big molecule (glucose) to small molecule (pyruvate), this is a catabolic reaction. Show me the math: x1 Glucose (6C) x2 Pyruvate (3C) x2 ATP x4 ATP (+2 ATP Net) x2 NAD+ x2 NADH Phosphofructokinase (enzyme): lots of ATP ATP binds allosterically to phosphofructokinase

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shuts phosphofructokinase down (feedback inhibition of an enzyme)

No oxygen? Diagram below. Yes oxygen? Next page.

What’s the point of anaerobic fermentation? It empties the energy trucks (2 NADH 2 NAD+) while creating a little bit of energy (ATP) (Note: You CANNOT do glycolysis without the empty energy trucks) This is OKAY for yeast and other little organisms who can live off the +2 ATP. However, big things have to use aerobic respiration to get enough energy out of glucose +26-­28 ATP.

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Okay, so we got some pyruvate. That still has lots of energy inside. But first, we need some more energy trucks (NADH and FADH2) The Krebs will do that, but we need to make pyruvate ready for Krebs. That’s the Bridge Reaction.

Bridge Math Pyruvate (3C) + Coenzyme A

Acetyl CoA (2C) + CO2 (1C) NAD+ NADH *Multiply by 2 for both pyruvate molecules

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Citric Acid/Krebs occurs in the mitochondrial matrix (random space inside cistae) Goal: Create tons of energy trucks (NADH + FADH2)

Krebs Math Acetyl CoA (2C) x2 CO2 (1C) x3 NAD+ x3 NADH FAD FADH2

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Aerobic: need oxygen or won’t happen We’re going through a series of redox reactions in which we are oxidizing and reducing molecules, ending with oxygen, the final electron acceptor. Note: Lose electron oxidize

Gain electron reduce “LEO says GER”

1. NADH and FADH2 arrive at the mitochondrial membrane (top row of circles is the outer bottom is the inner) 2. NADH arrives higher up in the electron transport chain. Therefore, it can pump more H+ across the membrane, effectively synthesizing 3 ATP. 3 FADH2 arrives lower down the electron transport chain. Therefore, it can pump ⅓ less H+ across the membrane, effectively synthesizing 2 ATP. 4. Pumping H+ across the membrane creates a chemiosmotic gradient. Because charged ions cannot simply diffuse across the membrane, they must diffuse across ATP synthase (integral protein) via facilitated diffusion. 5. This drives the reaction ADP + P ATP The electron transport chain creates a lot of ATP. Around 26-­28 molecules of ATP. If you don’t like my crummy drawing, go to the next page for a diagram.

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AMP (a cell resp. reactant) stimulates glycolysis ATP/Citrate (cell resp. products) inhibit glycolysis Next page has some general overviews of where all the products and reactants come from and go to.

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VIII. Protein Synthesis

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1. Central Dogma DNA (transcription) RNA (translation) Protein (processing) DNA strand is always read in the 3’ to 5’ direction. Thus, RNA polymerase builds mRNA in the 5’ to 3’ direction. AUG is the start codon (methionine) Codon: a 3 nucleotide sequence (note: Uracil replaces Thymine in RNA sequences) Bottom strand of DNA is called the template strand Top strand of DNA is called the coding strand mRNA: messenger RNA that leaves the nucleus for a ribosome in order to code for a polypeptide tRNA: transport RNA that carries amino acids from cytoplasm to ribosome, has complimentary anti-­codon to the mRNA rRNA: ribosomal RNA that makes up the ribosome’s subunits

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2. Why is Redundancy Important in Codons? As you can see in the diagram, there are usually 4 different codon sequences that can code for the exact same thing. This means that a point mutation (substitution) from ACU to ACC won’t screw you up. This is known as a silent mutation because you don’t notice any change. That variation in the 3rd base pair is known as wobble. Of course, some codons such as AUG (start) do not exhibit any redundancy and this can be problematic.

3. Transcription Once again, transcription involves us copying DNA to mRNA within the nucleus. There are 3 main steps to transcription: 1. Initiation Before DNA can be copied, the copier, RNA Polymerase must bind to the DNA strand at the promoter region (specifically at the TATA box). In order for RNA Polymerase to bind, you need a bunch of transcription factors. This provides an effective means for gene regulation (please see X. Gene Regulation for further detail) 2. Elongation DNA is unwound by transcription factors. RNA Polymerase then transcribes a single strand of mRNA complementary to the template DNA strand. 3. Termination RNA Polymerase and completed mRNA disconnect from the DNA strand upon reaching the termination sequence.

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Ok, so at this point, we got a complete mRNA strand. However, we only want the parts of it that are important-­ the coding regions (known as exons). The non-­coding regions are introns. So, how are we going to cut the introns out? mRNA editing Spliceosome (a complex of SNRPs) cuts introns out A poly-­Adenine tail is added (to 3’ end) A 5’ methylated cap is added

4. Translation 1. Initiation Assemble ribosomal subunits out of rRNA AUG is the start codon 2 subunits: large on top, small on bottom 5’ end enters first 2. Elongation Amino acids added to tRNA by Aminoacyl-­tRNA synthetase (an enzyme) Amino acid chain assembled out of the P-­site New amino acids carried by tRNA join to the complementary codon on the A-­site tRNA and mRNA exits via the E-­site 3. Termination Stop codons (UGA, UAA, UAG) signal the ribosomal subunits to break apart, releasing the completed polypeptide (string of amino acids)

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5. Post-­Translational Protein Editing • Rough-­ER bound ribosomes

Protein is synthesized in ribosome Enters lumen (area within the entire ER) Chaperonin (protein) folds new protein in secondary and tertiary structure Protein travels to Smooth-­ER (parts of ER without ribosomes) Buds off in a transport vesicle towards the Golgi Within the Golgi, travels in cis to trans direction At cis end, enzymes will begin modifying protein by phosphorylation or glycosylation Glycosylation adds/removes sugars. This decides where the protein will go At trans end, the finished protein will exit the Golgi in secretory vesicles If the vesicles fuse with lysosomes, the proteins will be for digestion of stuff

Protein examples: Nuclease, lipase, protease, etc. Stuff examples: Food, antigens, screwed up organelles, etc.

These vesicles can also carry the proteins out or to other organelles The proteins will leave the cell and enter the bloodstream via exocytosis Examples of RER proteins include: hormones (insulin) and digestive enzymes (lipase)

• Free ribosomes

Protein is synthesized in ribosome Receive little amount of modification (compared to RER proteins) Still fold into tertiary structure by chaperonin in the cytosol Cytosol: glycolytic enzymes, Actin for microfilaments (in cytoskeleton, muscles, etc.) Nucleus: histones, transcription factors, etc. very important! Mitochondria and Chloroplast

These organelles actually have their own genome and protein factories Still import most integral proteins (electron transport chain, etc.) from cytosol

Always inside the cell it was produced in!

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6. Mutations Mutation: a change in DNA during DNA replication, allows for methods of evolution Evolution: a change in allele/gene frequency Mutations arise from 1. DNA replication copying errors or 2. External factors (ie mutagens) There are 2 categories of mutations, point mutations and chromosomal mutations Point: (1 base pair)

Substitution Silent (Redundancy) Missense (Wrong amino acid) Nonsense (Stop codon)

Insertion or Deletion Adding in/ removing amino acids Can lead to a frameshift

Chromosomal: (change in entire chromosome) This can be a change in structure (losing part of it) or number (monosomy, etc.)

7. Universal Genome All domains of life share central genetic code (DNA). All domains of life share similar metabolic pathways. Just read Big Idea #1.

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IX. Meiosis and Inheritance Content courtesy of Chris Yao... with quite a bit of editing by yours truly.

Asexual Reproduction Sexual Reproduction

One parent Cell division by fission (mitosis),

budding, or regeneration Very efficient (think of bacteria

multiplying) Population vulnerable to being wiped

out due to lack of genetic variation

Two parents Gametes (egg and sperm) are both

haploid (single set of chromosomes) Gametes form a zygote (egg +

sperm) Genetic variation due to combination

haploid cells

Genetic variation

Crossing Over-­ alleles of two chromatids next to each other switch, so outer chromatids have alleles of the parent while the inner chromatids have the new mixture, therefore reproduction will yield new offspring.

Random Fertilization-­ 8 million potential ovum x 8 million sperm possibilities = trillions of potential zygotes.

Law of Segregation-­ Only one allele from each pair of alleles mixes in with the other alleles;; i.e. punnett square of Aa vs AA will yield 4 different types of alleles because each half of the alleles segregates and binds on its own.

Karyotypes

A picture of a cell’s chromosomes during the metaphase of mitosis. Chromosomes are in homologous pairs, starting with the smallest (1) and ending with

the sex chromosomes (23).

Mitosis Meiosis

Creates all of your non-­sex body cells (for example, new skin cells)

Genetically identical offspring (basically clones)

Note: Due to random mutation, there may still be very slight genetic variation

Chromosome number remains constant

Creates gametes for sexual reproduction

Allows for genetic variation (In humans) chromosome number is

halved from diploid to haploid

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Mendel’s Laws

Law of Segregation ⇒ Each gamete (sex cell) carries one allele (version of a gene). Each offspring then gets 1 allele from each parent for a total of 2 alleles (such as dominant brown hair from dad and recessive blonde hair from mom).

Law of Independent Assortment ⇒ Separate traits are inherited independently from each other. For example, your height and your eye color are coded for by different genes.

Law of Dominance ⇒ A dominant allele will take priority/override a recessive allele.

You should also know how to do Punnett Squares and Family Trees/Pedigrees/etc. This is some pretty basic stuff really. So pay attention in class and practice as much as you can. There aren’t any ‘tricks’ really, so I’ll leave you on your own here. Basically, I didn’t take notes for this part of the unit. And I’m not about to do so now, in August, when I have much better things to do. So once again, you’re on your own for this. Seriously, it’s not hard. Just pay attention in class and do your work. Okay fine. Even though I still refuse to put more effort into this, I happen to still have some examples that I can share with you. Also, some very important terms to know and definitely not to confuse (such as incomplete dominance and co-­dominance). Here’s the quiz (on dominance, I believe). Not only is it embarrassing but very silly and immature as well. Have fun. Don’t say I didn’t warn you. And no, there are no answers. That’s because you must take pride in your learning (ie I lost the answer key or there never was one).

Huntington Disease (Dominant) David Chen, Jay Wang, and Brian Lin

1. If Will-­da-­beast and Will-­powa-­showa, both with homozygous Pikachupacabra disease (dominant), have a child;; what is the probability that the child expresses the traits of the disease? 2. Sergei and Abby have a child, King Alfonso, and King Alfonso has a dominant disorder that makes him smile uncontrollably and is heterozygous. Give one possible set of alleles that Sergei and Abby could have so that the chance of their child having this smiling disorder is ½. 3. Little Ignoff has heterozygous Midas Touch disease (dominant), while his sister, Little Van Hindschtechtz, has the homozygous form of the disease. Give a possible set of genotypes for

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their parents, Sally and Bob. 4. Fill in the blanks! H = dominant h = recessive 5. The ultimate question: The members of the Chen family are affected by both hair color and Hokey-­Pokey disease (dominant). The father, Phat Dadda “Pkash” Money (the original Bile-­o-­G gangsta), has fluorescent purple hair (dominant) but does not express any alleles for Hokey-­Pokey disease. The mother, Val Mart-­Agupta, has normal brown hair (recessive) but has the dominant allele for Hokey-­Pokey disease. What is the probability that their new child, Alfred the Undulator, will have both purple hair and hokey-­pokey disease?

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X. Gene Expression Once again, written by Chris Yao, edited by me.

In Vivo Cloning In vivo (use dat spanish) = cloning within a living organism (in our case, using a bacteria

as a ‘factory’ of sorts to produce specific proteins!) Compare to In Vitro, which is cloning within a glass test tube (the Polymerase

Chain Reaction stuff you learned about) Class example = AMP experiment Isolate mRNA for desired gene... since it’s mRNA, there are no exons. Use reverse transcriptase to create cDNA from the mRNA template. Use a restriction enzyme to cut the plasmid once and the ends of the gene of interest

twice. Combine plasmid and gene of interest. They will be attracted to each other since the

sticky ends (cut by the restriction enzyme) will be complementary. Ligase will seal with covalent bonds (phosphodiester). Now that our gene has been successfully introduced into the bacteria’s plasmid (a

chromosome), the bacteria will start producing whatever we wanted it to! Microarrays

Using reverse transcriptase and DNA polymerase cDNA is synthesized from a RNA template (typically mRNA from the cells of interest), binds with certain ssRNA in the microarray, the ones that bind glow under the fluorescence detector, indicating that these are the genes expressed.

Operons

Promoter is like a door knob, promoters of many operons are similar, like a keyhole because only a specific regulatory protein binds it.

Co-­repressor ⇒ binds to repressor to help prevent transcription of the gene Repressor ⇒ prevents transcription of the gene by blocking the attachment of RNA

polymerase Activator ⇒ protein that increases gene transcription

Types of Regulation Please just use your class notes (ppt. slides) + diagrams for this... SO MUCH easier. Inducible (lactose)

The system begins as off. However, it can be induced (aka turned on). Repressor starts off attached to the operator (that’s why it’s off). Under certain conditions, the repressor will be removed, turning the system on.

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Repressible (tryptophan)

The system begins on. However, it can be repressed (turned off). When the levels of the expressed gene exceed the needs of the cell, the repressor

activates and inhibits expression. When trp levels are high enough (and you therefore need to get rid of it), activators bind

to the repressor to get it off. Positive

cAMP accumulates when glucose is scarse used to activate CAP CAP is a regulatory protein ⇒ activator when cAMP is low cap stops activating

Methylation

Addition of methyl caps to histones prevent expression Histone Acetylation

Add more space, make expression more likely to happen RNAi

siRNA-­ Small interfering RNA that degrade a specific mRNA upon recognition (RISC ) siRNA made from dsRNA using a dicer, which dices the dsRNA into siRNA RNAi can abolish gene function of specific genes, because they are created in vitro

(shRNA/siRNA), RNAi allows us to control timing Applications include gene therapy, Problems include stability, delivery, toxicity, off target miRNA is like siRNA but longer, made using dicers and takes out homologous mRNA

XI. Immune Response Content courtesy of Christopher Yao, edited by me.

I happened to have some book on the Immune System so I never had to take notes for this.

Pathogen ⇒ a disease causing infectious agent such as a bacteria, fungi, virus, etc. 1. Levels of Defense First level of defense physical and chemical barriers that prevent a pathogen from infecting cells ie) skin, stomach acids, mucous, enzymes, cough reflex, etc. non specific Second Level of defense also known as non specific immune response or innate immune

Inflammatory response upon detecting an infection, mast cells release histamines

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causing vasodilation Vasodilation⇒blood vessels and capillaries increase in diameter allowing

phagocytes easier access to the infected cells, this causes swelling and redness Phagocytes⇒Neutrophils, eosinophils and Macrophages all are phagocytes that

eat infected cells Cytokines ⇒ chemicals released by cells for cell to cell communication, ie) Helper

T Cells release Cytokines to activate B cells. Pyrogens ⇒ chemicals released by phagocytes that cause fevers in an attempt to

denature invaders through heat Interferons ⇒ infected cells also release interferons which are the cytokines that

Third Level of Defense specific immune response

Macrophages, after eating infected cells, uses MHC to present antigen fragments on their surface

Helper t-­cells become activated if they recognize the antigen fragments Helper t-­cells activate the killer T cells (AKA Cytotoxic T Cells) and B cells

Humoral Response

Plasma B cells (activated B cells) produce antibodies which bind onto their respective antigen (specific)

Antibodies are Y shaped proteins that bind onto an antigen, they then either mark the antigen for destruction (via killer t-­cells for example) or they can block the pathogen from further spreading.

Cell Mediated Response Cytotoxic t cells Helper t cell binds to macrophages presenting a virus on its mhc Activates cytotoxic t cell for that specific infection, finds all cells with that infection

and kills them using perforin Humoral vs Cell Mediated-­ What’s the Difference?

Cell mediated is a direct attack versus humoral which marks for an attack later both produce memory cells which remain for second incidence part of acquired immunity

Passive Immunity Natural: Transfer of antibodies from mom to child during pregnancy Artificial: Addition of antibodies through some other means to an individual

who cannot create the necessary antibodies Active Immunity

Natural: Exposure to a pathogen and going through b cells/t cells Artificial: Being ‘infected’ through a vaccine which stimulates the body to

create the necessary antibodies/memory cells for future attacks The thing you just read (passive/active) confuses a lot of people. Let me (Brian) elaborate a little. Passive immunity means that you get antibodies.

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Active immunity means that you make antibodies. Here’s an analogy: Passive immunity is like getting $100 for your birthday as a gift whereas active immunity would be like getting a job so that you can continually make money. Natural means that no voodoo science stuff is going on. Artificial means that we ‘use science’ (whatever that means) to create the immunity (such as getting a shot).

HIV

Destroys the body’s ability to fight disease by disabling helper t cells. Blood Type

People can only take in specific blood types that match with their own Each blood type has a specific antigen on their surface and antibodies around them.

ex. Type A blood is marked with ‘a’ antigens but has antibodies that destroy stuff marked with ‘b’.

AB is a universal receptor, O is a universal donor. If you have both A and B blood, then you’ll recognize everything. If you have type

O, you can only recognize type O blood. Allergies

Body detects non-­self (such as some pollen) and releases histamine to fight something that’s not even dangerous.

This causes inflammation and all the other typical allergy symptoms. Organ Transplantation

Organs need to be accepted by the host, otherwise they will be destroyed as non-­self. Body uses the MHC to identify self vs non-­self.

Autoimmune Disorders

Body somehow confuses self with non-­self and begins destroying self cells.

XII. Cellular Signaling

Content courtesy of Pulkit. However, I could tell that he copied it from somewhere else because the formatting was absolutely atrocious. In order to attest to this, I’m leaving it as is so you all can suffer unnecessarily. Hahaha. But seriously, I’m not about to spend an hour fixing this mess so

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pay attention in class and make your own notes lol. I tried fixing this page (added the bullet points, the original picture was absolute crap since you couldn’t read any words, but then I realized that this stuff is basically worse than the textbook so I’m reaching out to you guys for help here).

Long Distance Neurons = Electrical signals (chem for short paths), used for regulation

and information Dendrites-­ branched extensions that receive signals Axon-­ extension that transmits signals to other cells (information);; branched at one end,

hillock at other Cell Body-­ where neurons organelles are located Axon Hillock-­ signals that are transferred down the Axon generated here Synaptic Terminals-­ Branched ends of the axon, neurotransmitters transmit information

from the axon to the receiving cell from here;; the cell sending the signal is presynaptic, postsynaptic is the cell that receives. Dendrite conc.= synapse conc. Electrical synapses are rare but serve for really fast reactions. Usually chemical reactions. Presynaptic neuron packages and transports its neurotransmitters in synaptic vesicles towards the terminals of the recipient neuron. This change in action potential causes the neurons membrane to become permeable because it depolarizes which in turn means Ca+2 concentration goes up and then that causes some vesicles to fuse and dump their contents in the receiving neuron

Myelinated neuron-­ sheets that surround axons (produced by oligodendrocytes) -­> electrical insulation, space eficient

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Unmyelinated neuron-­ slower, travels in waves Sensory Neurons-­ transmit information from eyes and other sensors that detect external stimulation (light, sound, touch, heat, smell, taste) Motor output-­ necessitates nerves (bundles of neurons) to make muscles function properly CNS-­ brain and longitudinal nerve cord, integration up here (analyzing and interpreting the sensory information) Peripheral-­ send and take out information from the CNS

Brian edit: What is going on here?

Neurotransmitters have more than a dozen diff. receptors Sodium-­Potassium pumps are used for the maintenance of resting potential. They send out NA+ and bring in K+. Clusters of proteins make ion channels. These ion channels are selectively permeable to NA+ or K+ depending on the channel. K+ is taken out , leaving a negative charge behind, and NA+ comes in, the movement of these charges causes the generation of potential. The buildup of negative charge behind the movement of K helps create the membrane potential Eion = 62 mV ( log ([ion outside]/ [ion inside] )) Gated Ion channels open or close in response to stimuli when neurons are active. This in turn means that membrane potential changes (and permeability changes). Ex. Resting neurons k+ ion channels open up again, making it more negative, polarity goes up (hyperpolarization-­> increases the outflow of positive or in flow of negative ions, either way end result is a negative inside). Depolarization-­ reduction of membrane potential by opening gated sodium channels, these are graded potentials a bigger stimuli = bigger change. These have a major effect on the generation of nerve signals. Voltage gated ion channels open or close to a change in the membrane potential. If depolarization opens voltage-­gated sodium channels, then the resulting flow of Na+ causes more depolarization which opens more gates which in turn opens more gates and all of this changes the membrane potential , called an action potential. Action potentials are transmitted along the axon, occur whenever membrane voltage gets to the threshold, act independently of stimuli and are an all-­or nothing (happen or do not happen). During this period, the sodium channels close up till after the undershoot. Therefore if a stimuli occurs during the undershoot period no action potential will occur, this is called the refractory period. When an action potential is generated, it can only move towards the synaptic terminals because the area behind the generation point (the hillock) prevents another potential from being formed. Action potentials go as far as the synpases which allow the current to flow from one neuron to another Synaptic Terminals-­ Branched ends of the axon, neurotransmitters transmit information from the axon to the receiving cell from here;; the cell sending the signal is presynaptic, post synaptic is the cell that receives. Dendrite conc.= synapse conc. Electrical synapses are rare but serve for

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really fast reactions. Usually chemical reactions. Presynaptic neuron packages and transports its neurotransmitters in synaptic vesicles towards the terminals of the recipient neuron. This change in action potential causes the neurons membrance to become permeable because it depolarizes which in turn means Ca+2 concentration goes up and then that causes some vesicles to fuse and dump their contents in the receiving neuron Ligand gated ion channels are clustered in the membrane of the post synaptic cell, binding of the neurotransmitter to a particular part allows specific ions to diffuse across the membrane. Post Synapatic Potentials-­ vary depending on the concentration of neurotransmitter sent, the potential degenerates as it gets farther from the synapse. ESPS is too small to effectively generate a reaction Temporal summation-­ two ESPS occur at once almost (one happens and then another happens before first done) – same synapse Spatial summation-­ different synapses-­ but made simultaneously Excitatory -­ bringing membrane potential closer to threshold (cap) Inhibitory-­ taking away from threshold (cap);; It’s almost like a cycle. One neuron sends a signal via neurotransmitters to another neuron. The connection of neutransmitters to the post synaptic cell’s membrane causes channels to open that depolarize the cell, this depolarization causes excitatory postsynaptic potential which brings the cells potential up to the threshold. When this happens to twice in one synapse, its called temporal separation and can cause an action potential to be generated. When this happens with two different synpases at the same time, an action potential is generated. The generation of an action potential then gets the axon hillock to transmit it down the axon to the synpases which in turn starts the cycle all over again with another cell, ISPS (hyper polarization) can lower the threshold and balance out with the ESPS. REFLEX ARC Reflexes-­ the body’s automatic response to certain stimuli, produced by spinal cord Ex: touching a hot stove, knee buckling, hitting knee w/ hammer How knee-­jerk reflex response works: 1) Muscle is tapped 2) Sensory Neurons detect a sudden stretch in quadriceps muscle 3) Information is conveyed by these sensory neurons back to the spinal cord (white matter) 4) Motor neurons, thanks to this information, signal the quadriceps to contract 5) In the meanwhile, sensory neurons are also communicating with inter neurons to prevent inhibition of the reflex Spinal Cord runs to and fro the brain, therefore it generates basic patterns of locomotion/movement CNS/PNS

Describe how the nervous system components work together to maintain homeostasis.

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Define the functions of the CNS and PNS (include the following: brain, spinal cord, autonomic nervous system, somatic nervous system, interneurons, sensory neurons). Brain-­ contains white matter on the inside, used predominantly for signaling, sensory information processing, feeling emotions, generating commands, and gray matter consists mainly of neuron cell bodies, dendrites, and unmyelinated axons. Integrates sensory neuron information;; Spinal Cord-­ white matter on the outside, used for transmitting information from CNS to sensory/motor neurons of the PNS;; generates basic patterns of locomotion (reflexes too) Astrocytes-­ Provide structural support for neurons and regulate the extracellular concentrations and neurotransmitters. Astrocytes cause blood vessels to dilate which increases the flow of oxygen to neurons, they create the blood-­brain barrier, radial gilia help move the new neurons from the neural tube Cranial nerves-­ connect the brain with locations in organs of head/upper body, some are afferent only i.e. the one for smell (Peripheral) Spinal nerves-­ run between spinal cord and parts of the body below head (Peripheral) Afferent-­ The Sensory neurons that tell the CNS whats going on, Efferent = the neurons that tell the muscles what to do (motor) Motor System (Somatic) -­ consists of neurons that carry signals to skeletal muscles, mainly in response to external stimuli, it is voluntary since we can consciously control it, but there is also a major reflex aspect to it. Autonomic nervous system-­ regulates internal environment by controlling smooth and cardiac muscles ;; Controls the organs of the digestive, cardiovasulcar, excretory, and endocrine systems;; involuntary control, three divisions-­ sympathetic, parasympathetic, and enteric-­ Sympathetic division—energy generation (“fight or flight” response-­ heart beats faster, digestion is inhibited, liver converts glycogen to glucose, adrenaline. parasympathetic division-­ calming, return to self-­ maintenance functions (rest and digest) **need relation to homeostasis** T6-­ Hypothalamus-­ endocrine gland in brain;; receives information from nerves throughout the body and from other parts of the brain. It initiates endocrine signaling appropriate to environmental conditions;; Pituitary Gland-­ a gland located at base of hypothalamus, size and shape of lima bean, two parts (posterior and anterior). Posterior-­ Extension of hypothalamus that grows downward towards the mouth, stores and secretes two hormones made by the hypothalamus;; releases oxytocin and antidiuretic hormone;; hormones released travel along the axon’s of the neurosecretory cells to the posterior pitiuary. Impulse stimulates a neurosecretory cell to release neurohormone which diffuses into bloodstream. (nerve impulse from hypothalamus making oxytocin get released).oxytocin-­ regulate milk release;; Anterior-­ regulated by hormones secreted by the hypothalamus;; Anterior pituitary hormones are all controlled by some hypothalamus hormonone which determines their release (the hormones from the hypothalamus are released near the base by capillaries

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which in turn go into portal vessels which then go into another layer of capillaries by the anterior pituitary. Brian edit: WTF is with this picture? Why would you stretch it out to the point where no one can read it?

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Long distance regulators: Animal hormones are cheimcal signals that are secreted into the circulatory system and commnicate regulatory msgs within the body hormons reach all parts of body, but only target cells have receptors of that hormo

What Is a hormone-­ secreted cells that serveto maintain homeostasis, mediate responses to environmental stimuli, regulate growth, development, and reproduction. Hormones coordinate the body’sr esponse t ostress, dehydration, low blood glucose;; control appearances. COME FROM ENDOCRINE SYSTEM!! Insulin-­ Hormone. Polypeptide. Cleavage of longer protein chain forms insulin;;

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Epinephrine & Thyroxine are amine hormones which come from an amino acid;; Cortisol-­ lipids that contain four fused carbon rings Polypeptide/Amine hormones are water soluble while Steroids are lipid soluble (membranes are hydrophobic so they let the steroids diffuse through but don’t let the polypeptides through) Protein Hormones: -­Receptors on the outside, on the plasma membrane -­ Secreted by exocytosis, bind to the receptor on the outside, and initiate a change in gene transcription (serve as transcription factors for the mRNA, allow it to translate -­ signal transduction: converting the extra-­cellular signal (the binding of the hormone to the receptor) to a intracellular response (change in transcription etc.) -­second messenger: ex. cAMP, activates protein Kinase A which leads to activation of an enzyme required for glycogen A breakdown and inhibits the synthesis of more glycogen which in turn releases more glucose via the liver into the blood which helps you chase the bus (example provided based on hormone epinephrine) Hormone binds to G protein coupled receptorà releases G protein(uses GTP for transport)-­à gets to Adenylyl Cyclaseà bind and w/ help of ATP make cAMPà activates protein kinase Aà (in the case of epinephrine) activates the inhibition of glycogen synthesis & the promotion of glycogen breakdown

Steroid Hormones: -­Receptors are located within the cell -­bind to intracellular receptors, cause gene transcription changes, go through the plasma membrane

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-­ hormone binds to receptor, this directly activates cell response (directly regulate gene expression usually), bind to DNA (in nucleus) and transcribe certain parts of mRna i.e. binding of estradiol leads to the transcription and translation of Vitellogenin which goes to the reproductive system in birds for egg yolk production NEED: SHORT DISTANCE (WATER SOLUBLE) + LONG DISTANCE (LIPID SOLUBLE)

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