5.5 Plant & Animal Responses Flashcards

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1
Q

Describe the central nervous system

A

-Brain : relay neurones, multiple connections for complex neural pathways. Mostly non-Myelinated grey matter.
-Spinal Cord: non-myelinated central grey matter, myelinated outer white matter ( carries APs down spinal cord for rapid, long distance communication ).
Protected by vertebral column.

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2
Q

Describe the peripheral nervous system

A
  • sensory and motor neurones bundled in a connective tissue sheath to form nerves
  • ensures rapid communication between sensory receptors, CNS, and effectors.
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3
Q

Describe the motor nervous system

A
  • conducts APs from CNS to effectors
  • somatic nervous system: motor neurones that conduct APs from CNS to voluntary effectors (e.g skeletal muscles). mostly myelinated for rapid responses. one motor neurone only.
  • autonomic nervous system: motor neurones that conduct APs from CNS to involuntary effectors (e.g glands cardiac muscle, smooth muscle ) mostly non-myelinated (don’t need rapid response). At least 2 motor neurones, connected at ganglia.
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4
Q

Describe the sensory nervous system

A

-sensory neurones conduct APs frim sensory receptors to the CNS. cell body in dorsal root leading into spinal cord short axon connects to CNS neurones.

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5
Q

Describe the sympathetic (autonomic) motor system

A
Sympathetic (prepares for activity)
-many nerves leading out CNS, each to a separate effector.
-ganglia just outside CNS
-short pre-ganglionic neurones
-long post-ganglionic neurones
-noradrenaline neurotransmitter
-increases activity
-most active during stress
Effects: -increases heart rate
-dilates pupils
-increases ventilation rate
-reduces digestive activity
-orgasm
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6
Q

Describe the parasympathetic (autonomic) motor system

A
Parasympathetic (conserves energy)
-few nerves leading out CNS which divide to different effectors 
-ganglia in effector tissue 
-long pre-ganglionic neurones
-short post-ganglionic neurones
-acetylcholine neurotransmitter
-decreases activity
-active during sleep/ relaxation
Effects: - decreases heart rate
-constricts pupils
-reduces ventilation rate
-increases digestive activity
-sexual arousal
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7
Q

Briefly describe the parts of the brain

A
  • Cerebrum: largest part, organises most higher thought processes ( conscious thought & memory )
  • Cerebellum: coordinates movement and balance
  • Hypothalamus and Pituitary Complex: organises homeostatic responses and controls physiological processes
  • Medulla Oblongata: coordinates autonomic responses
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8
Q

Describe the cerebrum

A

-2 cerebral hemispheres connected by corpus callosum (neurones)
-outer layer = cerebral cortex (nerve cells)
Controls : -conscious thought
-conscious actions
-emotional responses
-intelligence, reasoning, judgement, decision making
-factual memory
Divided into Areas:
-sensory areas receive APs indirectly from sensory receptors. size of region = sensitivity of area inputs are from
-association areas compare inputs to previous, interpret and judge a response
-motor areas send APs to effectors. size of region= complexity of movement. motor areas on left side of brain control right side of body.

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9
Q

Describe the cerebellum

A
  • balance and fine coordination of movement. receives info from many sensory receptors (e.g. retina spindle fibres)
  • balance, judging position of objects and limbs, tensioning muscles to use tools, coordinating contraction and relaxation of antagonistic skeletal muscles.
  • nervous pathways strengthened by practise
  • connected to cerebrum by pons
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10
Q

Describe the hypothalamus

A

-controls homeostatic mechanisms
-contains its own sensory receptors
-acts by negative feedback
Temperature regulation: hypothalamus detects change in body temperature & receives input from sensory receptors in skin. initiates response for change via nervous or hormonal system.
Osmoregulation: osmoreceptors monitor water potential of blood, osmoregulatory centre initiates a response to reverse the change via the hormonal system.
* if via hormonal it acts via the pituitary gland

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11
Q

Describe the pituitary gland

A
  • posterior lobe linked to hypothalamus by neurosecretory cells. hormones such as ADH pass down the neurosecretory cells and are released into blood from pituitary gland
  • anterior lobe produces hormones that are released in response to releasing factors produced by hypothalamus. control response to stress, growth, reproduction, lactation
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12
Q

Describe the medulla oblongata

A

-controls non-skeletal muscles ( cardiac and involuntary smooth ) by sending APs via the autonomic NS.
Contains centres to regulate:
-cardiac centre: heart rate
-vasomotor centre : circulation and BP
-respiratory centre: rate and depth of breathing
*coordinate functions by negative feedback
-receive sensory information

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13
Q

explain the blinking reflex

A

-causes temporary closure of eyelids to protect the eyes from damage
-cranial reflex (passes through the brain)
-reflex arc as receptor and effector in same place
Stimulated by changes in environment:
-foreign object touching eye (corneal reflex)
-sudden bright light (optical reflex)
-loud sounds
-sudden movements close to eye

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14
Q

explain the corneal reflex

** what’s special about it?

A
  • sensory neurone from cornea enters the pons. synapse connects sensory and relay which passes the AP to the motor neurone. motor passes out brain to facial muscles. rapid (0.1s). usually causes both eyes to blink.
    • sensory neurone also passes the AP to myelinated neurones in the pons. carry it to sensory region in cerebral cortex. this allows the reflex to be overridden by conscious control. the cerebral cortex can send inhibitory signals to the motor centre in the pons. the myelinated neurones transmit the AP more rapidly than the non myelinated neurones in the pons. the inhibitory AP prevents the formation of the AP in the motor neurone.
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15
Q

explain the optical reflex

A

protects light sensitive retina cells from damage. retina detects stimulus and optical centre in cerebral cortex mediates the response. slower than the corneal reflex.

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16
Q

explain the knee jerk reflex

A
  • spinal reflex
  • involved in coordinated movement and balance
  • quadriceps contracts to straighten leg, attached to lower leg by patella tendon. when muscle at front of thigh stretched ( knee bent / leaning backwards ), stretch receptors detect. if unexpected a reflex action causes contraction of the muscle.
  • rapid
  • sensory -> motor
  • higher parts of the brain told that its happening but cant inhibit ( no relay )
  • when walking / running cerebellum inhibits the reflex via inhibitory action potentials to the reflex arc to prevent contraction of opposing muscle.
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17
Q

Explain the physiological changes during the fight or flight response

A
  • pupils dilate: more light enters eyes making retina more sensitive
  • Heart rate and BP increase: increases rate of blood flow to deliver more oxygen and glucose to muscles and to remove CO2 and toxins
  • arterioles to skin and digestive system constricted whilst those to muscle and liver are dilated : diverts blood flow away from skin and digestive system to muscles.
  • blood glucose levels increase: supplies energy for muscular contraction
  • Metabolic rate increases: converts glucose to usable forms of energy such as ATP
  • erector pili muscles in skin contract: hairs stand up, sign of aggression
  • Ventilation rate and depth increase: increases gaseous exchange so more O2 enters blood for aerobic respiration
  • Endorphins released in brain: wounds don’t prevent activity
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18
Q

briefly describe how the fight or flight response is coordinated

A

1) inputs from sensory receptors feed into sensory centres in the cerebrum
2) cerebrum passes signals to association centres
3) if a threat is recognised, the cerebrum stimulates the hypothalamus
4) hypothalamus increases activity in the sympathetic nervous system and stimulates the release of hormones from the anterior pituitary gland.

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19
Q

explain how the sympathetic nervous system brings about the long term fight or flight response ( adrenaline ) (D)

A

-sympathetic nervous system activates the adrenal medulla to secrete adrenaline into the bloodstream.

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20
Q

describe the mechanism of adrenaline action

A
  • first messenger (AA derivative that cant enter cells)
  • binds to adrenaline receptor on plasma membrane, receptor associated with a G protein which is stimulated to activate adenyl cyclase
  • adenyl cyclase converts ATP to cAMP which is the second messenger
  • cAMP causes a series of enzyme controlled reactions that bring about the response
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21
Q

explain the use of releasing hormones in the fight or flight response (D)

A
  • hypothalamus secretes releasing hormones into blood. they pass down a portal vessel to the pituitary gland and stimulate the secretion of tropic hormones from the anterior pituitary.
    1) Corticotropin-releasing hormone CRH from Hypo causes release of Adrenocorticotropic hormone ACTH. ACTH causes adrenal cortex to release corticosteroid hormones ( e.g. glucocorticoids- cortisol )which regulate carb metabolism to release more glucose ( from glycogen or fat/ protein )
    2) Thyrotropin-releasing hormone TRH causes release of thyroid-stimulating hormone TSH which stimulates thyroid gland to release more thyroxine (hormone) which acts on many cells, increases metabolic rate and makes cells more sensitive to adrenaline.
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22
Q

how can heart action be modified?

A
  • raising or lowering heart rate (bpm)
  • altering force of contractions of ventricular walls
  • altering stroke volume
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23
Q

explain the control of the heart rate by the cardiovascular centre

A
  • at rest the SAN controls the heart rate. however the frequency of the waves can be altered by output from the cardiovascular centre in the medulla oblongata
  • nerves from cardiovascular centre ( part of autonomic NS ) supply the SAN, altering frequency of contraction
  • APs sent down a sympathetic (accelerans) nerve and cause the release of neurotransmitter noradrenaline at the SAN to increase heart rate.
  • APs sent down parasympathetic (vagus) nerve release neurotransmitter acetylcholine which reduces the heart rate
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24
Q

give examples of sensory inputs to the cardiovascular centre

A
  • stretch receptors in muscles detect movement of the limbs. these send impulses to the cardiovascular centre to inform it that extra O2 may be needed soon and so heart rate is increased
  • chemoreceptors in the carotid arteries, aorta and brain monitor blood pH. during exercise muscles produce more CO2 which reacts with water in blood plasma to produce carbonic acid which reduces blood pH and affects O2 transport. chemoreceptors detect change in pH and send APs to the cardiovascular centre to increase heart rate.
  • when exercise stops, concentration of CO2 in blood falls, this reduces activity of accelerator pathway to decrease heart rate.
  • stretch receptors in walls of carotid sinus ( swelling in carotid artery) monitor blood pressure, if it gets too high (e.g. during exercise) they send APs to the cardiovascular centre to reduce heart rate.
25
Q

describe involuntary (smooth) muscle

A
  • spindle shaped individual cells
  • uninucleate
  • non-striated?
  • cells contain bundles of actin and myosin
  • in walls of tubular structures
  • arranged in longitudinal and circular layers that oppose each other
26
Q

describe cardiac muscle

A
  • myogenic
  • striated
  • uninucleate
  • cells form fibres which branch to form cross bridges which ensure even spreading of stimulation, and squeezing
  • cells joined by intercalated discs ( allow free diffusion of ions )
27
Q

describe voluntary ( skeletal/ striated) muscle

A
  • causes movement of the skeleton
  • muscles in antagonistic pairs ( one contracts, other elongates)
  • cells form fibres
  • multinucleate
  • striated
  • sarcolemma surrounds fibre
  • sarcoplasm, sarcoplasmic reticulum
  • fibres form myofibrils divided into sarcomeres which contain actin and myosin protein filaments
  • banded pattern gives striped appearance.
28
Q

describe how skeletal muscle contraction is stimulated

A
  • APs arrive at end of axon open V-gated Ca2+ ion channels in the membrane. Ca2+ flood into the axon
  • vesicles of acetylcholine move towards and fuse with the end membrane
  • acetylcholine molecules diffuse across gap and fuse with receptors in the sarcolemma
  • this opens sodium ion channels allowing Na+ ions to enter the muscle fibre and depolarise the sarcolemma
  • a wave of depolarisation spreads along the sarcolemma and down transverse tubules into the muscle fibre
29
Q

what is a motor unit

A

where a motor neurone divides and connects to several muscle fibres which contract together, providing a stronger contraction.

30
Q

briefly describe the structure of a myofibril

A
  • thin filaments make up light band, held together by Z line (sarcomere = distance between 2 Z lines)
  • thick filaments make up dark band
  • thin + thick overlap but middle where they don’t = H zone
31
Q

describe the thin filaments

A
  • 2 chains of actin subunits twisted around each other
  • tropomyosin wound around actin, attached to globular troponin molecules
  • each troponin= 3 polypeptides. one bound to actin, tropomyosin and calcium.
  • at rest, tropomyosin covers binding sites for thick filaments
32
Q

how does the sarcomere vary during contraction

A
  • light band and H zone get shorter
  • Z lines move closer together
  • sarcomere gets shorter
33
Q

Explain the mechanism of muscle contraction

A
  • when muscle is stimulated action potential passes along sarcolemma and down t-tubules into the muscle fibre
  • the AP is carried to the sarcoplasmic reticulum which stores calcium ions and causes the release of calcium ions into the sarcoplasm
  • Calcium ions bind to troponin altering the shape of tropomyosin, exposing the binding sites on the actin for the myosin heads
  • myosin head binds to actin forming cross bridges between filaments.
  • myosin head moves, pulling the actin filament past the myosin filament
  • myosin head detaches and can bind further up the actin.
  • after contraction Ca2+ ions actively pumped back into sarcoplasmic reticulum
34
Q

Explain the role of ATP in muscle contraction

A
  • myosin head forms cross bridge with actin filament
  • head tilts back causing the thin filament to slide past the myosin filament (power stroke) during this ADP and Pi are released from the myosin head
  • after the power stroke, ATP attaches to the head, breaking the cross bridge
  • the head returns to its original position (swings forward) ATP is hydrolysed to release energy for this . the myosin head can then form a new cross bridge.
35
Q

how is the supply of ATP maintained in muscle

A
  • aerobic respiration in mitochondria. bohr effect helps release more O2 from haemoglobin in the blood. limited by O2 delivery
  • anaerobic respiration in sarcoplasm. releases a little more ATP but leads to production of toxic lactate. build up of this causes fatigue
  • CREATINE PHOSPHATE in sarcoplasm = phosphate group reserve, transferred to ADP to create ATP ( creatine phosphotransferase ) .
36
Q

explain the plant responses to abiotic conditions

A
  • thicker waxy cuticle when hot to lose less water by transpiration
  • more lignin in windy conditions
  • stomata close when hot/dry due to abscisic acid
  • root growth slows during drought
37
Q

explain how plants can physically avoid herbivory/ grazing

A

Mimosa pudica responds to tough by a sudden folding of the leaves- thigmonasty. This is a nastic response as it is a non-directional response.

38
Q

explain how plants chemically avoid herbivory/grazing

A
  • Tannins ( phenolic compounds in vacuoles or surface wax) are toxic to microorganisms and herbivores. in the upper epidermis of leaves and make them taste bad. in roots they prevent infiltration by pathogens or microorganisms
  • Alkaloids ( derived from AA and contain N, bases ) taste bitter. in growing tips, flowers. peripheral stem and roots. e.g. nicotine, morphine
  • Pheremones - released by one individual and affect the behaviour and physiology of another. produced when leaf eaten to tell other leaves/ plants.
39
Q

explain the types of tropism

A

( directional growth response)

  • phototropism (+) shoots grow towards the light to photosynthesise
  • geotropism: roots grow towards the pull of gravity to anchor them in soil and help them take up water for support and turgidity and for photosynthesis and cooling. also take up minerals e.g nitrates for AA syntheisis. shoots show negative geotropism.
  • chemotropism- pollen tubes grow down style attracted by chemicals to the ovary for fertilisation
  • thigmotropism- shoots of climbing plants such as ivy wind around other plants or solid structures to gain support
40
Q

how do hormones move around plants?

A
  • active transport
  • diffusion
  • mass flow in phloem sap or xylem vessels
41
Q

explain the role and commercial use of auxins

A
  • Auxins e.g. IAA promote cell elongation in shoots causing them to grow
  • high conc inhibits root growth (inhibits root elongation)
  • maintains apical dominance - inhibits growth of lateral shoots/buds
  • inhibits leaf and fruit abscission by preventing ethene production from increasing

commercial uses

  • cuttings dipped in rooting powder (low conc) to promote root growth
  • weedkiller- promotes rapid shoot growth, plant cant support itself and falls and dies
  • helps make seedless fruit ( parthenocarpy ) - promotes ovule growth triggering auxin production
42
Q

explain the role and commercial use of cytokinins

A
  • overcome apical dominance, promote lateral bud growth
  • high levels of auxin inhibit
  • low levels of auxin allows promotion of lateral bud growth
  • promotes cell division and cell expansion
  • delays leaf senescence

commercial uses

  • prevents yellowing of lettuce leaves (senescence)
  • in tissue culture, promotes many side shoots which can be gown into new plants so higher production of new plants
43
Q

explain the role of abscisic acid

A
  • e.g ABA
  • inhibits seed germination and growth to ensure seeds only germinate in optimum conditions
  • causes stomata to close when water availability is low
  • inhibits lateral bud growth ( apical dominance )
  • high auxin level keeps abscisic acid levels high which prevents lateral bud growth
44
Q

explain the role of giberellins

A
  • e.g GA
  • promotes seed germination
  • when seed absorbs water, embryo releases gibberellin
  • gibberellin travels to aleurone layer causing production of amylase
  • starch-> maltose, hydrolysed to glucose for respiration enabling growth
  • promotes internodal stem growth
  • promotes cell elongation and cell division
45
Q

explain the commercial use of giberellins

A
  • elongate internodal cells in stalks of grapes - grapes spread out and get bigger
  • elongation of internodal cells in sugar cane- more sugar
  • beer production needs malt ( dried, ground seeds ). giberellins encourage barley seed to make amylase so starch -> maltose. germination then stopped by drying.
  • (delays senescence in citrus fruits)
  • ( with cytokinins makes apples elongate )
  • ( induce seed production )
  • (gibberellin inhibitor keeps flowers short and stocky, keeps crop plants short to prevent lodging)
46
Q

explain the role and commercial use of ethene

A
  • promotes leaf abscission
  • promotes fruit ripening

commercial uses

  • spray fruit to speed up ripening (e.g. in bananas)
  • promotes fruit abscission (e.g in cherries)
  • promotes female sex expression in cucumbers reducing chance of self pollination (bitter) and increasing yield
  • promotes lateral growth in some plants yielding compact flowering stems

cold, little O2 and high CO2 prevents ethene synthesis and fruit ripening during shipping - stored for longer, increases shelf life.

47
Q

explain the experimental evidence for the role of auxins in controlling apical dominance

A

-if you remove tip- no apical dominance
tip makes auxins, no tip= no auxin suggests auxin causes apical dominance.
-cut tip + apply auxin paste = apical dominance
-ring of auxin transport inhibitor below tip stopped auxins from going down stem.
side shoots grew therefore auxin causes apical dominance

  • high auxin keeps abscisic acid high to prevent lateral bud growth
  • cytokinins applied to bud can override apical dominance. high auxin make shoot apex a sink for cytokinins produced in roots, when apex removed cytokinins spread evenly.
48
Q

explain the experimental evidence for the role of gibberellin in the control of stem elongation

A

-applied gibberellic acid to dwarf plants, they grew taller ( internodal regions grew )
suggests giberellins cause stem elongation but doesn’t tell us if tall plants in nature are due to this.

-compared GA1 levels in tall pea plants (Le le) and dwarf pea plants (le le) (Le is dominant allele). higher GA1 were taller.
-to show that GA1 directly caused growth, need to know how its formed. Le gene responsible for enzyme that converted GA20 to GA1
-chose pea plant with mutation that blocks gibberellin production earlier on in the pathway (don’t produce gibberellin). they grafted a shoot onto a homozygous le plant ( which cant convert GA20 to GA1 )and it grew tall.
-shoot still had enzyme, used unused GA20 to make GA1, causing stem elongation.
this suggest GA1 causes stem elongation.

49
Q

explain the experimental evidence for the role of gibberellin in seed germination

A
  • application of gibberellin to seeds can cause early germination
  • abscisic acid inhibits gibberellin. if abscisic acid inhibited during ripening, the seeds inside the fruit will begin germinating during ripening.
  • mutant plants that don’t make gibberellin wont germinate but they will if you spray them with gibberellin.
50
Q

Where does plant growth occur ?

A
  • apical meristems at tips of roots and shoots
  • lateral bud meristems in buds
  • lateral meristems on outer layer of shoots and roots
  • intercalary meristems between nodes
51
Q

How would you investigate phototrophic responses ?

A
  • take 3 sets of 10 seedlings
  • place one in the dark, one with illumination from all sides and one with illumination from one side.
  • mark each shoot every 2mm
  • leave for several days
  • work out the mean and standard deviation of the distances between the marks - both should increase for the shaded side.
52
Q

How would you investigate geotropic responses?

A
  • use a klinostat
  • control plant spun to ensure the effect of gravity is applied equally to all sides of the plant
  • switch of for experimental plant so gravity is only applied to one side
  • for experimental plant root bends downwards and shoot bends upwards
  • in the control plant, roots and shoots grow horizontally
53
Q

What were darwins experiments and what did they show?

A
  • control
  • tip removed
  • tip covered by opaque cap
  • tip covered by transparent cap
  • base covered by opaque shield

Shoot tip is responsible for phototropic responses

54
Q

What were boysen-Jensens experiments and what did they show?

A
  • top separated by gelatine block
  • tip separated by mica

Water/solutes need to be able to move backwards from the tip of the plant for phototropism to happen

55
Q

How can you artificially do an experiment to test the phototropic effect ?

A
  • place shoot tip on agar block, auxin diffuses into the agar
  • cut shoot tip off 6 plants
  • leave one control
  • one with auxin agar directly on top of shoot- grows up
  • one with auxin agar offset left- bends right ( curved growth )
  • one with auxin agar offset right- bends left (curved growth)
  • one with agar but no auxin
  • one with agar but no auxin offset
56
Q

How do you create a serial dilution of auxin?

A
  • set up 5 10ml screw-top bottles
  • use a syringe to add 10ml auxin solution at 100 ppm to the first boiling tube
  • use a separate syringe to add 9ml of distilled water to the other 4 test tubes
  • remove 1ml of auxin from the first tube and add it to tube 2
  • shake tube 2 vigorously
  • remove 1ml from tube 2 and add it to tube 3
  • repeat
  • each tube is 10 times more dilute than the previous
57
Q

Explain a practical to investigate the effect of IAA on shoot growth

A

-take 15 wheat seedlings, measure and cut the final 2mm from the tip. Take 5 further seedlings and measure but don’t remove tip
-treat 5 with lanolin to cover the tip (A)
-treat 5 with lanolin infused with IAA (B)
-leave 5 untreated (C)
-leave intact seedlings (D)
Return to beaker with roots surrounded in wet cotton wool
-leave for 3 days
-measure again
-A and C won’t grow
-B and D will grow
(Cell elongation is proportional to auxin concentration)

58
Q

What is the mechanism for auxins effect?

A
  • auxin increases stretchiness of cell wall by promoting the active transport of H+ by ATPase enzyme on the plasma membrane into the cell wall, low pH is optimum for wall loosing enzymes ( expansins ). These break bonds within cellulose ( and H+ disrupt H bonds ) so walls become less rigid and can expand as the cell takes in water.
  • phototropin ( enzyme ) activity is promoted by blue light so lots of activity on illuminated side of plant, less active on dark side. Gradient causes redistribution of auxin by effect on PIN proteins in plasma membranes, cause the auxin to move between cells in different directions.
  • PIN protein activity controlled by PINOID , therefore phototropins affect PINOID activity .
59
Q

Explain how auxin is involved in the geotropic responses of roots.

A

In a root lying flat, auxin accumulates on the lower side where it inhibits cell elongation. Upper side continues to grow and root bends downwards

  • in shoot auxin promotes cell elongation on the lower side making the shoot bend upwards
  • root and shoot cells in zone of elongation exhibit different responses to the same concentration of auxin .