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Module 5 revision

Sara Bean
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OCR A Level Biology Module 5 - Communication, homeostasis and energy

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Why is coordination needed? Organisms have to coordinate all their different cells and organs to make sure they're operating effectively overall Have to be able to respond to changes in their internal and external environments Neuronal communication Neurones have: cell body --> contains the nucleus with a cytoplasm full of endoplasmic reticulum and mitochondria which are involved in the production of neurotransmitters dendrons --> responsible for transmitting the impulse TOWARDS the cell body axons --> transmit the impulse AWAY from the cell body Three types of neurone: sensory --> transmit impulses from receptor to the relay neurone, motor neurone or the brain --> have one dendron and one axon relay --> transmit impulses between sensory and motor neurones --> short dendrons and axons motor --> transmit the impulse to the effector --> one long axon and many short dendrites Myelination: Schwann cells produce layers of plasma membranes around the axon The layers of plasma membrane act as an insulating layer which makes the impulse faster than non-myelinated as it has to "jump" between the gaps (aka the nodes of Ranvier) This "jumping" = saltatory conduction Sensory receptors Specific to a single type of stimulus Act as transducer --> convert stimulus into a nerve impulse by generating a generator potential Four types: mechanoreceptor = pressure and movement chemoreceptor = chemicals thermoreceptor = heat photoreceptors = light Pacinian corpuscle is a type of mechanoreceptor has special sodium ion channels in its plasma membranes --> stretch-mediated channels when these channels change shape / stretch the permeability to sodium ions changes too Resting potential Resting potential = no impulse in the neurone -70mV Generated by: sodium-potassium ion pump actively pumps 3 sodium ions OUT for 2 potassiums IN the sodium ion channels are mostly closed so they can't diffuse in the potassium ion channels are open so they diffuse back out of the axon ^^ this combines to give an overall resting potential of -70mV Action potential The neurone has a resting potential (some K ion channels are open but the Na voltage-gated channels are closed) Energy of the stimulus triggers some of the voltage-gated Na channels to open so Na ions diffuse into the axon down their electrochemical gradient This change in charge triggers more of the voltage-gated Na channels to open (positive feedback) When the potential difference reaches +40mV the voltage-gated Na channels close and the voltage-gated K channels open K ions diffuse out the axon, down their electrochemical gradient to make the axon more negative Lots of K ions move out, making the axon super negative (-90mV) so the voltage-gated K channels close The Na-K pump takes over again to restore the resting potential of -70mV This is followed by a refractory period where another impulse cannot be fired -70mV = resting potential -70mV --> +40mV = depolarisation +40mV --> -70mV = repolarisation -70mV --> -90mV = hyperpolarisation -90mV --> -70mV = restoration of resting potential Propagation of action potentials The depolarisation of one region on the membrane of an axon acts as a stimulus for the next region along ^^ this continues along the length of the axon  Refractory period prevents the propagation of the action potential BACKWARDS down the membrane --> makes sure the impulse is unidirectional ^ also ensures the action potentials don't overlap Action potentials are sped up by: axon diameter --> the bigger the diameter, the faster the impulse because there is less resistance to the flow of ions temperature --> higher the temperature, the faster the impulse because the ions have more kinetic energy All or nothing principle A certain level of stimulus must be achieved before a response is triggered (threshold value) No matter how large the stimulus, the same action potential is always triggered The size of the stimulus effects the number of action potentials generated at a given time (larger stimulus = more frequent action potentials) Synapses Types of neurotransmitter excitatory --> results in the depolarisation of the post synaptic neurone --> acetylcholine inhibitory --> results in hyperpolarisation of the post synaptic neurone to prevent an action potential from being triggered --> GABA in the brain Action potential reaches the end of the presynaptic neurone Depolarisation of the presynaptic neurone causes Ca2+ channels to open Influx of Ca2+ cause the vesicles containing the neurotransmitter to fuse with the presynaptic membrane --> neurotransmitter released by exocytosis Neurotransmitter diffuses across the synaptic cleft and binds to the specific receptors in the membrane of the postsynaptic neurone This causes the Na+ channels to open which triggers an action potential in the postsynaptic neurone Once the neurotransmitter has triggered this action potential it is removed from the receptors and left in the cleft They are often broken down by enzymes and the products diffuse back to the presynaptic neurone to be reformed into the neurotransmitter Acetylcholine synapses are often found between motor neurones and muscle cells The acetylcholine is hydrolysed by acetylcholinesterase which is also released from the presynaptic neurone The products of the hydrolysis are choline and ethanoic acid Role of synapses Ensure impulses are unidirectional Allow a single stimulus to create a number of simultaneous responses - divergence Allows the results from different stimuli to create a single result - convergence Summation and control When the neurotransmitter from a single impulse isn't enough to trigger an action potential, the neurotransmitter isn't removed from the cleft until it builds up to trigger an action potential --> summation Types: temporal --> release of a neurotransmitter several times over a period to trigger an action potential in the postsynaptic neurone spatial --> number of presynaptic neurones connect to one postsynaptic neurone --> each releases neurotransmitter which builds to a high enough level in the synapse to trigger an action potential Organisation of the nervous system Central Nervous System --> brain and spinal cord Peripheral Nervous System --> neurones that connect the CNS to the rest of the body PNS splits to Somatic nervous system --> concious control (move a muscle) Autonomic nervous system --> subconcious control (peristalsis) Autonomic nervous system splits to: Sympathetic nervous system --> "fight or flight" Parasympathetic nervous system --> "rest and digest" The brain Protected by the skull Surrounded by protective membranes --> meninges  Cerebrum --> voluntary actions (thinking, memory, personality, learning) split into cerebral hemispheres which control each side of the body outer layer of the hemispheres = cerebral cortex Cerebellum --> unconscious functions (posture, balance) Medulla oblongata --> autonomic control (heart and breathing rates) Hypothalamus --> regulatory centre for water balance and temperature (produces hormones like ADH) Pituitary gland --> stores and releases hormones anterior produces 6 hormones including FSH posterior stores and releases the hormones made in the hypothalamus (ADH) Reflexes Stimulus, Receptor, Sensory, Relay, Motor, Effector, Response Silly, Rabbits, Sometimes, Rob, My, Enormous, Radishes Blinking reflex: cornea is stimulated  impulse along fifth cranial nerve (sensory neurone) impulse passes to relay neurone in lower brain stem impulses sent along seventh cranial nerve (motor neurone)  the eyelids close Survival importance being involuntary responses --> the brain is left to deal with more complex responses so its not overloaded not having to be learned --> present at birth and provide immediate protection extremely fast --> the reflex arc is very short many are what we consider everyday actions like standing upright Voluntary and involuntary muscles Skeletal muscle striated voluntary control regularly arranged to get contraction in one direction rapid contraction speed short contraction fibres tubular and multinucleated Cardiac muscle specialised striated involuntary control cells branch and interconnect to simultaneously contract intermediate contraction speed fainted striations than skeletal muscle fibres are branched and uninucleated Involuntary / smooth muscle non-striated involuntary control different cells contract in different directions slow contraction speed no cross striations fibres are spindle shaped and uninucleated Structure of skeletal muscle Muscle fibres enclosed in plasma membrane AKA sarcolemma contain large number of nuclei longer than normal cells shared cytoplasm = sarcoplasm parts of sarcolemma fold inwards to help spread electrical impulses = T tubules lots of mitochondria to provide ATP for muscle contraction modified endoplasmic reticulum = sarcoplasmic reticulum with calcium ions for muscle contraction Myofibrils each muscle fibre contains many myofibrils myofibrils = organelles made of protein and specialised for muscle contraction lined parallel to provide maximum force when they contract together two types of protein filament: actin --> thinner filament (two strands twisted together) myosin --> thicker filament (rod-shaped fibres with bulbous heads)  alternatig light and dark bands light bands = areas where actin and myosin DON'T overlap --> called the I bands dark bands = areas where myosin are present, edges even darker because they overlap with the actin --> A bands Z line = line found at centre of each light band --> distance between two is a sarcomere (when a muscle contracts, the sarcomere shortens) H zone = lighter region at the centre of each dark band where only myosin are present (when a muscle contracts, the H zone decreases) Sliding filament model Myosin pulls actin inwards towards the centre of the sarcomere so  the light band becomes narrower the Z lines move closer together H zone becomes narrower Structure of myosin globular heads which are hinged --> allow them to move back and forth on the heads, there's one binding site for actin and one for ATP Structure of actin filaments have binding sites for the myosin heads binding sites often blocked by tropomyosin which is held in place by troponin How muscle contraction occurs Acetylcholine released into neuromuscular junction  Causes depolarisation of sarcolemma This travels deep into the fibre through the T tubules When the action potential reaches the sarcoplasmic reticulum, the calcium ion channels are opened The Ca2+ diffuse down their concentration gradient to flood the sarcoplasm with Ca2+ The Ca2+ bind to the troponin, causing it to change its shape, pulling the tropomyosin away from the binding sites on the actin The myosin heads bind to the actin, forming a actin-myosin cross-bridge The myosin heads flex, pulling the actin along ATP binds to myosin head, causing it to detach because of the ATPase activity of the myosin The myosin can now attach to the next binding site and the cycle continues until the Ca2+ detach from the troponin
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Endocrine system is made of endocrine glands which are a group of cells specialised to secrete chemicals (hormones) directly into the bloodstream Pituitary gland = growth hormone, ADH, FSH, LH Thyroid gland = thyroxine Adrenal gland = adrenaline, noradrenaline, aldosterone Testis = testosterone Ovaries = oestrogen Pancreas = insulin, glucagon Thymus = thymosin Hormones Secreted directly into the blood They then diffuse to bind to specific receptors on target cells or organs Once bound they cause the organ to produce a response Steroid hormones --> lipid soluble so pass through the cell membrane of the cell and bind to receptors in the cytoplasm or nucleus --> forms a hormone-receptor complex which has a transcription factor attached so a gene is either activated or inhibited as a result Non-steroid hormone --> hydrophillic so bind to specific receptors on the cell surface membrane --> triggers cascade reaction in cell involving secondary messengers like cAMP Adrenal glands Adrenal cortex --> outer region of the glands where cortisol and aldosterone are made controlled by hormones released from the pituitary gland Glucocorticoids (release controlled by hypothalamus) --> cortisol which regulates metabolism and corticosterone which works with cortisol to regulate the immune response and suppress inflammatory reactions Mineralcorticoids (release controlled by signals from the kidneys) --> aldosterone which helps control blood pressure and maintain water and mineral balances in the blood  Andorgens --> small amounts of sex hormones  Adrenal medulla --> inner region of the gland where adrenaline and noradrenaline are made released when the sympathetic nervous system is stimulated adrenaline --> increases heart rate, raises blood glucose levels (glycogenolysis and gluconeogenesis) noradrenaline --> works with adrenaline to increase the heart rate, dilate the pupils, widen air passages and narrow blood vessels to non-vital organs Fight or flight response Once a threat is detected by the autonomic nervous system, the hypothalamus is stimulated Hypothalamus stimulates sympathetic nervous system The sympathetic nervous system stimulates the adrenal medulla and smooth muscles to secrete adrenaline and noradrenaline Hypothalamus stimulates the pit. gland to release ACTH ACTH travels to the adrenal cortex and activates the release of about 30 hormones to help with the response  heart rate increases to pump more oxygenated blood to the muscles for respiration pupils dilate to take in as much light as possible for better vision aterioles near skin constrict  to send more blood to major muscle groups blood glucose rises to increase glucose available for respiration  smooth muscle in airways relaxes to let the most amount of air into the lungs non-essential systems shut down to focus energy to muscles Action of adrenaline Adrenaline is non-steroid based so binds to specific receptors in the cell membrane When it has bound, the enzyme adenylyl cyclase inside the cell is activated Adenylyl cyclase triggers the conversion of ATP to cyclic AMP or cAMP on the inner surface of the membrane in the cytoplasm The increase in cAMP activates protein kinases which phosphorylate and in turn activate other enzymes (e.g. enzymes that break down stored glycogen to glucose) The pancreas Endocrine gland --> produces hormones (insulin and glucagon) that are released into the bloodstream Exocrine gland --> produces enzymes (amylases, proteases and lipases) which are released into the duodenum  Islets of Langerhans have alpha and beta cells Alpha cells produce glucagon Beta cells produce insulin Alpha cells are bigger and more numerous in the islets than the beta cells Beta cells are usually stained blue and alpha cells are pink Controlling blood glucose Example of negative feedback loop Increased via diet, glycogenolysis and gluconeogenesis Decreased via respiration and glycogenesis Role of insulin high blood glucose is detected by the beta cells and they respond by secreting insulin into the bloodstream virtually all body cells have insulin receptors in their plasma membranes when insulin binds to its glycoprotein receptor it changes the tertiary structure of the glucose transport channel proteins in the membrane this increases the cell's permeability to glucose so more is removed from the blood insulin also activates the enzymes that convert glucose to glycogen in the cell (glycogenesis) insulin also increases the respiratory rate of cells and inhibits the release of glucagon by the alpha cells Role of glucagon low blood glucose is detected by the alpha cells and they respond by secreting glucagon into the bloodstream only liver and fat cells have receptors for glucagon so they are the only ones that can respond to the hormone glucagon causes glycogenolysis, reduced respiration and increased gluconeogenesis Control of insulin secretion Normal glucose levels --> K channels on the beta cells are open and the cell has a potential of -70mV When glucose levels rise, the concentration of glucose inside the cell increases too as it moves in via a glucose transporter The glucose is metabolised inside the mitochondria resulting in ATP synthesis The ATP binds to the K channels and causes them to close as they are ATP-sensitive potassium channels As K cannot leave the cell so the potential rises to -30mV and depolarisation occurs This causes the voltage-gated calcium channels to open The Ca2+ diffuses in and causes the insulin-containing vesicles to move to the membrane and release the insulin via exocytosis Diabetes Type 1 = patients are unable to produce insulin (usually due to an autoimmune disease that attacks the beta cells) --> usually treated with insulin injections inject too much and they'll suffer from hypoglycaemia (low blood glucose) and fall unconcious inject too little and they'll suffer from hyperglycaemia (high blood glucose) and fall unconcious and possibly die if left untreated Type 2 = patients cannot effectively use or make insulin in order to deal with their blood glucose levels, or their insulin receptors have become unresponsive to the hormone (usually due to diet and often associated with obesity) --> treated via diet and exercise, sometimes with injections but they aren't particularly effective  Pancreas transplants are also effective for type 1 sufferers but transplants come with their own risks (rejection or infection from the surgery) and the waiting list is very long Beta cell transplants have also been tried but they're not very effective as the immunosuppressants that must also be taken increase the metabolic demand on the beta cells which exhausts them Stem cells have the potential to help but it seems like the best stem cells to use will be embryonic ones which bring their own ethical issues donor availability wouldn't be an issue reduced likelihood of rejection people wouldn't have to inject themselves with insulin anymore Controlling the heart rate Heart rate is controlled by the autonomic nervous system The medulla oblongata is responsible for controlling it and making changes Two centres of the med. oblongata which are linked to the SAN via motor neurones accelerator nerve increases the heart rate by sending impulses along the sympathetic nervous system vagus nerve decreases the heart rate by sending impulses along the parasympathetic nervous system Two types of receptor that provide information that affects the heart rate baroreceptors --> detect blood pressure --> aorta, vena cava and carotid arteries chemoreceptors --> detect changes in the levels of chemicals (like carbon dioxide) in the blood --> aorta, carotid artery and medulla Chemoreceptors: sensitive to changes in the pH of the blood CO2 increases --> pH of blood decreases due to more carbonic acid --> centre in med. oblongata increases frequency of impulses via accelerator nerve to SAN (sympathetic nervous system) --> increase in heart rate --> more blood flow to lungs to remove the CO2 quicker CO2 decreases --> pH of the blood increases due to less carbonic acid -->  centre in med. oblongata decreases frequency of impulses to the SAN --> decreases the heart rate --> less flow to the lungs as its not needed Baroreceptors: blood pressure too high --> med. oblongata sends impulses along vagus nerve to the SAN (via parasympathetic nervous system) to decrease the heart rate --> puts the pressure back to normal blood pressure too low --> med. oblongata sends impulses along accelerator nerve to the SAN (via sympathetic nervous system) to increase the heart rate --> puts pressure back to normal Hormones also effect the heart rate --> adrenaline and noradrenaline bind to SAN to affect it in the fight ot flight response
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Endotherms and ectotherms Ectotherms --> use their surroundings to warm their bodies (reptiles and amphibians) behavioural responses --> they bask in the sun, orientating as much surface area toward the sun to absorb the most head by radiation or they can increase their body heat by conduction by pressing their bodies against warm ground or can use some exothermic metabolic reactions they shelter from the sun or dig burrows to cool down or they press their bodies against cool rocks or stones or they orientate their bodies so that a small surface area is in the sun physiological responses --> they use the fact that dark colours absorb more heat radiation than light and some increase or decrease their heart rate to effect their metabolic activity Endotherms --> rely on metabolic processes to heat themselves, usually maintain a steady body temperature regardless of their environment (mammals and birds) behavioural responses --> basking in the sun, pressing themselves to warm surfaces, wallowing in water and mud or digging burrows --> humans wear clothes and build houses physiological responses --> peripheral temperature receptors, thermoregulatory centres in the hypothalamus, the skin and muscles anatomical adaptations --> animals in hot climates have large SA:Vol to increase heat loss (big ears) and pale fur or feathers to reflect the sun but animals in cold climates do the opposite often having a thick insulating layer of blubber cooling down vasodilation --> vessels near the skin dilate so more heat is lost via radiation through the skin increased sweating --> as sweat evaporates from the surface of the skin, heat is lost and the blood below is cooled reducing the insulating effect of hair --> erector pili muscles in the skin relax and hairs lay flat to remove the insulating layer of air warming up vasoconstriction --> vessels near the skin constrict so less heat is lost via radiation through the skin decreased sweating --> reduces the cooling provided by the evaporation of water from the surface of the skin raising of body hairs or feathers --> erector pili muscles contract to lift the hairs or feathers which traps a layer of air to insulate the body and reduce heat loss shivering --> rapid and ivoluntary contracting and relaxing od the large voluntary muscles to increase respiration which releases heat  Changes to the temperature of the blood are detected in the hypothalamus which sends impulses along motor neurones and the autonomic nervous system to effectors in the skin and muscles to create these ^^^^ responses The Liver Has a very rich blood supply Blood supplied by hepatic artery Blood removed by hepatic vein Blood loaded with products from digestion supplied by the hepatic portal vein Hepatocytes (liver cells) have large nuclei, prominent Golgi apparatus and lots of mitochondria Blood from hepatic artery and portal vein mixed together in spaces aka sinusoids which are surrounded by hepatocytes  Mixing increases the oxygen content to satisfy the needs of the hepatocytes Sinusoids contain Kupffer cells which act as macrophages Hepatocytes secrete bile which drain into the canaliculi that drain into the bile duct to the gall bladder   Functions of the liver carbohydrate metabolism  hepatocytes are particularly responsive to insulin and glucagon they convert glucose to glycogen and store it and reverse this when glucagon is about deamination of excess amino acids hepatocytes synthesise most of the plasma proteins hepatocytes carry out transamination where one amino acid is converted to another hepatocytes carry out deamination where the amine group is removed from the molecule the amine group is converted to ammonia and then to urea to be removed  the rest of the amino acid can be used in respiration or the formation of lipids ammonia is converted to urea through the ornithine cycle (ornithine --> ammonia added, CO2 added, water produced --> citruline --> ammonia added, water produced --> arginine --> water added, urea produced --> ornithine) detoxificiation hydrogen peroxide --> by-product of metabolic pathways --> hepatocytes contain catalase which splits it into oxygen and water ethanol --> hepatocytes contain alcohol dehydrogenase --> ethanol converted to ethanal --> ethanal converted to ethanoate which can be used to make fatty acids The kidneys Made of millions of nephrons Ultimately, urine is made which is taken to the bladder by the ureters and it then leaves the body via the urethra Medulla --> contains the tubules of the nephrons and the collecting ducts Cortex --> where the blood is filtered through the dense capillary network Pelvis --> central chamber where the urine collects before going to the bladder Nephrons Bowman's capsule --> contains the glomerulus with its afferent and efferent arteriole Proximal convoluted tubule --> in the cortex, many of the substances are reabsorbed into the blood Loop of Henle --> creates a region of high solute concentration in the medulla to increase water reabsorption Distal convoluted tubule --> in the cortex, fine-tuning of water balance, ions and pH, permeability of walls to water controlled by ADH Collecting duct --> more fine-tuning of water balance and also controlled by ADH Ultrafiltration wide afferent arteriole of glomerulus but narrower efferent arteriole this means the glomerulus has a high pressure which forces blood out through the capillary wall the fluid then pushes through the basement membrane AND podocytes with pedicels into the Bowman's capsule the fluid in the Bowman's capsule contains water, ions, glucose and other substances Reabsorption PCT all the glucose, amino acids, vitamins and hormones moved back into the blood via active transport Na ions move by active transport and Cl ions follow passively PCT cells covered in microvilli and have many mitochondria once removed from the nephron, the substances diffuse into the capillary network down steep concentration gradients Loop of Henle ascending limb is very permeable to sodium and chloride ions in the early limb they just diffuse out but further up they are actively transported out this makes the region hypertonic compared to the descending limb descending limb is very permeable to water and due to the hypertonic region created by the ascending limb the water moves out passively by osmosis DCT permeability of tubule controlled by ADH have many mitochondria for active transport if the body lacks salt, the ions are pumped out water can also leave if there's ADH and aquaporins Collecting duct main site that's effected by ADH the ion concentration in the surrounding solution increases as you go down meaning water can move at any point --> produced hypertonic urine Osmoregulation ADH in produced in the hypothalamus and secreted by the posterior pituitary gland ADH increases the permeability of the CD and DCT to water The hormone is released into the bloodstream It binds to the receptors on the cells and triggers the formation of cAMP cAMP causes the vesicles lining the collecting duct to fuse to the surface membranes and insert the aquaporins into these membranes This provides a route for water to move via osmosis out of the CD and into the capillaries more ADH = more aquaporins so more water is reabsorbed When ADH levels fall, the process is reversed --> cAMP levels fall so the aqauporins are removed from the membranes and they are made less permeable When water levels are low, the osmoreceptors detect that ion concentration of the blood is high and the water potential of the blood and tissue fluid is more negative --> ADH released When water levels are high the blood becomes more dilute and the water potential of the blood and tissue fluid becomes less negative --> the release of ADH is inhibited Kidney failure Shown by protein or blood in the urine Results in loss of electrolyte balance, build up of urea, high blood pressure, weakened bones, pain and stiffness in joints and anaemia If the levels of creatinine in the blood increase it is a sign that the kidneys are damaged Dialysis Haemodialysis --> blood taken from an artery, blood thinners are added, it passes over a semi-permeable membrane where nutrients either diffuse in or out to the optimum levels then returns to the body (uses a countercurrent system to maintain the concentration gradients) Peritoneal dialysis --> inside the body, used the peritoneum as the membrane, dialysis fluid is introduced through a catheter --> excess urea and ions pass out of the capillaries, into the tissue fluid across the membrane and into the dialysis fluid where its drained off Transplants risk of rejection --> match between antigens is made as closely as possible recipient is treated with immunosuppressants for the rest of their lives --> can't respond effectively to any infections transplant doesn't last forever waiting lists can be very long Pregnancy tests Work using monoclonal antibodies that complement hCG (human chorionic gonadotrophin) which is made by the development of the placenta Main stages: Wick is soaked in the first urine passed in the morning Test contains mobile monoclonal antibodies that have dye attached that will only bind to hCG If she's pregnant, the hCG binds to the antibody making a hCG-antibody complex (with the dye) The urine moves up the test by capillary action 1st window has immobilised antibodies that only bind to hCG-antibody complex (if they do the dye attached will show the positive shape) 2nd window has immobilised antibodies that will bind to the mobilised ones regardless of whether they have a hCG attached --> this proves that the test has worked Other urine tests Anabolic steroids  tested with gas chromatography and mass spectrometry  sample is vapourised with a known solvent and passed along a tube a lining of the tube absorbs the gases and is analysed to give an image that can be read to show the presence of drugs Drug testing immunoassay which uses monoclonal antibodies that bind to the drug or its breakdown product ^ if this is positive, they use gas chromatography and mass spectrometry to confirm the presence of a drug
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Auxins cell elongation, prevent leaf abscission, apical dominance, stimulate release of ethene IAA --> growth stimulant made in cells at tips of roots and shoots and meristems move in the transport tissues and cell to cell high concentrations inhibit gibberellins --> supports apical dominance bind to specific receptors in the cell membrane, cause pH to fall to 5 which makes the cell walls flexible and plastic which enables elongation, as the cell matures hormone levels fall and the cell walls become more fixed in shape and inflexible low concentrations promote root growth --> produced in the tips and they get some from the shoot when its little --> less auxin means less growth Gibberellins cause stem elongation of lateral shoots, trigger seed germination, stimulate pollen tube growth in fertilisation add water to seed --> embryo produces gibberellins --> gibberellins + water = gibberellic acid -->activates the transcription of amylase --> amylase breaks the stored starch to maltose --> maltase breaks the maltose to glucose --> glucose is respired for ATP to build materials for growth they effect the length of the internodes (regions between the leaves the stem) and can make them long and spindly Ethene causes fruit ripening, promotes abscission lengthening of the dark period of the day triggers abscission and a period of dormancy --> falling light = falling auxin to which the leaves respond my making ethene --> the base of the leaf has an abscission layer with two layers of ethene sensitive cells --> these cells produce enzymes that digest and weaken the cell walls of the abscission layer when ethene is present --> vascular bundles are sealed off and fatty material is deposited to form a protective scar when the leaf falls --> hormones made cells retain water and put more pressure on the separation layer --> abiotic factors like the wind make the break ABA (abscisic acid) maintains dormancy of seeds and buds, stimulates cold protective responses, stimulates stomatal closure leaf cells release ABA under abiotic stress --> ABA binds to receptors in the plasma membranes --> this changes the ionic concentrations of the cell so water leaves the vacuoles and the stomata are closed Chemical defences to herbivory Tannins --> bitter taste and put animals off eating the plant Alkaloids --> bitter tasting, nitrogenous compounds which act as drugs affecting the metabolism of the animals that take them in or even poisoning them Terpenoids --> form essential oils and act as toxins to insects and fungi Pheremones --> communication between groups of the same species ("I'm being attacked, protect yourselves!") or they attract parasites to eat their attackers rather than let their attackers eat them (wasps lay eggs in over larvae so that the baby wasps eat the larvae but leave the plant alone) How're they used? Ethene used commercially to make fruit perfect ripeness for sale Auxin is used in rooting powder Synthetic auxins can act as weedkillers that only kill broad-leafed plants (their growth rate increases to a point where its unsustainable and it dies) Auxins can be used in the production of seedless fruit Ethene is used to promote early abscission Cytokinins are used to prevent aging of ripened fruit Gibberellins are used to delay ageing and ripening in fruit
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