Edexcel Biology as Revision Notes

Edexcel AS Biology Revision Notes Written by Tim Filtness

AS Biology Revision NotesAS Biology Revision NotesAS Biology Revision NotesAS Biology Revision Notes

“Science is organised knowledge. Wisdom is

organised life” - Kant

Merchant Taylors’ School


Understanding the jargon:

1. The 9 Core Practicals are not discussed here. Don’t forget to revise them too!

2. All Key Words are given underlined in red, these are words specifically mentioned on the syllabus!

3. There are many blue “How Science Works” boxes in the text book. In past years these have almost always been the basis of a number of exam questions...

A word of caution

These revision notes are designed to help you, NOT do the job of revision for you. Ultimately, only you can learn this material: you can’t pay, cajole or persuade anyone to do it for you! Additionally, these notes are the bare bones (your text book and class notes are almost certainly better sources of information if you’re aiming for the highest grades). So treat these notes as a minimalist approach for someone aiming for a solid B grade. At this point you might want to get your own notes to cross-reference with the material here. Why not add your own annotations to improve what’s already here?


Unit 1: Lifestyle, Transport, GenesUnit 1: Lifestyle, Transport, GenesUnit 1: Lifestyle, Transport, GenesUnit 1: Lifestyle, Transport, Genes & & & &

HealthHealthHealthHealth Topic 1: Lifestyle, health & Risk 1.1.2

Water molecules are polar

H = Positively charged (δ+) O = Negatively charged (δ-) This allows them to form Hydrogen

Bonds with other water molecules. This gives water some useful properties;

Property Explanation

Less dense as a solid Arctic ecosystems float, ice insulates water beneath it etc

High SHC Cells do not heat up or cool down easily, therefore can hold a fairly stable temp. (cf enzymes)

Present naturally in all three states

Allows the water cycle to function

Transparent Allows photosynthesis underwater

Cohesion Generates surface tension, capillary uptake, transpiration etc

Good solvent Essential role in transport in biological systems

Immiscible with hydrophobic molecules

Allows membranes to form and, therefore, control movement in / out of cells

High latent heat of evaporation

Evaporation of water has a strong cooling effect and comparatively little water is required to lose a lot of heat

Buffer Water is capable of accepting and donating protons, therefore acts as a buffer

Edexcel AS Revision


1.1.3 Saccharides are made from sugar molecules, which are made from combinations of the elements Carbon, Hydrogen and Oxygen only

Saccharides are used for;

1. Fuels for respiration (e.g. glucose) 2. Energy storage molecules (e.g. starch and glycogen) 3. Structural molecules (e.g. cellulose)

Monosaccharides – one sugar molecule only Disaccharides – two sugar molecules joined together Oligosaccharides – a few sugar molecules joined together Polysaccharides – many sugar molecules joined together You need to know the different structures of glucose. You should be able to draw this out if requested.

Disaccharide Name Component monosaccharides

Maltose Glucose + Glucose

Sucrose Glucose + Fructose

Lactose Glucose + Galactose

α Glucose Β Glucose

H

OH


There are three polysaccharides specifically mentioned on your syllabus (starch, glycogen and cellulose). Cellulose is in Topic 4 (2.4.3) but is included here for reference.

Polysaccharide Structure and Function

Glycogen

1. Made from Poly (α Glucose).

2. Found in muscle and liver cells for energy storage

3. Insoluble, so no osmotic effect in tissues

4. Lots of branches (i.e. 1-6 glycosidic bonds present), which allows quick access to glucose

5. Compact shape, so good for storage

Starch

1. Actually made from two molecules in combination; Amylose and Amylopectin

2. Both are made from Poly (α Glucose).

3. Found in Amyloplasts (starch grains) inside plant cells for energy storage

4. Insoluble, so no osmotic effect in tissues

5. Amylose has no branches (i.e. 1-4 glycosidic bonds only), so access to glucose is slow

6. Amylopectin has some branches (i.e. both 1-4 & 1-6 glycosidic bonds)

Cellulose

1. Made from Poly (β Glucose).

2. Main component of cell walls as it is a very strong structural molecule

3. Insoluble… for obvious reasons!

4. Cellulose has no branches (i.e. 1-4 glycosidic bonds only), so adjacent cellulose chains line up close

5. Hydrogen bonds form between adjacent chains, creating very strong cellulose fibrils


Saccharides join together in condensation reactions, which produce water. A glycosidic bond forms between the saccharide molecules. The opposite of a condensation reaction is a hydrolysis. This requires;

1. Heat + HCL 2. OR an enzyme (e.g. Amylase)

1.1.4

Tests for Sacharides:

- Iodine solution turns brown → blue/black in the presence of starch

- Benedict’s solution turns blue → brick red in the presence of a reducing sugar

- Non reducing sugars (most disaccharides and all polysaccharides) will give a positive result to Benedict’s if heated in acid first.


1.1.5

Triglycerides are either fats or oils. They are made from the elements C, H & O only.

Triglycerides are used for;

1. Long term energy storage molecules 2. Insulation 3. Protection (e.g. pericardium) 4. Buoyancy 5. Synthesis of specific hormones (e.g. steroids)

The C=C bonds form ‘kinks’ in the fatty acid chains, which push adjacent triglycerides away from each other. This lowers the effect of intermolecular forces (e.g. van der vaal’s forces), which lowers the boiling and melting temp.

Triglycerides are formed in condensation reactions between;

1 x glycerol 3 x fatty acid An ester bond forms between the fatty acid and the glycerol

Saturated triglycerides have no C=C bonds in them. They form fats. Unsaturated triglycerides DO have C=C bonds in them. They form oils.

Test for a triglyceride (Emulsion test):

1. Add ethanol (dissolves fat) 2. Add water 3. White precipitate indicates a positive result


1.1.6 Fick’s law: Rate of Diffusion = Surface Area x Conc Gradient

Distance If we apply this to a cube, the rate at which O2 reaches the centre of the cube is a product of the ratio of the Surface Area compared to the Volume (i.e. SA:Vol) In humans the mass transport system is the circulatory system and the heart. The specialized exchange organs include the lungs and the digestive system.

Amoeba Large SA:Vol ratio Can rely on diffusion through its surface.

Human Small SA:Vol ratio Diffusion through surface is too slow to supply O2. Therefore require a mass transport system and specialized exchange organs


1.1.7

You need to know;

1. the names of the 4 chambers of the heart

2. the names of the 2 arteries and 2 veins attached to the heart

3. The names of the two sets of valves in the heart

4. The cardiac cycle

5. The initiation and conduction pathways of the heartbeat Contraction in the heart:

Remember, the atria contract first. The L & R atria contract at

the same time. The ventricles contract second. The L & R

Ventricles contract at the same time.

Aorta

Pulmonary Artery

Vena Cava

Vena Cava

Cuspid Valve

Semi-lunar Valve


0 – 0.2s Atrial Systole The atria contract, atrial pressure rises and blood is pushed from atria → ventricles

0.2 – 0.3s Ventricular

Systole The ventricles contract, ventricular pressure rises above atrial pressure and the cuspid valves shut (1)

Ventricular pressure rises, but no blood leaves the heart yet!

When ventricular pressure rises above pressure in the arteries the semi-lunar valves open (2)

Blood leaves the heart

0.3 – 0.4s Diastole The ventricles relax. Ventricular pressure falls and when pressure in the arteries > ventricular pressure the semi-lunar valves shut (3).

0.4 – 0.7s Diastole The entire heart is relaxed. The cuspid valves open (4) and both atria and ventricles fill with blood.


1. SAN sends a wave of electrical activity (depolarization) around the walls of the atria.

2. A ring of insulating tissue blocks the wave from passing into the ventricles.

3. The AVN conducts the wave into the Ventricles slowly, which gives the ventricles time to fill.

4. The Purkinje fibres are fast-conducting and take the wave to the apex of the heart first, so the ventricles contract bottom upwards.

1.1.8

Artery: Arteries carry high pressure blood away from the heart.

Key Points:

collagen & connective tissue

smooth muscle& elastic tissue

lumen (blood)

0.1-10mm

SAN: Sino-Atrial Node AVN: Atro-Ventricular Node Purkinje Fibres (in bundle of His)


1. Thick muscle layer to withstand high pressure blood 2. Elastic tissue allows artery to stretch when blood is forced

into it. The elastic layer recoils during diastole, converting pulsatile into laminar (continuous) blood flow.

3. Protective collagen layer 4. Round shape 5. Relatively small lumen

Vein: Veins carry low pressure blood towards the heart.

Key Points:

1. Thin muscle layer (low pressure blood) 2. Valve to stop backflow 3. Protective collagen layer 4. Not a round shape (wall not thick enough to hold shape) 5. Large lumen (decreases effect of friction)

Capillary: Capillaries are adapted for exchange – they are not connected directly to the heart.

basement membrane(collagen)

endothelium cell

red blood cell

8 µm

collagen & connective tissue

smooth muscle& elastic tissue

lumen (blood)

semilunar valve

0.1-20mm

Small hole


Key Points:

1. Walls are one cell thick (cells are called endothelial cells) 2. Lumen is the same width as one RBC (therefore more of RBC

in contact with wall, therefore smaller diffusion distance) 3. No muscle or elastic tissue 4. Tiny (compare the scales and remind yourself what a чm is)

1.1.9

Dig up your Daphnia Core Practical notes in the Practical Handbook

1.1.10 & 1.1.11 Atherosclerosis is a disease in which the wall of arteries becomes furred up with fatty deposits called plaques or atheromas. The sequence of atherosclerosis is as follows;

1. Endothelial layer on the inside of an artery is damaged

2. Inflammation (an A2 topic) of the artery wall occurs

3. White blood cells move into the artery wall

4. Cholesterol begins to accumulate at the site of damage

5. Atheroma forms

6. Lumen narrows

7. Pressure increases After atherosclerosis has developed there is a chance that a blood clot might form in the damaged area. This makes the problem much worse!

As hypertension speeds atheroma formation these steps are a vicious cycle!


Clot formation:

1. Platelets are activated by substances released by the damaged artery wall

2. Platelets become “sticky” and form a “platelet plug” on the surface of the atheroma

3. Platelet plus releases chemicals which activate thromboplastin

4. Thromboplastin initiates the clotting cascade

There is a real danger of the blood clot becoming dislodged from the site of formation. It could be carried around the bloodstream and deposited elsewhere. If this occurs; - in the brain a stroke occurs - in the coronary arteries, CHD or even an infarction might occur - anywhere else, ischaemia and even gangrene are possible

1.1.12 Risk factors for CVD. There are lots, but these 7 are specifically mentioned on your syllabus

Thromboplastin


Risk Factor Explanation

Age Atherosclerosis occurs naturally as our arteries become less elastic with age. Less elastic = higher pressure during systole, ∴ hypertension, ∴ atherosclerosis… bummer.

Gender Girls have less atherosclerosis: fact. Two explanations;

1. Girls make oestrogen, which has a protective effect against atherosclerosis. Evidence to support this theory is that incidence of atherosclerosis in post-menopausal women rises to that of men.

2. Women tend to have less stressful jobs / be at home more ∴ less stress ∴ less hypertension, etc

Hypertension Speeds up atheroma formation AND causes endothelial damage (which is the 1st step in atherosclerosis)

Smoking Nicotine is very, very good at damaging the endothelium. Remember that next time you’re tempted to dally behind the bike shed…

Inactivity Allsorts of factors here; - lower BMI = less hypertension - fitter heart = less hypertension - exercise decreases LDL levels - exercise increases metabolic rate ∴ lowering BMI - Possibly some indirect contributing factors as well…

if you exercise regularly you probably put stock in looking after yourself ∴ are you likely to be smoking or drinking as well?

Genetic predisposition Some alleles give you less protection from / greater risk of developing atherosclerosis. To an extent, a higher chance of getting atherosclerosis does run in families

Diet Millions of contributing factors here; - High salt intake causes hypertension - Eating saturated fats decreases HDL level - Eating more calories than you need causes BMI to

increase. High BMI is associated with atherosclerosis

- Alcohol causes hypertension directly


1.1.13

Drug treatments for atherosclerosis and their side effects; Antihypertensives Diuretics – The Loop of Henle is the part of the nephron (in the kidney) that regulates water reabsorption. Essentially, it puts Na+ back into the blood by active transport. This lowers the water potential in the blood, so water follows the Na+ by osmosis. Most diuretics block the protein that actively transports the Na+, so less water is returned to the blood, thus reducing the pressure. Three problems with this, however;

1. The blood gets more viscous, which makes the heart beat harder

2. Dehydration can occur 3. Only treating the symptom

β Blockers – block the adrenaline receptor in the heart. This stops the heart from beating harder in response to stress and, therefore, reduces hypertension. There are some side effects in some cases (e.g. sleep disturbance, depression, vasoconstriction of the extremities) but generally they’re pretty good. One of the main problems is bradycardia, which can become serious if you have CHD. Can you explain why? Ca2+ channel blockers – stop the heart muscle from contracting too hard. You don’t need to know why, but if you’re interested look up Starling’s Law of the heart… Major side effect is arrhythmia, which can develop into fibrillation and infarction.


ACE Inhibitors – are REALLY complicated, but I don’t know how much of this you’re supposed to know, so here is the full version of things… Basically, our kidneys make Angiotensinogen all the time, but it doesn’t do anything itself (its not a hormone) it just circulates in the blood. However, when we are hyoptensive (i.e. have low blood pressure) the kidneys start to make Renin enzyme, which turns Antiotensinogen into Angiotensin I. After this, ACE enzymes (found in the endothelial cells lining arteries) quickly turn the Antiotensin I into Angiotensin II, which is a powerful hormone. It has the following effects;

1. General vasoconstriction 2. Causes the hypothalamus to release ADH (look it up from

GCSE, it was in Unit 3), which increases water reabsorption by the kidney

3. Stimulates the brain to release aldosterone, which causes the kidneys to increase salt reabsorption, which in turn increases water reabsorption.

All of these effects increase blood pressure, so ACE inhibitors will, therefore, do the opposite. The major side effect is kidney failure. Vasodilators – dilate blood vessels, reducing blood pressure. If this occurs too much you get hypotension, which can cause heart attacks (not enough blood returns to the heart to fill it properly)

Angiotensinogen Angiotensin I Angiotensin II Renin Enzyme ACE Enzyme

A protein made by the kidneys, which circulates in the blood

An intermediate, also circulating in the blood

The important one! This is the hormone that increases blood pressure!


Statins Two effects;

1. Block an enzyme in the liver that makes cholesterol. 2. Remove LDL from the circulation

Associated with liver failure. Anticoagulants As the second stage of atherosclerosis is associated with blood clotting (thrombosis), anticoagulants block the clotting process. There are many, many different ways of doing this. Blood clots slowly. Platelet inhibitory drugs These work in the same way as anticoagulants but target platelets, which are required to activate the clotting process. They, therefore, have the same side-effects.

1.1.14 Cholesterol is the major component in atheromas. High blood cholesterol level is, therefore, a bad thing. We get cholesterol from two sources;

1. Diet 2. It is made by the liver

Lipoproteins (also made by the liver) ferry cholesterol around in the bloodstream and play a role in pushing the liver towards making more cholesterol, or excreting more cholesterol. There are two types of lipoprotein;


High Density Lipoproteins (HDLs) take cholesterol out of the circulation to the liver, where it is converted into bile salts and (ultimately) excreted. HDLs lower cholesterol levels. Low Density Lipoproteins (LDLs) take cholesterol from the liver and put it into the circulation to the liver. LDLs increase cholesterol levels.

Crudely…

High HDL = good High LDL = bad High cholesterol = bad

1.1.15 You need to understand that scientists use their scientific knowledge of the effects of diet, exercise and smoking to try and predict risk of CVD and, therefore, to give people advice about how to reduce their risk.

1.1.16

Dig up your Vitamin C Core Practical notes in the Practical Handbook

1.1.17 Body Mass Index = Mass

(Height)2 Your energy budget balances the number of calories you require with those that you consume. Ideally, they ought to be the same.

Energy consumed > Energy expended → mass gain Energy consumed < Energy expended → mass lost

BMI < 18.5 Underweight BMI between 18.5 and 25 Normal BMI between 25 and 30 Overweight BMI > 40 Obese


1.1.18 & 1.1.19 You need to be able to analyze data on mortality rates to determine health risk. Be careful! If two sets of data follow the same pattern they are correlated

If two sets of data follow the same pattern because one factor directly affects the other they are causal In order to assess whether data is correlated or causal scientists experiment, the idea being to try and falsify the Null Hypothesis that one factor does not affect the other. However, be aware that the design of the experiment often affects the results. Things to watch out for;

1. People selected were not representative of the population (e.g. all students, all female, etc) i.e. not accurate

2. Only a few people were involved in the experiment (i.e. not very reliable)

3. Not all the variables were controlled i.e. a systematic error in the experiment (i.e. smokers included with non-smokers)

If you get a question on this section of the syllabus always

ask yourself WHERE HAS THE DATA COME FROM?

1.1.20 Why might people’s perception of risk be different from the actual risk?

1. They don’t understand the risk fully and underestimate it (e.g. if you smoke your risk of CVD is X and if you are obese your risk of CVD is Y. BUT if you are both your risk is not X + Y but XY… much greater!)


2. They don’t understand the risk fully and overestimate it (e.g. the person who thinks they actually might win the lottery this week…)

Broadly speaking, risk factors for CVD tend to be underestimated because people don’t realise that risk factors tend to be associated with other i.e. if you smoke and drink and are obese, chances are you also eat a diet high in saturated fat and salt. Quite quickly the risks stack up…

Oxygen Dissociation Curve This is not mentioned on the syllabus, but it is in the text book. The prudent man learns it anyway… Remember, each Haemoglobin (Hb) can bind up to 4 O2 molecules. The affinity of Hb for O2 changes depending on how many O2 are being carried. A: The haemoglobin is in the lung and is O2 loading. Affinity of Hb is high, therefore it “fills up” with O2 easily.

A B C


B: The haemoglobin is in the respiring tissues. Initially affinity is high, so Hb does not give O2 away easily to tissues that already have enough. However, when Hb gives up its 1st O2 the affinity suddenly drops, so Hb tends to unload 3 O2 just where it is required! C: With 3 O2 removed the affinity is high again, so the last O2 is kept as an “emergency”. It is only given up if the Hb passes through tissues with very low PO2 When the line shifts position

1. Foetal Hb has a higher affinity than adult Hb. This is so the foetus will load with O2 from the maternal Hb. Foetal ends with L, therefore shifts to the LEFT

2. Llamas (starts with L) live at altitude and need to have Hb with higher affinity to load O2 in the thin air.

3. Myoglobin (has an L in it) is an O2 store in muscles. It has very, very high affinity for O2 so only gives off O2 when in the “emergency” section of the graph. Whales and diving mammals have vast quantities of myoglobin in their muscles.

4. Bohr (ends in R) shift occurs when Hb is exposed to acid. The affinity drops and O2 is unloaded more easily. Acids tend to be

- carbonic acid (made from CO2) - lactic acid (made in anaerobic respiration)

Both acids are produced when O2 is in short supply, so it makes sense for Hb to give up more O2 in these circumstances.

End of Topic 1End of Topic 1End of Topic 1End of Topic 1


Unit 1: LifestyleUnit 1: LifestyleUnit 1: LifestyleUnit 1: Lifestyle, Transport, Genes & , Transport, Genes & , Transport, Genes & , Transport, Genes &

HealthHealthHealthHealth

Topic 2: Genes & Health 1.2.2 Cell membranes are made from a double layer (bilayer) of phospholipids, which align “heads” inwards and “tails” outward because of their attraction / repulsion from water. Sat in teh membrane are transmembrane proteins. The proteins have a number of roles;

- channels into / out of the cell (see 1.2.4)

- receptors for hormones (tend to be glycoproteins)

- cellular “glue” joining adjacent cells together (look up desmosomes if you’re interested)

- anchors for the cytoskeleton

Edexcel AS Revision

Notes

Charged phosphate “head” ∴ hydrophilic

Uncharged fatty acid “tails” ∴ hydrophobic


1.2.3 “Osmosis is the movement of water molecules from high

concentration to low concentration through a partially permeable

membrane.”

Water molecules cannot pass through the bilayer itself because they are charged and are repulsed by the fatty acid “tails”. There are a few theories about how the water actually gets through, but these are the best so far;

1. Passes through special channels called aquaporins 2. Moves through ion channel as ligands on ion complexes (e.g.

with Na+ or Mg2+)

1.2.4 How do molecules move in / out of the membrane?

1. Uncharged hydrophobic molecules (e.g. steroid hormones, cholesterol, ethanol) pass freely between fatty acid tails by diffusion

2. Large hydrophilic molecules (e.g. enzymes) move in by endocytosis and out by exocytosis

3. Small hydrophilic molecules (e.g. glucose, mineral ions, water) move in and out via proteins in the membrane. There are 3 types of these;

Channel Proteins


Movement is governed by molecules diffusing freely through the channel. Sometimes the channel will only open under specific circumstances (i.e. if a certain hormone is present, or under certain environmental conditions e.g. temp, pressure etc). These are gated channel proteins Facilitated Diffusion proteins Protein channel has an active site specific to a particular hydrophilic molecule. It attaches to the molecule, spins around in the membrane and deposits it on the other side. Movement is governed by the concentration gradient. Active Transport proteins As above, but the movement is against the concentration gradient. Energy (in the form of ATP) is required to get movement to occur.

1.2.5

Dig up your Beetroot Core Practical notes in the Practical Handbook

1.2.6 Fick’s law: Rate of Diffusion = Surface Area x Conc Gradient

Distance

1111 3333 2222


You should be able to explain breathing in terms of volume and

pressure changes in the Thoracic Cavity (GCSE idea)

Adaptations for rapid gas exchange (all related to Fick’s Law)

Remind yourself why humans need lungs in the first place, why

can’t we just breathe through our skin like Amoeba do?

Larynx (voicebox)

Bronchiole

Bronchus

Intercostal Muscle

Thoracic Cavity contained within pleural membranes

Diaphragm

Thachea

Ribs

Alveolus

Human Respiratory System

Element of Fick’s Law Adaptation

Surface Area Each alveolus has a small SA, but there are millions, which produces a huge total SA

Distance Each alveolus is one cell thick, as are the capillaries which surround them. Therefore, the total diffusion distance is only two cells!

Conc Gradient Ventilation maintains a constantly high PO2 in the alveoli. Additionally, as soon as O2 has been collected by haemoglobin the circulation removes it, therefore maintaining a low PO2 in the blood. This keeps the concentration gradient high!


1.2.7

Amino acids are connected by peptide bonds. They are formed in condensation reactions and broken up in hydrolysis reactions.

Primary Structure – a long chain of amino acids connected by peptide bonds. Most proteins do not function in their primary form Secondary Structure – the long chain of amino acids is folded into two types of structure;

- Alpha helix - Beta sheet

Both are held together by hydrogen bonds

Test for Protein:

- Biuret solution turns blue → “purple halo” in the presence of protein

Proteins are polymers of amino acids. There are ~20 amino acids, each of which has the same basic structure with a different variable group (R group)


As the shape of a protein determines its function (think about the active site of an enzyme, for example) it is really important that all the bonds holding the shape together form in the right places. The most important bonds are those that hold the 3o and 4o structure together and these all form between R groups of specific amino acids. Therefore;

The specific sequence of specific amino acids determines

the shape of the protein and, therefore, its function.

1.2.8 In the Lock and Key hypothesis, the active site and the substrate are completely complementary.

1. Substrate diffuses into the active site 2. Substrate binds to the active site 3. Bonds in the substrate are broken as a result 4. Products form and unbind from the active site 5. Products diffuse out of the active site

Tertiary Structure – sections of secondary structure are folded up further, forming a protein with a 3D shape. The shape is held together by covalent bonds (e.g. disulphide

bridges) between R groups of specific amino acids. Quarternary Structure – formed when two or more tertiary proteins are combined e.g. haemoglobin is made from 4 x haem proteins


In the Induced Fit hypothesis the mechanism of action is the same except that the active site changes shape to fit the substrate once the substrate has bound. The shape change causes bonds in the substrate to break, forming the products. All enzymes work by reducing the Activation Energy (Ea). This is the energy required to get the reaction to start. Enzymes provide an alternate reaction pathway (i.e. a different way for the reaction to happen – in the active site), which requires less energy to start.

1.2.9

Dig up your Enzyme Core Practical notes in the Practical Handbook

1.2.10

DNA is made from many nucleotides joined together. It is, therefore, a polynucleotide Each nucleotide contains 3 things;

(i) Sugar molecule, (ii) Nitrogenous base (iii) Phosphate group (negatively charged)


There are 2 types of nucleotide;

(i) Ribose nucleotides - make RNA (ii) Deoxyribone nucltodies - make DNA

DNA nucleotides have 2H atoms on the C2 carbon atom

RNA nucleotides have an H and an OH on the C2 carbon Other differences: • RNA is single – stranded, DNA is double – stranded • RNA has different bases • RNA used to make 3 different things (mRNA, tRNA & rRNA),

DNA only used to determine genetic code • DNA only found in nucleus, RNA in nucleus & cytoplasm

Polynucleotides are formed by connecting the phosphate group of one nucleotide with the 3rd carbon atom of another, forming the Sugar-

Phosphate Backbone

DNA is made from 2 strands of DNA polynucleotides, held together by hydrogen bonds between the bases. Because the strands face in opposite directions DNA is an antiparallel molecule.

H / OH


1.2.11 DNA Synthesis: The proof that DNA Replication is semi-conservative (rather than conservative, or dispersive – the other theories) was provided by Meselson & Stahl. Their experiment is shown on the next page (you need to know what they did), but you should be able to interpret their results as follows;

RNA

Adenine (A) pairs with Uracil (T) Guanine (G) pairs with Cytosine (C)

DNA

Adenine (A) pairs with Thymine (T) Guanine (G) pairs with Cytosine (C)

DNA synthesis is semi-conservative (i.e. half of each new strand is old DNA & half is new DNA)

1. Helicase unwinds the DNA forming the replication fork.

2. New nucleotides diffuse into the fork and hydrogen bind with their complementary partners

3. DNA Polymerase joins the nucleotides together forming the new sugar phosphate backbone

You can make this more complicated by looking closely at what happens on the lagging strand, but you don’t need to know it (if you’re interested look up “Okazaki fragments”)

Original DNA, all heavy ∴ DNA band at bottom of centrifuge

1st generation DNA, ½ old, ½ new ∴ DNA band in middle of centrifuge

2nd generation DNA, some ½ and ½ (forms one band at top) & some all new ∴ second band in the middle of centrifuge. No other theory predicts formation of TWO BANDS


1.2.12


1.2.12 & 1.1.13 The genetic code is read from the sequence of bases in the DNA. Each of the ~30,000 instructions in the code is a gene and tells the body how to make one specific protein. Genes, therefore, code for proteins. The genetic code is read in sequences of 3 bases, called codons each codon represents one specific amino acid. e.g. in this gene the code is ATG CCA CTA GCA CGC, which corresponds to the following amino acids

1.2.14

Protein Synthesis occurs in two stages;

(i) Transcription

(ii) Translation

A Gene

A Protein


Transcription: • Takes place in nucleus • A complementary copy of the gene is made using RNA 1. Gene opens up. Hydrogen bonds break between bases

2. RNA nucleotides attracted to complementary bases and form hydrogen bonds.

3. RNA nucleotides joined together by enzyme RNA Polymerase.

4. Complementary RNA copy of gene now made. It is called mRNA (messenger RNA)

5. Single stranded mRNA molecule diffuses out of gene

6. mRNA molecule leaves nucleus through nuclear pore (large holes in nuclear envelope)

7. Many mRNA strands are made before gene closes.

MRNA is complementary, not a copy!

DNA TAC GAA TCT GAG CAC GGC TAT ATC

mRNA. AUG CUU AGA CUC GUG CCG AUA UAG

Translation: • Takes place in cytoplasm • MRNA code read by ribosome and amino acids assembled in

correct order to make protein 1. mRNA strand binds to cleft in ribosome. Start AUG codon fits

into bottom of P site

2. tRNA diffuses into P site and recognises the mRNA codon using its specific anticodon


3. A second tRNA diffuses into the A site and recognises the

mRNA codon there.

4. The amino acids between the two tRNAs join together forming a peptide bond

5. The tRNA in the P site diffuses into the cytoplasm and binds to another specific amino acid.

6. The ribosome moves one codon down the mRNA chain so that the P site is filled with the tRNA from the A site and the A site is empty

7. When the ribosome reaches the stop codon it releases the mRNA and the amino acid chain.

Most ribosomes translate whilst attached to the rER. The completed primary protein is inserted into the rER, where enzymes fold it into its secondary and tertiary shape. Many ribosomes can translate the same piece of mRNA at the same time. A polysome forms


A Mutation = a change in the genetic code. By changing the genetic code mutations ultimately change the sequence of amino acids in primary proteins. This changes the sequence of R groups in the protein and, therefore, the way in which the protein folds up. This affects on the function of the protein

Any mutation in the CFTR gene that stops / impairs the function of the CFTR protein causes Cystic Fibrosis. To date over 2000 different mutations have been catalogued, each of which causes CF.

Mutation Explanation

Neutral mutations

The function of the protein is unchanged after the mutation (i.e. the protein still does its job as well as it did before the mutation). There are 2 possible causes;

One codon is altered. However, the codon still codes for the same amino acid. Therefore, the protein is the same

A codon is changed, leading to a different amino acid in the primary protein. However, this protein is not in a place crucial for folding, so the protein is still the same shape and functions the same.

Deletion mutations A nucleotide is deleted from the DNA code, which changes all the codons after the deletion. This causes frame-shift.

Insertion mutations A nucleotide is inserted into the DNA code, which changes all the codons after the insertion. This causes frame-shift.

Frame-shift

mutations

All the codons in the sequence are altered, meaning that every amino acid after the addition / deletion is different. Normally, this has a huge impact on the function of the protein.

Non-sense mutations

One of the altered codons in the frame-shifted sequence changes to become a stop codon. Protein synthesis stops half-way through the gene, resulting in only half of the protein being made. Almost always the protein does not function.

1.2.15


1.2.16

Key Definitions:

Gene: a sequence of DNA coding for a specific protein Allele: an alternative version of a gene Genotype: the pair of alleles an individual possesses Phenotype: the physical appearance Recessive: allele does not affect the phenotype in the presence of a Dominant allele Dominant: always affects the phenotype Homozygote: individual possesses two copies of the same allele Heterozygote: individual possesses two different alleles

A Genetic Diagram

♀ ♂

Parents’ Phenotype: Brown eyes Brown eyes

Parents’ Genotype: B b B b

Gametes: F1 Genotype: B B B b B b b b F1 Phenotype: 3 : 1 Brown eyes : blue eyes

Note the gametes are always put in circles

B b B b

B b

B

b


You also need to interpret inheritance problems involving seed morphology (shape) and plant height.

1.2.17

Goblet cells secrete mucus onto the surface of the epithelium, which lines the lungs. Epithelial cells regulate the water content of mucus. In the alveoli mucus is very watery to allow it to be wafted easily by cilia. However, higher up the lungs water is drawn out of mucus to reduce its volume: one cannot fit the mucus from 6 small bronchioles into one larger one, so water is removed. In Cystic Fibrosis the mechanism controlling the water content of the mucus does not work properly and the water removal process is constantly switched on in all parts of the lung. This means the mucus is too sticky in the alveoli and cannot be wafted.

Disease Heritability Effect

Sickle Cell Anaemia Recessive

A mutation in the haemoglobin genes Cause haemoglobin molecules to stick together inside red blood cells. RBCs become distorted into a “sickle” shape. They can become stuck inside capillaries leading to clots and stroke. RBCs have limited oxygen carrying capacity.

Thalassaemia

Recessive

A mutation in (usually) the gene coding for alpha haem causes very slow haemoglobin production. This results in anaemia and reduced haemocrit (% RBCs per unit volume of blood). Regular transfusions are required.

Achondroplasia

Dominant

Caused by a mutation in one of genes controlling collagen production in bones. As a result bone growth plates fuse too early, leading to shortening of the long bones. Homozygous dominant genotype is fatal.

Albinism

Recessive

A mutation in the gene coding for melanin protein stops melanocytes from producing melanin. Melanin colours hair, skin etc and provides protection from UV rays.


Normally:

Cystic Fibrosis:

The sticky mucus causes the effects of CF and affects;

a) Lungs, b) Digestive system c) Reproductive system

Cl-

Na+

Mucus

Tissue Fluid

Water

Water

Cl-

Na+

Mucus

Tissue Fluid

Water

Water

X

Cl- moves out of epithelial cells into mucus via the CFTR protein. Na+ is drawn into mucus to balance the charge. Na+ passes between epithelial cells. The combined effect of Na+ and Cl- reduces water concentration making hypertonic mucus. Water is drawn into mucus by osmosis and mucus is dilute.

CFTR is blocked or absent, so Cl- stays inside epithelial cells. Na+ does not move into mucus as there is no charge to balance. Mucus is hypotonic. Water is drawn into epithelial cells by osmosis and mucus is sticky.


1.2.18

The problem with genetic diseases is that they are caused by a mutation that is present in every cell of the body. In order to cure the disease you need to change the DNA in every cell of the body, which is impossible. However, in the case of CF because the CFTR protein is only transcribed by epithelial cells (the cells lining the lungs, digestive system and reproductive tracts) only these cells need to be targeted. So how can you change DNA inside living cells? Answer: use gene therapy, which attempts to add a normal copy of the CFTR gene to the DNA inside epithelial cells. Gene Therapy (in humans – no plasmids are used) Step 1: cut out a working copy of the gene from normal DNA using a restriction enzyme. OR use reverse transcriptase enzyme to make a copy of the gene from CFTR mRNA

Step 2: add the gene to a vector, which will insert the new gene into the DNA of the target cell

Step 3: hope the gene is successfully incorporated in the DNA in the nucleus

Tissue Effect of CF

Lungs

Mucus produced is too sticky and blocks the alveoli. This makes the person breathless. The mucus also provides ideal conditions for bacteria, so chest infections are common.

Reproductive system

Mucus blocks the vas deferens in boys and the fallopian tubes in girls, making the individual infertile

Digestion

Mucus blocks the bile duct and the pancreatic duct. Enzymes do not reach the small intestine and food is not digested properly.


Vectors are used to get the working gene into the epithelial cells. Somatic Cells = Body cells. Somatic Cell Gene Therapy therefore only affects the targeted cells

Germ Cells = Gametes. Germ Cell Gene Therapy therefore affects the entire organism that is produced when the gamete is fertilised. NB: Genetic engineering of bacteria is different and involves plasmids and DNA ligase enzyme as well (look it up)

1.2.19

Genetic screening is used to determine whether a person has a genetic disease or not.

Vector Explanation

Liposome

An artificial vesicle. A little bubble of membrane in which the CFTR gene is placed. When the liposome is inhaled the gene can enter the epithelial cell by endocytosis.

Virus

Viruses naturally insert their own DNA into host cells DNA. So, if we remove the viral DNA and replace it with the CFTR gene that ought to be inserted instead.

Method Summary

Amniocentesis

A long needle is inserted through the mother’s abdomen into the amniotic fluid of the developing embryo. As this is produced by the embryo it will contain embryionic cells and, therefore, embryo DNA

Chorionic villus

sampling

As above, but cells are taken from the placenta, which is also made by the embryo.

Pre-implantation

genetic diagnosis

(PIGD)

Gametes are fertilized in vitro (outside of the body) and the resultant embryos are then tested. Only embryos known NOT to have the disease are implanted in the uterus.


1.2.20


Advantages of genetic testing

• Can opt for termination • Can get counselling • Can buy special medical

equipment / care in preparation for birth

• Can opt not to have children (if parents are tested)

• Utilitarian argument

Disdvantages of genetic testing

• Abortion is morally wrong • Tests can be inaccurate • Small chance of test

resulting in miscarriage • Unnatural procedure • Embryos right to life • Embryos cannot give

informed consent


Unit 2Unit 2Unit 2Unit 2: : : : Development, Plants & the Development, Plants & the Development, Plants & the Development, Plants & the

EnvironmentEnvironmentEnvironmentEnvironment

Topic 3: The Voice of the Genome 2.3.2 & 2.3.3

Prokaryotic Organelles:

Ribosomes. Same function as eukaryotic cells (protein synthesis), but are smaller (70s rather than 80s).

Nuclear Zone. The region of the cytoplasm that contains DNA. There is no nuclear membrane.

DNA. Always circular, and not in chromosome form.

Plasmid. Very small circles of DNA, containing non-esential genes. Can be exchanged between different bacterial cells.

Edexcel AS Revision

Prokaryotic Cell


Cell membrane. made of phospholipids and proteins, like eukaryotic membranes.

Mesosome. Tightly-folded region of the cell membrane containing all the proteins required for respiration and photosynthesis.

Cell Wall. DIFFERENT from plant cell wall. Made of murein (a protein). There are two kinds of cell wall, which can be distinguished by a Gram stain:

A: Gram positive bacteria have a thick cell wall and stain purple B: Gram negative bacteria have a thin cell wall with an outer lipid layer and stain pink.

Capsule (or Slime Layer). Thick polysaccharide layer outside of the cell wall. Used for:

1. Sticking cells together 2. As a food reserve

3. As protection against desiccation (drying out) and chemicals, and as protection against phagocytosis (being broken down by a white blood cell).

Flagellum. A rotating tail used for propulsion.

Eukaryotic Cell


Endoplasmic Reticulum. Site of protein folding (see 2.3.4)

Ribosome. Site of protein synthesis

Nucleus. DNA “store” & site of mRNA synthesis.

Golgi apparatus. Site of protein folding and packaging (see 2.3.4)

Centriole. Makes spindle protein, which pulls chromosomes apart during cell division

Vesicle. “Bubble” of membrane, used to transport materials around a cell and between cells

Lysosome. A vesicle filled with digestive enzymes. Protects against bacterial attack and removes cell debris.

Cell membrane. Made of phospholipid and protein, controls movement in / out of the cell

Mitochondrion. Site of respiration

Chloroplast. Site of photosynthesis

Prokaryotic Cells Eukaryotic cells

Small cells (< 5 mm) Larger cells (> 10 mm)

Always unicellular Often multicellular

No nucleus or any membrane-bound organelles

Always have nucleus and other membrane-bound organelles

DNA is circular, without proteins DNA is linear and associated

with proteins to form chromatin

Ribosomes are small (70S) Ribosomes are large (80S)

No cytoskeleton Has a cytoskeleton

Cell division is by binary fission Cell division is by mitosis or

meiosis

Reproduction is always asexual Reproduction is asexual or sexual


2.3.4 Amino acids are “stuck together” in the correct order during translation. This take place using ribosomes, which are therefore the site of protein synthesis.

After synthesis, proteins are put into the rER, which folds primary proteins into their specific secondary and tertiary forms. 20 and 30 proteins are packaged into vesicles and sent to the Golgi In the Golgi, 30 proteins are stuck together to form completed 40 proteins. They are packaged into large secretory vesicles, which bud off the Golgi and go the cell membrane for exocytosis. The Golgi also makes lysosomes.

2.3.5 Tissue: a group of specialized cells, which all carry out the same function.

Organ: a group of different tissues. Although every cell contains the entire library of genes, each tissue only expresses a select few of them. This is because, as cells become specialized, they progressively switch off genes. This is called cell differentiation.

2.3.6

The Cell Cycle

G1 Phase: Growth phase Approximately 40% of cell cycle

S Phase: DNA replication occurs Approximately 45% of cell cycle

G2 Phase: Preparation for mitosis Organelles replicate

Mitosis: Cell divides Approximately 10% of cell cycle

Cytokinesis: Cell physically splits Approximately 5% of cell cycle


Underlined comments = definition of stage end

Stage Explanation

Stage is: Prophase

1. DNA coils up onto chromosomes 2. Centriole divides 3. Centrioles move to cell poles 4. Nuclear envelope disappears

Stage is: Metaphase

1. Chromosomes move to equator 2. Spindle attaches to centromeres 3. Centrioles split 4. Chromatids separate

Stage is: Anaphase

1. Chromatids separate completely 2. New nuclear envelope grows

Stage is: Telophase

1. Cytokinesis occurs 2. Cells separate

Stage is: Interphase As above (G1, S & G2)


Dig up your Mitosis Core Practical notes in the Practical Handbook

2.3.8 Mitosis produces genetically identical daughter cells, whereas Meiosis produces genetically dissimilar gametes. The variation in gametes comes from;

1. Random fusion of gametes

Each individual makes many gametes, each of which is genetically different. This creates a huge number of potentially different embryos as which two gametes are selected for fertilization is largely random.

If the number of different gametes made by both parents is n, therefore the total number of possibilities is n2, which is huge!

2. Independent assortment

During meiosis, chromosomes pair up at the equator (they don’t at during mitosis). Whichever way up the pair are aligned will affect the combination of alleles in the gamete. i.e. AA BB → AB aa BB → aB aa bb → ab AA bb → Ab

3. Crossing Over

When the chromosomes are paired up during metaphase

sections of DNA are swapped between chromatids (this is called crossing over). This means that alleles which were

previously linked with others (i.e. in set combinations of

alleles) become unlinked, thus increasing the potential

number of combinations of alleles

2.3.7


2.3.9

Follicle cells (from ovary)

Lipid droplets

Zona Pellucida

Cytoplasm

Nucleus

Lysosomes

Cell membrane

A Mammalian Ovum:

Part of Ovum Adapted for…

Nucleus Contains only one copy of each chromosome (haploid)

Follicle cells Secrete chemicals that secrete the acrosome reaction

Cytoplasm Very large so fertilised cell can divide immediately

Lipid droplets Source of energy for future growth and division

Zona pelludica Hardens once sperm has entered ova, stops further cells entering.

Lysosomes Cause the zona pellucida to harden once a sperm’s nucleus has entered the ova.

Adaptations:


A Mammalian Sperm:

Adaptations:

Part of Ovum Adapted for…

Nucleus Contains only one copy of each chromosome (haploid)

Head Detachable. Contains the nucleus.

Middle Contains lots of mitochondria, which make ATP

Tail Made from motor proteins, which use ATP to propel the sperm forwards

Acrosome An adapted lysosome on the top of the sperm’s head. The acrosome swells and bursts when the sperm embeds in the zona pellucida (zona pellucida releases chemicals that trigger this). The enzymes in the acrosome digest the follicle cells and the zona pellucida and allow the cell membranes to fuse.

Cytoplasm Very little cytoplasm, which means cells are small and therefore can be released in large numbers.


2.3.10 Fertilization is the successful fusion of two haploid gametes to create a diploid cell (a zygote). The zygote then divides rapidly by mitosis to become an embryo. Mammalian fertilisation:

1. The sperm is attracted to the ovum by hormones released by the follicle cells surrounding the ovum

2. When the sperm reaches the ovum it embeds its head in the zona pellucida, triggering the acrosome reaction

3. The acrosome swells and bursts, releasing proteolytic enzymes

4. The enzymes digest a hole into the ovum

5. Sperm membrane fuses with ovum membrane and the sperm nucleus enters the ovum by endocytosis

6. Lysosomes in the ovum cause the zona pellucida to harden once the sperm’s nucleus has entered the ovum, stopping further sperm from penetrating the ovum.

Plant fertilisation:

1. The pollen grain (male gamete) lands on the stigma

2. Pollen grain grows a pollen tube down into the stigma. The pollen nucleus is at the tip of the tube

3. The pollen tube enters the ovule

4. The pollen tube reaches an ovum and the nucleus enters it by endocytosis forming a zygote.

5. Many pollen grains may fertilize many ova


2.3.11 Stem Cell: an undifferentiated cell (i.e. a cell that can grow into more than one type of cell).

Totipotent Cell: an undifferentiated cell capable of growing into a new embryo

Pluripotent Cell: an undifferentiated cell capable of growing into any cell, but not a new embryo

Multipotent Cell: an undifferentiated cell capable of growing into a few types of cell

Stem Cells are very useful because they can be used to grow replacement organs. However, it is not yet possible to get a differentiated cell to revert to being a stem cell. Therefore, stem cells tend to be harvested from embryos, which causes serious ethical problems. You might like to consider;

� Where do the embyos come from? � Is an embryo a human? � Do embryos have the same rights as adult humans? � Can we use animal embryos (or human-animal hybrids) instead? � The utilitarian argument � The right to life (for both adult and ambryo)

2.3.12

Dig up your Plant Culture Core Practical notes in the Practical Handbook

2.3.13 Cells become specialized (or differentiated) by progressively switching genes off. This is sometimes done by adding methyl groups to the gene, which stop it being opened in transcription. The


gene is then permanently inactivated in the adult cell, but also in any daughter cell produced through mitosis. In addition, some genes may require a transcription factor to activate them i.e. the gene is normally off, but will be transcribed in the presence of a TF. Usually the TF is a hormone (e.g. Steroids -think about their effects), but sometimes it can be an environmental factor (e.g, the presence of lactose in E.coli – see text book)

2.3.14 The phenotype is a product of the genotype and the environment. For some genes the environment has minimal effect (e.g. blood group), but for the majority the environment plays a significant role. You need to know 4 examples Animal Hair Colour: Some animals have fur colour that is a product of the environment e.g. Siamese cats should have black fur all over as their genotype codes for the enzyme tyrosinase that converts tyrosine into melanin (which is a dark protein – remind yourself of Albimism in 1.2.16). However, the enzyme is denatured by body heat, so only the cold parts of the animal are black (tail, ears etc) and teh rest is white. Human Height: Is controlled by many genes, each with a range of alleles, making it an example of polygenetic inheritance (i.e. controlled by lots of genes). In addition, diet has a huge effect on height. Mono Amine Oxidase A (MAOA): MAOA enzymes break down neurotransmitters released by nerves in the brain. High levels of MAOA have been linked to risk-taking and aggression, whereas low levels of MAOA can cause depression


and Parkinsons disease. Mutations of MAOA are the genetic component to these conditions, but environmental factors such as stress levels also have a profound effect. Cancer: A tumour is a ball of cells dividing quicker than they should. Tumours that split apart and spread around the body (metastasis) are the most dangerous (malignant) The rate of cell division is controlled by;

Oncogenes – speed cell cycle up Tumour Supressor Genes – slow cell cycle down

Mutations in either of these genes can cause tumours. Although mutations occur naturally, the environment can have an effect e.g. radiation, free radicals, carcinogen chemicals all increase the mutation rate.

2.3.15 Discontinuous variation: phenotypes appear in discrete categories (i.e. blood group). Usually controlled by one gene where the environment has little effect. Continuous variation: phenotypes appear in a range of categories (i.e. height). Usually controlled by many gene (polygenes) where the environment has a large effect.



Unit 2Unit 2Unit 2Unit 2: : : : Development, Plants & the Development, Plants & the Development, Plants & the Development, Plants & the

EnvironmentEnvironmentEnvironmentEnvironment

Topic 4: Biodiversity & Natural Resources 2.4.2 Animal and plant cells are both eukaryotic cells, they have common eukaruyotic features. However, plant cells also have some features unique to them.

Cell wall: A structure made from cellulose fibrils and pectin cross-links. It strengthens the cell and allows it to be turgid without bursting.

Amyloplast: A membrane-bound organelle full of starch (starch grain)

Chloroplast: Site of photosynthesis.

Vacuole: A water-filled membrane-bound organelle that helps a cell maintain turgor pressure

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Notes


Tonoplast: The vacuolar membrane

Plasmodesmata: A junction between adjacent cells where the cytoplasm of one cell joins the cytoplasm of the other. Used for intercellular communication

Pit: A thin patch in the cell wall where plasmodesmata can form or have formed previously

Middle lamella: A pectin “glue” attaching one cell wall to another

2.4.3 Plant cells are strong because they are wrapped in a protective layer of cellulose. This forms the cell wall. Cellulose is a polysaccharide made from β glucose monomers. Alternate glucose molecules “flip over” in the chain, forming hydrogen bonds between adjacent cellulose chains. Because cellulose has no side branches the chains can be packed closely which increases the strength of the hydrogen bonds further.

Alternate glucose molecules “flipping over” Individual cellulose chains are packaged together into microfibrils. The microfibrils wind around each other forming cellulose fibres. The cell wall is build from layers of these fibres.


2.4.4 Primary cell wall: First to form, cellulose fibres laid down in the same direction Secondary cell wall: Forms later, cellulose fibres laid down at right angles to those in the primary wall. Provides much greater strength. Collenchyma: found around the outside of the stem have their cell walls further strengthened with more cellulose (secondary thickening) to form thick supporting cells. Sclerenchyma: in larger plants strings of collenchyma begin to lay down the protein lignin in their cell walls to form very strong fibres within the stem. These tend to form as a cap to the vascular bundles in the stem. Sometimes the sclerenchyma can be extracted by humans for making into rope (e.g. hessian) or clothes (e.g. flax or jute).

2.4.5

Vessel Location in stem Purpose

Xylem Inside of vascular bundle

Carries water and minerals up the stem

Phloem Middle of vascular bundle

Carries sucrose up & down the stem

Sclerenchyma Cap on vascular bundle

Support for the stem

Collenchyma Inside epidermis Lesser support for the stem


2.4.6 Plant materials are used for three main reasons;

1. Sustainable - they are not a limited resource as, although they are used, they can be replanted.

2. Carbon neutral - do not contribute to rising CO2 levels (although they may give off CO2, replanting uses the CO2 up again).

3. Biodegrade.

Plant materials are used as fibres (wood, cotton etc) as they have a high tensile strength and can be used in clothing, building industry etc. Oils from plants can be used as biofuels and starch can be used in packaging, glues, absorbants as well as for food.

2.4.7

Xylem

Sclerenchyma

� Regular rings of lignin � Wide lumen � No end walls (continuous

tube) � Location at inside of VB

� Irregular layers of lignin � Tiny lumen � End walls with pits � Location as cap to VB � Presence of sclerids


2.4.8

Dig up your Celery Fibres Core Practical notes in the Practical Handbook

2.4.9

Plants also need water for;

1. Photosynthesis (~5%) 2. Cooling via transpiration (~90%) 3. Transport of substances (e.g. sucrose, mineral ions) 4. Maintain turgor 5. Solvent for chemical reactions 6. Gamete distribution

2.4.10

Dig up your Plant Mineral Deficiencies Core Practical notes in the Practical Handbook

2.4.11

Dig up your Mint / Garlic Core Practical notes in the Practical Handbook

2.4.12 William Withering experimented with foxglove extract as a cure for dropsy (oedema caused by congestive heart failure). He gave the drug in increasing amounts until the patient became ill, then he

Mineral Function in plant

Nitrate Used to make amino acids, which the plant uses to form proteins

Calcium Used to make pectin for cell walls

Magnesium Central ion in the chlorophyll molecule.


worked out a dose based on that. He also killed someone. His studies, though important are NOT ethical and do not follow the basis of modern clinical trials Clinical Trial Process:

Stage Purpose of stage

Pre-clinical testing

1. Proposed drug is tested in a lab with cultured cells to see the general effects of the drug

2. Proposed drug is given to animals to see the effects on a whole animal. Any side effects away from target cells are noted.

Clinical Trials – Phase 1

1. A small group of healthy volunteers are given different doses of the drug. They are told what the drug does

2. The distribution, absorbance rate, metabolism & excretion profile of the drug are assessed.

3. The effects of the different doses are assessed to try and determine the optimum dose

4. An independent organisation (UK Medicines Control Agency) assesses whether it is appropriate to move to Phase 2


1. A small group of people with the disease are given the drug.

2. Studies are very similar to Phase 1 3. The optimum dose is worked out


1. A large group of people with the disease are given optimum doses of the drug

2. The patients are either given the drug or a placebo in a double-blind test

3. The results are analysed 4. If the drug has had a significant positive effect in the

treatment of the disease it is put forward to licensing authority


2.4.13 Biodiversity: The number of species, the number of individuals within those species and the number and variety of alleles those individuals. Endemic: Where a species is found only within a particular niche in a particular ecosystem. Species richness: is a measure of biodiversity where the number and variety of species in an area is recorded. Can be measured in different ways;

• Indicator species i.e. the presence of specific species (usually those least tolerant to pollution / climate change etc) are used to indicate the “health” of the ecosystem.

• Population of keystone species i.e. the population of crucial species (usually those providing prey for the rest) are used to measure the “health” of the ecosystem

• Quantitative sampling – a direct way of sampling the biodiversity using quadrats

• Capture / recapture – a direct way of working out populations of species.

Genetic diversity: the number of different alleles within the gene pool. The greater the diversity, the more likely the species is to survive environmental change or disease.

2.4.14 A niche is the specific part of the ecosystem in which a species lives and any adaptations the species has that make it successful there. Adaptations can be; Behavioural e.g. Iguana on the Galapagos islands dive for seaweed - they are the only lizards to venture into the sea.


Physiological e.g. some Ethiopians have evolved a different shaped haemoglobin molecule that resembles foetal Hb. It loads O2 much more efficiently at altitude (see end of Topic 1)

2.4.15 Darwin made two observations and a conclusion; O1: More offspring are born than can survive O2: There is variation within a species Conclusion: There is a “struggle for survival” only the “fittest can survive and reproduce.” This is Natural Selection In order for NS to lead to evolution a few extra conditions are required;

1. Isolation (see table below) so no flow of alleles

2. Small population & inbreeding

3. Mutation (generates new “fitter” alleles)

4. Mutations accumulate within population

5. Eventually the isolated population cannot reproduce with the originals. At this point a new species has formed (speciation)

Anatomical e.g. the Fiddler crab has two very different claws. One is huge and is used for “fiddling” i.e. signalling for a mate. The smaller claw is, rather disappointingly, used for feeding.


Allopatric speciation occurs when species are far from each other Sympatric speciation occurs when species are close to each other

2.4.16 The taxonomic classification system follows a hierarchy of groups (the 5 Kingdoms at the top, individual species at the bottom) in which all species are categorised according to their anatomy. However, this is not necessarily the best approach as species with similar anatomies (e.g. dolphin and shark) are not necessarily closely related. A better system is based on molecular phylogeny i.e. comparing the molecules species are comprised of. The best molecule to examine is DNA. A recent proposal along this line (the three domain theory) argues that all organisms evolved into three broad groups; Bacteria – prokaryotes, fundamentally different structures

Archaea – those species that exhibit characteristics of both (i.e. “early eukaryotes” and their descendents)

Eukaryotes – eukaryotes, fundamentally different structures

Method of isolation Description

Ecological isolation The species occupy different parts of the habitat

Temporal isolation The species exist in the same area, but reproduce at different times

Behavioural isolation The species exist in the same area, but do not respond to each other’s courtship behaviour

Physical incompatibility Species coexist, but there are physical reasons which stop them from copulating

Hybrid inviability In some species, hybrids are produces but they do not survive long enough to breed

Hybrid sterility Hybrids survive to reproductive age, but cannot reproduce


2.4.17 Seed banks and Zoos help because they allow us to preserve

biodiversity, reintroduce species, set up captive breeding

programmes, educate people about ecology and generate money from tourism.

However, be aware that some species (those that have a lot of leaned behaviours e.g. tigers) do not tend to fare well on reintroduction programmes.

Cohesion-Tension Theory of Transpiration This is not mentioned on the syllabus, but it is in the text book. The prudent man learns it anyway… Epidermis: A single layer of cells often with long extensions called root hairs, which increase the surface area enormously. A single plant may have 1010 root hairs.

Cortex: A thick layer of packing cells often containing stored starch.

Stele: contains the Xylem, Phloem & Cambium and is protected by a layer of endodermis cells

epidermiscortexendodermispericyclephloemcambiumxylem

vascula

rtis

sue

roothairs


Endodermis: A single layer of tightly-packed cells containing a waterproof layer called the casparian strip. This prevents the movement of water between the cells and helps “waterproof” the stele – keeping water in.

Water moves through the root by two paths: (i) Symplast pathway (10%) (ii) Apoplast pathway (90%)

cellwall

cellmembrane

cytoplasm vacuolecasparian

strip


Symplast pathway: water moves from cytoplasm to cytoplasm through plasmodesmata (holes in the cell walls, where cell membranes of adjacent cells are joined - so there are no membranes for the polar water molecules to cross). Apoplast pathway: water moves from cell wall to cell wall. The cell walls are quite thick and very open, so water can easily diffuse through cell walls without having to cross any cell membranes. However the Apoplast pathway stops at the endodermis because of the waterproof casparian strip. At this point water has to cross the cell membrane and enter the symplast pathway. This effectively water-proofs the Stele, which stops water loss higher up the root.

Root Pressure:

Water moves from high water potential to low water potential by osmosis. However, most soils are dry (especially in the desert) and the water potential of the soil is low. Plant cells are full of water, so why doesn’t water leave the plant cells and enter the soil? The answer is that plant roots take up lots of ions from the soil, which lowers the water concentration of their cytoplasm enough for water to enter the root by osmosis, even if the soil if very dry. The ions are taken up by active transport, by proteins in the cell membrane of the root hairs. This uses up lots of energy (uses lots of ATP). Because of the low water potential root cells become very turgid. This creates a small pressure, which forces water up the xylem in the stem. This is called Root Pressure. In small plants root pressure is very important for transpiration. In woody plants it does not have a significant effect.



Xylem Tissue

Xylem tissue is composed of dead cells joined together to form long empty tubes.

Different kinds of cells form wide and narrow tubes, and the end cells walls are either full of holes, or are absent completely.

Before death the cells form thick cell walls containing lignin, which is laid down in rings, giving these cells a very characteristic appearance under the microscope.

H

H

O

H

O

O

H H

H H

O

H

large xylem vessel

small xylem vessels(tracheids)

thick cell wall

empty interior

remainsof end wall

perforatedend walls

lignin rings

Transverse Section (T.S.)

Longitudinal Section (L.S.)

Water molecules are polar and bind to each other by hydrogen bonds forming a strong column of water (for it’s diameter the column is stronger than steel!)

1. Water evaporates out of the leaves and causes low pressure in the leaves.

2. This creates a suction (or tension) force which sucks water up the stem

3. Because water molecules are polar they stick to each other and the entire column of water in the Xylem moves upwards.

4. This mechanism is called the cohesion-tension theory.

Lignin makes the xylem vessels very strong, so that they don’t collapse under pressure, and they also make woody stems strong. The xylem vessels form continuous pipes from the roots to the leaves. Water can move up through these pipes at a rate of 8m h-1, and can reach a height of over 100m.

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