A2 Biology Unit 5 Model Answers Flashcards
Homeostasis
Maintenance of a constant internal environment at a set point
Regulation of body temperature in ectotherms
Basking Solar re-orientation Taking shelter Gaining warmth from the ground Change in physical activity Colour variation Thermal gaping
Regulation of body temperature in endotherms - cold environment
Vaso constriction
Shivering
Raising of body hair - contraction of pilo-erector muscles
Decrease in sweating
Behavioural mechanisms - sheltering, huddling
Increased metabolic rate
Regulation of body temperature in endotherms - warm enviornment
Vaso dilation
Increase in sweating
Lowering of body hair - relaxation of pilo-erector muscles
Behavioural mechanisms - seeking shade
Modes of heat loss
Evaporative
Radiative
Response to a decrease in blood glucose
Detected by alpha cells in pancreas
Glucagon is produced
Liver cells have receptors to glucagon
Enzyme activates converyting glycogen to glucose (glycogenolysis)
Liver cells increase convergen of amino acids and glycerol into glucose (gluconeogenesis)
Adrenaline raises blood glucose by activating enzyme that causes the breakdown of glycogen to glucose in the liver (glycogenolysis) and inactivating an enzyme that synthesises glycogen from glucose (glycogenesis)
Increased blood glucose causes alpha cells to reduce glucagon secretion - negative feedback
Negative feedback
Changes that result in the system returning to a specific set point
Positive feedback
Changes that result in the system deviating away from a specific set point
Second messenger model - the role of adrenaline in increasing blood glucose
The hormone adrenaline is the first messenger
It binds to specific receptors on the membranes of target cells to form a hormone-receptor complex
Adenylate cyclase activated inside the membrane
This enzyme converts ATP to cyclic AMP
Cyclic AMP acts as a second messenger by activating other enzymes that convert glycogen to glucose (glycogenolysis)
Control of the oestrus cycle
Pituitary gland releases FSH
Stimulation of the development of follicles in the ovary
Growing follicles secrete small amounts of oestrogen causing uterus lining to build up
FSH and LH from the pituitary are inhibited - negative feedback
More oestrogen is produced growing follicles
FSH and LH is stimulated - positive feedback
The surge in FSH and LH production causes ovulation
LH stimulates the empty follicle to form the corpus luteum which secretes progesterone and small amounts of oestrogen
Progesterone maintains uterus lining and inhibits the release of FSH and LH - negative feedback
Corpus luteum degenerates and stops producing progesterone
Lower levels of progesterone mean that the uterus lining breaks down and FSH is no longer inhibited
manipulation of the oestrus cycle
farmers give animals progesterone implants
when implant is removed all animals come into season at the same time
this saves money on the AIT
bull or ram only brought to the farm once
lambs all born at once
Type 1 diabetes
insulin is not produced
Type 2 diabetes
glycoprotein receptors on the target cells lose their responsiveness to insulin
or
inadequate insulin is released from the pancreas
regulated by controlling the diet
The hormonal system
- transmission is by the blood
- transmission is slow
- response is widespread
- response is long-lasting
- effects may be permanent and irreversible
- hormones travel to all parts of the body but only target organs respond
The nervous system
- transmission is by neurones
- transmission is fast
- response is localised
- response is short-loved
- effects are temporary and reversible
- nerve impulses to specific parts of the body
Humans produce a large number of different hormones but only a small number of neurotransmitters. Explain the significance of this.
Hormones reach all cells by the blood
Neurotransmitters secrete directly onto target cells
Different hormones are specific to different target cells
Tropisms
Growth movement of part of a plant in response to a directional stimulus
Control of tropisms by IAA
Cells in tip produce IAA
IAA initially transported to all sides of the plant as it moves down the shoot
Light causes movement of IAA towards shaded side
Greater concentration of IAA builds up on shaded side
Cells on shaded side become elongated
Shaded side grows faster causing shoot to bend towards the light
Benefit of seedlings exhibiting positive phototropism
Growing shoots grow towards the light
Chloroplasts absorb more light
For photosynthesis
Taxis
A simple response to an external directional stimulus
Kinesis
The random non-directional movement of an organism in response to a stimulus in which the rate of movement depends on the intensity of the stimulus
Advantage to woodlice of moving away from a bright area
Prevents dessication
Helps protect against predation
Helps prevent temperature rising above optimum - enzymes not denatured
May help them to find food if their usual habitat is dark
Reflex
Rapid response to a stimulus which is automatic and not under conscious control
Comprisors of the reflex arc
Stimulus Receptor Co-ordinator Effector Response
Importance of reflex actions
Protect the body from harmful stimuli that do not have to be learned
Fast because the neurone pathway is short
Involuntary and do not require decision-making powers of the brain
Control of heart rate by chemo-receptors (CO2 increase)
Respiration produces increase in CO2
Blood pH is decreased
This is detected by chemo-receptors in the carroted and aortic bodies
Increased frequenct of impulses sent from medulla along the sympathetic nerve
SAN increases heart rate
Control of heart rate by pressure receptors (pressure increased)
Pressure receptors in the carroted arteries and arota detect an increase in blood pressure
Nervous impulses sent to the medulla
Medulla sends more imoulses down the parasympathetic nerve
SAN decreases heart rate
Functions of the pacinian corpuscle
Pressure is applied
The membrane around the neurone becomes stretched
Stretch mediated sodium channels are widened
NA+ ions diffuse into the neurone
Membrane potential changes
It becomes depolarised and proidueces a generator potential
which then creates an action potential that is passed along the neurone
How connections of neurones make it possible to see in dim light
Several rods have connection with one bipolar neurone
Uses spatial summation aka retinal convergence
To allow impulses to exceed threshold for action potential
Rod cell bits
Rod cells contain rhodopsin
Rhodopsin can be broken down in low-light intensity
But a consequence of retinal convergence means that light received by red cells sharing the same neurone will only generate a single impulse, regardless of how many neurones are stimulated
This results in low visual acuity
Cone cell bits
Cone cells respond to higher levels of light intensity
Their pigment iodhopsin requires more light to break it down
Cone cells can respond to colour and are connected to single neurones so they have have higher visual acuity
Hence we can’t see colours at night and can see much more detail in colour
Fovea
Point directly behind the pupil
Receives most light
Only cone cells found here
Blind spot
Part of the eye where the optic nerve attaches and there are no rod or cone cells
Periphery
Only red cells found
Peripheral vision tends to be blurry
Low visual acuity
Resting potential
Na+ ions actively transported out of the axon
K+ ions actively transported into the axon
Active transport of Na+ is greater
Electrochemical gradient caused by inbalance of +ve ions
Na+ begin to diffuse back into the axon
K+ starts diffusing back out of the axon
Na+ channels close so more K+ leaves than Na+ enters
Equilibrium is established as outside of axon is more positive and K+ cannot diffuse out
What do the different pumps at channels do at different stages?
Resting potential maintained by sodium and potassium ion pumps
Depolarisation caused by sodium gates opening
Repolarisation caused when potassium gates open
Refractory period where sodium gates cannot open
Resting potential re-established by ion pumps.
Action Potential
Energy of stimulus causes sodium voltage-gated channels to open
Na+ ions diffused into axon along an electrochemical gradient
This triggers a reversal in the potential difference across the membrane (depolarisation)
Repolarisation
Voltage-gated sodium channels close, preventing further influx of Na+ ions
Voltage-gated potassium channels open
K+ diffsues out causing repolarisation
Temporary overshoot of electrical charge (hyperpolarisation) causes K+ channels to close
Resting potential is re-established
Factors affecting the speed of impulse
Presence of a myelin sheath - impulse jumps from node to node when the myelin sheath insulates rest of axon so impuse speeds up
Diameter of axon - when larger conductance is faster as there is less resistance and less ion leakage
Temperature - higher temps are faster to do faster diffusion of ions (higher resp. rate (inc. ATP production) and higher kinetic energy)
Metabolic Poisons - Inhibit production of ATP during respiration meaning less energy for sodium/potassium ions to be pumped out/in and resting potential cannot be achieved
Refractory Period
Where inward movement of Na+ ions is prevented due to closure of the sodium voltage-gated channels - impossible to create a further action potential during the time
Ensures that action potentials are propagated in only one directions
Ensure only discrete impulses are produced
Limits the number of AP’s
All or Nothing principle
Below the threshold value there is no action potential and therefore no impulse will be generated
Any stimulus above the threshold value will produce an action potential regardless of strength or size of the stimulus
Release and binding of Acetylcholine
How an impulse carries across the synapse
Energy from stimulus causes calcium ion channels to open and Ca2+ ions enter the synaptic knob
Synaptic vesicles fuse with presynaptic membrane and release acetylcholine into the synaptic cleft
Acetylcholine fuses with complementary receptors on the postsynaptic neurone
Sodium channels open and Na+ ions to diffuse in along a concentration gradient
Depolarisation occurs and a new AP is generated on the post synaptic neurone
Recycling of Acetylcholine
Acetylcholinesterase hydrolyses acetylcholine into choline and ethanoic acid
The products diffuse across the synaptic cleft into the presynaptic neurone
ATP is used to recombine the choline and ethanoic acid.
Why is acetylcholine recycled?
Avoids build of transmitter in the synaptic cleft
Allows the neurotransmitter to be reused
Prevent the formation of continuous APs in the post synaptic neurone (because sodium gates would remain open and axon be constantly depolararised)
Temporal Summation
The same presynaptic neurone releases neurotransmitter over time in order for the concentration to accumulate exceeding the threshold.
Spatial Summation
Different presynaptic neurones release neurotransmitter into the same cleft in order for the concentration to accumulate exceeding the threshold
Why is nervous transmission delayed at synapses?
It takes time for enough neurotransmitter to be accumulated to exceed the threshold.
Synapse inhibition
Cl- ion channels on postsynaptic neurone open
Cl- ions diffuse into the axon
Charge is made more negative than at resting (hyperpolarizing)
New action potential is less likely to form.
Sometimes inhibition is a good thing: natural chemical GABA causes most epilepsy and is treated with a drug that binds to receptors that binds receptors and inhibits nerve transmission
Drugs can act on synapses in two ways:
- Stimulate by creating more AP’s
- mimic a neurotransmitter
- stimulate release of neurotransmitter
- inhibit enzymes that breakdown neurotransmitters
- enhance the binding of neurotransmitters to its receptors
- Inhibit by creating fewer action potentials
- inhibit release of neurotransmitter
- block receptors on postsynaptic neurone - e.g. painkillers block receptors in pain pathways reducing pain experienced
- enhance the binding of neurotransmitters to its receptors - e.g. Valium enhances the effect of GABA which inhibits nerve transmissions
Muscle Contraction Diagrams:
Sarcomere shortens Z lines move closer together H zone is shorter I band is shorter A band remains same size-size of Myocinn filaments do not change.
Role of calcium ions in contraction of a myofibral
Calcium ions bind to Troponin
This moves Tropomyocin
This reveals the binding sites on the Actin
This allows myocin heads to bind to the Actin-forming a crossbridge
Myocin Head moves pulling the Actin along in a ratchet mechanism (power stroke).
This activates ATPase-energy is released from ATP
Describe how nerve impulses arriving at a neuromuscular junction result in the shortening of Myofibrils:
Nerve impulses causes calcium ions enter the presynaptic membrane.
Vesicles fuse with the membrane by exocytosis releasing acetylcholine (NT).
NeuroTransmitter diffuses across the synapse.
NeuroTransmitter binds to receptors in the post synaptic membrane.
Depolarisation.
Release of calcium ions from within the muscle.
Calcium ions bind to Troponin
This moves Tropomyocin
This reveals the binding sites on the Actin
This allows myocin heads to bind to the Actin-forming a crossbridge
Myocin Head moves pulling the Actin along in a ratchet mechanism (power stroke).
This activates ATPase-energy is released from ATP
Role of ATP and Phosphocreatine in producing a muscle fibre contraction:
ATP allows Myocin to detach from Actin.
Phosphocreatine allows regeneration of ATP by providing inorganic phosphate to combine with ADP.
This only happens in anaerobic conditions.
Importance of recyclingthe Neurotransmitter (contextual-acetylcholine in muscle contraction)
ACH stays bound to the receptors on the Post-synaptic membrane.
Sodium channels will be permanently open.
Cell will be continually depolarized.
Continuous formation of action potentials.
Muscle will be permanently contracted and unable to relax.
Slow twitch fibres:
properties:
- Contract more slowly
- Less powerful
- Adapted to endurance work
- Adapted for aerobic respiration(avoiding build up of lactate)
- Lots of Myoglobin (higher affinity for O2+appears darker
- Good supply of Glycogen (can be hydrolysed into a glucose for respiration, production of ATP)
- Good supply of blood vessels to circulate O2 and Glucose and remove Carbon Dioxide.
- Numerous Mitochondria (more respiration-production of ATP)
Fast Twitch Fibres:
Properties:
- Contract more rapidly
- Powerful contractions over a short period of time.
- Adapted for intense exercise
- Thicker and more umerousMyocin Filaments.
- High concentration of enzymes that are involved in anaerobic respiration
- Good store of phosphocreatine (generates ATP from ADP quickly to provide energy.
Muscle Relaxation
When stimulation ceases calcium ions actively transported into the sarcoplasmic reticulum using ATP
Tropomyocin re-blocks Actin binding site.
Myocin heads unable to bind Actin.
No crossbridge is formed-contraction ceases.
Rigormortis
No respiration. No ATP produced. Myocin Head unable to detach from Actin binding site. Crossbridges remain firmly bound. Muscles unable to relax.
Roles of ATP in Muscle Contraction:
1 - Formation of Crossbridges between Myocin Head & Actin binding site.
2- Powerstroke movement of Myocin Head
3 - Detachment of Myocin Head
4 - recovery stroke movement of Myocin Head (return to original position)
Comparison of DNA & RNA
1- DNA contains Deoxribose sugar - RNA contains Ribose
2- DNA contains Thymine - RNA contains Uracil
3- DNA is double stranded - RNA is single stranded
1- Both contain Cytosine, Guanine & Adenine
2- Both contain Phosphate Groups
3- Both contain Pentose sugars
Comparison of mRNA and tRNA
1- mRNA is a single helix linear molecule-tRNAis a clover leaf shaped molecule
2- mRNAis chemically unstable - tRNA is chemically more stable
3- mRNA does not have areas of complementary based pairing - tRNA does.
4- mRNA has no hydrogen bonding - tRNA does.
5- mRNA length is variable - tRNA length is specific and standard.
6- mRNA has no AA attachment sites - tRNA does.
1- mRNA has a Codon - tRNA also has a Codon however technically called AntiCodon.
2- Both have the same bases
3- Both contain Pentose sugar ribose
Transcription
- DNA double helix unzips, hydrogen bonds are broken
- Transcriptional factor binds promoter of gene
- RNA polymerase binds to promoter
- Free mRNA nucleotides complementary base pair with exposed DNA nucleotides (only on the template strand)
- RNA polymerase seals the new backbone of mRNA (catalyses the formation of new phosphodiester bonds between adjacent nucleotides)
- When RNA polymerase reaches a stop codon it detaches and pre-mRNA is formed
- DNA strands rejoin
Translation
- Ribosome attaches to mRNA at start codon (AUG)
- tRNA is activated in the cytoplasm by binding to a specific amino acid
- This process requires ATP
- tRNAs with complementary anticodon sequence base pair with mRNA codons
- Ribosome moves along the mRNA bringing together two tRNAs at any one time
- Two amino acids on the tRNA are joined by a peptide bond, this also requires ATP
- tRNA is released from the amino acid and is recycled
- Synthesis continues until the ribosome reaches a stop codon
- The polypeptide chain then detaches and is folded into a functional protein
Post-transcriptional modification of pre-mRNA (splicing)
- Pre-mRNA copies whole section of a gene including non-coding regions
- Introns are removed (spliced) from the mRNA by enzymes
- Functional exons are joined together
- Mature mRNA molecules leave nucleus via a nuclear pore
Uses of SiRNA
- to identify the role of genes in biological pathways
* to block the genes that cause genetic diseases
Totipotency
Cells that are able to differentiate into any body cell
Ways to isolate a DNA fragment
- Identify the gene using a DNA probe and cut it out using restriction enzymes
- Artificially synthesise the gene, after working out its base sequence from knowing the primary protein structure
- Using mRNA and reverse transcriptase to produce cDNA
Using reverse transcriptase to produce DNA fragments
- a cell that readily produces the required protein is selected
- the large quantities of relevant mRNA are extracted from the nucleus
- reverse transcriptase (isolated from retroviruses) enzyme catalyses the formation of cDNA from the mRNA
- via complementary base pairing
- DNA polymerase is used to build up the complementary DNA nucleotides
Ways to get multiple copies of a gene
- PCR (in vitro gene cloning)
- In vivo gene cloning (inserting a gene into a plasmid and transforming bacteria) – this one gets you a desirable protein product!
Primer
Short single-stranded molecules of DNA, which complementary base pair with specific regions on the DNA molecule
Function of primers in PCR (in vitro cloning)
- Primers prevent the single strands of DNA re-joining
* Provide a short double stranded section of DNA for the attachment of Taq polymerase
Advantages and disadvantages of PCR
- extremely rapid
- does not require living cells
- can be v. inaccurate
- cannot be used to make genes to be used in humans for things like gene therapy as it may give rise to further mutation
PCR (in vitro cloning)
- DNA is heated to 95°C to separate the strands
- By breaking the hydrogen bonds
- Mixture is cooled to 55°C
- Primers are added (see below) – lower temperature allows primers to anneal
- Molecules are reheated to 72°C (optimum for Taq polymerase)
- Taq polymerase (DNA pol) joins nucleotides together
In vivo gene cloning (gene transfer) – to make lots of a useful protein e.g. insulin, human growth hormone
- required gene is identified from DNA strand using a DNA probe and is isolated by cutting at specific recognition sequences using restriction endonucleases
- the same restriction endonuclease is used to cut the plasmid vector
- to produce complementary palindromic sticky ends
- DNA ligase is used to seal the DNA of the required gene into the plasmid vector; this produces a recombinant plasmid
- bacteria are then given an electric or thermal shock to encourage them to take up the recombined plasmid
- successful recombinants are identified using a marker gene e.g. antibiotic resistance, luciferin / GFP, lactase
- colonies containing bacteria possessing the recombined plasmid are selected and cultured in a batch fermenter; the required protein is extracted and purified
Advantages of In vivo cloning (gene transfer)
- useful for delivering a gene into another organism
- involves no risk of contamination (due to matching of sticky ends)
- very accurate (mutations are very rare)
- cuts out specific genes
- produces transformed bacteria, which can be used to produce large quantities of gene products
Marker genes
3 types:
• antibiotic resistance e.g. ampicillin, tetracycline
• makes a fluorescent protein e.g. luciferin / GFP
• produces an enzyme with an identifiable action e.g. lactase turns a particular substrate blue
Using antibiotic resistance marker genes (replica plating)
- bacteria are cultured on a plate containing ampicillin – those that survive are known to have taken up the recombinant plasmid
- a sterile gauze is used to transfer the colonies onto a second plate containing tetracycline
- the colonies of bacteria containing the recombinant plasmid will not survive on the second plate
- as the gene for tetracycline resistance will have been disrupted due to insertion and subsequent ligation of the required gene
- the colonies transferred are in the same position as the originals
- so comparison of the plates can identify the required colonies (i.e. the colonies that appear on the first plate but not on the second plate)
GM Plants
- tomatoes that do not soften (the enzyme causing softening has its expression blocked, as the mRNA cannot be translated)
- herbicide-resistant crops
- disease-resistant crops e.g. modified rice to withstand a particular virus
- pest-resistant crops e.g. maize produces a toxin, killing the beetles that feed on it
- plants that produce plastics
- rice that expresses beta-carotene to avoid the deficiency problems in some Asian countries
GM animals
- disease-resistance
- transfer of growth hormone genes to increase yield e.g. salmon
- sheep/goats with modified milk that can express useful proteins e.g. spider silk or anticoagulants such as factor IX (antithrombin)
Gene therapy
The replacement or supplementation of defective genes in an individual with genes cloned from healthy individuals (or with DOMINANT ALLELES in the case of gene supplementation – but only useful if the disease-causing gene is a recessive allele)
Cystic Fibrosis
- mutant recessive allele with 3 bases missing (deletion mutation)
- amino acid left out of protein for chloride ion channels (CFTR protein)
- chloride ions are not transported out of epithelial cells
- so water does not move out cells by osmosis (water potential gradient not produced)
- so epithelial membranes dry out and produce a sticky mucus, which blocks the airways
CFTR Gene therapy using a viral vector
• adenoviruses made harmless by interfering with a gene involved in their replication
• adenoviruses grown in epithelial cells along with recombinant plasmids containing the normal CFTR gene
• gene becomes incorporated into the DNA of the viruses
• viruses are isolated from the cells and purified
• viruses containing the gene are introduced into the patient’s nostrils
viruses inject their DNA into epithelial cells of the lungs
CFTR gene therapy using lipid-molecule wrapped genes
- CFTR genes isolated and inserted into plasmid vectors
- vectors are reintroduced into host cells and gene markers used to detect successful recombinants
- bacteria are cloned to produce multiple copies of the CFTR gene
- plasmids extracted and wrapped in lipid molecules to form a liposome
- liposomes sprayed into nostrils as an aerosol and are drawn into the lungs
- liposomes pass across the phospholipid portion of the cell membrane of lung epithelial cells
Problems with gene therapy
- patient could become resistant to the viral vectors
- patient’s immune system could recognize the viral vectors as non-self antigens and destroy it
- effects are only short term
- viral vectors may cause infections
- protein may not be expressed
Treatment of SCID
- normal ADA gene isolated from human tissue and cut using restriction endonuclease
- ADA gene inserted into a retrovirus
- Retroviruses are grown with host cells to increase their number
- Retroviruses mixed with patient’s T cells
- Retroviruses inject a copy of the normal ADA gene into the T cells
- T cells are reintroduced into the patient’s blood to provide the code needed to make ADA
ONLY EFFECTIVE FOR 6-12 MONTHS
What is SCID?
Disease caused by a defective version of a gene coding for adenosine deaminase (ADA).
The normal enzyme destroys toxins that kill white blood cells.
The mutant enzyme cannot destroy the toxins and therefore white blood cells are affected and are unable to produce antibodies.
DNA sequencing (Sanger method) Determining the exact order of nucleotides in a DNA sequence
- Four tubes set up containing ssDNA fragments (of the gene to be sequenced) – these act as a template for synthesis of the complementary strand
- Mixture of nucleotides added (ATCG) plus a small quantity of modified nucleotide terminators added to each tube (A* to tube 1, T* to tube 2 etc)
- Primer added (as DNA polymerase only works on short sections of dsDNA) – the primer is labeled with a fluorescent dye or is radioactively tagged
- DNA polymerase added to synthesise new DNA
- addition of a modified nucleotide to the sequence (which is a random process) truncates the synthesis depending on where this happens, different size fragments are produced
- the fragments from tube 1 all have one thing in common – they all end in A (for example) and all the fragments from tube 2 end in T etc. Fragments can be identified due to the radioactive or fluorescent labeling.
- The fragments are then separated using gel electrophoresis (based on density)
Genetic fingerprinting
- DNA is extracted from the sample and restriction endonucleases cut the DNA into fragments; this is inserted into wells on an agar jelly
- Fragments are separated using gel electrophoresis where an electrical charge is applied to the gel
- DNA moves to the positive end as it is negatively charged
- Smaller, lighter fragments move the furthest up the gel
- Southern blotting occurs to transfer the DNA fragments from the gel to a nylon membrane
- DNA probes are added to radioactively label the fragments
- The membrane is placed onto an x-ray film and developed – a banding pattern is revealed
Effects of a Gene Mutation:
Changes the nucleotide base sequence on DNA.
Changes the sequence of mRNA codons.
tRNA brings different Amino Acids to the Ribosome (incorrect).
Changes in the primary sequence of AAs may changer the tertiary structure of the protein.
Bonds form in diff places and therefore the folding pattern is different.
CONTEXT
Enzyme-active site changes shape.
ABS-AGS complexes do not form.
Hb-Quaternary structure changes shape-Haem group can no longer transport O2
Characteristics of Stem cells
Pluripotent-power to differentiate into a limited number of type of cells- i.e. bone marrow stem cells.
Totipotent-power to differentiate into all types of cells.
Stem Cells are constantly replicated and replaced.
Totipotent cells are only found in the unborn foetus.
Plants have meristem cells-totipotent-throughout life.
Role of proto-oncogenes:
Normal role is to stimulate cell division.
Mutation causes the formation of an Oncogene.
This can permanently activate the membrane receptor protein so:
1- Cell division is switched on even in the absence of growth factors.
2- Oncogene may code for a growth factor which would then be produced in excessive amounts.
Role of tumour suppressor gene:
Normal role is to inhibit cell division.
Mutation can cause inactivation.
Cell division is no longer inhibited and becomes uncontrollable.
Effect of Oestrogen on Transcription:
In the cytoplasm, Oestrogen combines with a receptor on the transcriptional factor molecule (due to its complementary shape).
Oestrogen changes the shape of the receptor molecule (non competitive inhibition)
Inhibitor molecule is released from the transcriptional factor.
Transcriptional factor can then enter the nucleus and bind to the DNA.
This stimulates transcription of a particular gene.
CONTEXT
Gene that causes mutations in Oncogenes - Angelina Jolie
Effect of siRNA on gene expression:
dsRNA is broken up by an enzyme dicer into siRNA (small interfering)
1 strand of siRNA combines with an enzyme.
siRNA strand (within the RISC Complex) pairs with complementary bases on a mRNA strand (which has just left the nuclear pore).
The RISC Complex (bound with the siRNA) cleaves the mRNA into smaller sections.
translation cannot take place fully because the full sequence of AAs would not join.
PCR and DNA replication:
PCR uses heat to separate the strands-DNA uses the enzyme Helicase to separate the strands.
PCR uses primers to attach DNA Polymerase-DNA does not.
PCR uses TAQ Polymerase which works at 72c - DNa uses a Polymerase which works at body optimum temperature (36.5c)
Both involve breaking hydrogen bonds.
Both use Polymerase.
Both involve complementary base pairing.
What is a Gene Probe?
A DNA probe is a short single stranded section of DNA with a radioactive or fluorescent marker label.
The probe is designed in the lab so that the bases are complementary to part of the genetic sequence in the target gene.
Usually used to screen for genetic diseases or identify sequences in DNA samples (criminal/paternity)
Response to an increase in blood glucose
blood glucose level increases detected by beta-cells of pancreas
insulin is produced which causes:
-increased cellular respiration
-conversion of glucose to glycogen (glycogenesis)
-conversion of glucose to fat
-absorption of glucose into cells
lowering of blood glucose causes beta-cells to reduce insulin secretion (negative feedback)
adrenaline also raises blood glucose by activating an enzyme that causes the breakdown of glycogen to glucose in the liver (glycogenolysis) and by inactivating an enzyme that synthesizes glycogen from glucose (glycogenesis)
Definition of ectotherm
An organism that relies on environmental/external heat sources to maintain a constant core body temperature.
Def. of endotherm
An organism that has internal temperature regulation, and metabolic process responses to ensure the maintenance of core body temperatures.
