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BIOLOGY REVISION > Plant and animal responses 5.5 > Flashcards

Plant and animal responses 5.5 Flashcards

1
Q

(plant) what are three examples of plant stimuli and their responses?

A

Stimuli:

  • high temperature = thicker waxy cuticle
  • strong wind = more lignin
  • herbivory = chemical defences
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2
Q

(plant) What are three chemical defences for herbivory?

A

Chemical defences to herbivory:

  • tannins
  • pheromones
  • alkaloids
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3
Q

(plant) what do tannins do?

A

Tannins can be toxic and make the leaf taste bad. They are found in the upper epidermis and roots

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4
Q

(plant) what do pheromones do?

A

Pheremones are released by plants and affect the behaviour and physiology of herbivores

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5
Q

What do alkaloids do?

A

Alkaloids are a feeding deterrenet as they make the plant taste bitter. they are found in the gowing tips, flowers and peripheral cells of stems and roots

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6
Q

What is a tropisms?

A

A tropism is a directional growth response

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7
Q

What are 4 examples of tropisms?

A

Phototropism- shoots grow towards light
Geotropism- roots grow towards the pull of gravity
Chemotropism- pollen tubes grow down the style towards the ovary
thigmotropism - shoots of climbing plants wind around structures for support

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8
Q

What is a nastic response and an example?

A

Nastic responses are non directional responses to a stimuli for example thigmonasty where leaves curl whenever touched

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9
Q

What do cytokinins do?

A

Cytokinins:

  • promote cell division
  • delay leaf senescence
  • overcomes apical dominance
  • promotes cell expansion
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10
Q

What does abscisic acid do?

A

Abscisic acid:

  • inhibits seed germination and growth
  • stomatal closure in times of water stress
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11
Q

What do auxins do?

A

Auxins:

  • promote cell elongation
  • inhibits growth of side shoots
  • inhibits leaf abscission (leaf fall)
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12
Q

What do gibberellins and ethene do?

A

Gibberellins:
-promotes seed germination and stem growth
Ethene:
-promotes fruit ripening

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13
Q

What do synergic hormones do?

A

Synergic hormones amplify other hormones effects

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14
Q

What do antagonistic hormones do?

A

Antagonistic hormones cancel out other hormones effects

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15
Q

What is apical dominance?

A

Apical dominance = inhibition of lateral bud growth further down the shoot by chemicals produced in the apical bud at the tip of the shoot (breaking off the apex of the shoot causes growth of side shoots

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16
Q

What was the theory of auxins and plant growth (apical buds)?

A

It was thought auxins from the apical bud prevent lateral bud growth. When the tips were removed the auxins levels drop and the buds grow.

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17
Q

What were two experiments researchers did to support their auxins and apical growth?

A

Experiments supporting auxins in apical bud:

  1. applied auxin paste to a cut tip of a plant and saw that the lateral buds did not grow
  2. Applied auxin paste to cut tip of plant and then added auxin transport inhibitor and the lateral buds grew
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18
Q

How is ABSCISIC ACID relevant in the updated theory of apical dominance and auxins?

A

-Abscisic acid inhibits lateral bud growth and auxins keep the level of abscisic acid high in the bud. When the tip is removed the levels of abscisic acid drop so it can no longer inhibit lateral bud growth

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19
Q

How is CYTOKININS relevant in the updated theory of apical dominance and auxins?

A

-Cytokinins promote bud growth and when there is high auxins the apex becomes a sink for the cytokinins so growth is restricted to the apex, when the tip is removed the cytokinins spread evenly

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20
Q

What are the 2 functions of gibberellins?

A

Gibberellins:

  • stem elongation
  • seed germination
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21
Q

Describe how gibberellins affect seed germination

A

Seed germination:

  1. seed absorbs water
  2. embryo releases gibberellins which travel towards the aleurone layer in the endosperm region
  3. gibberellin enables amylase production (amylase converts starch to glucose)
  4. the glucose provides a substrate for respiration for the embryo as it grows
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22
Q

what is the synthesis pathways for gibberellins that causes stem elongation?

A

Synthesis pathway for gibberellins:

  1. ent kaurene
  2. GA -12 aldehyde
  3. GA -20
    - –enzyme caused by Le—-
  4. GA-1 ( stem growth)
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23
Q

What does G1 cause and what is it?

A

GA 1 is gibberellic acid and causes plants to grow TALL

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24
Q

What gene is responsible for producing the enzyme converting GA -20 to GA -1?

A

Le gene produces the enzymes that converts GA-20 to GA-1 and therefore what causes the plant to grow tall

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25
Q

How did researchers prove GA-1 directly causes stem growth?

A
  1. chose LeLe plant that had a mutation where the transition from ent kaurene to GA -12 aldehyde was blocked so produced no GA-1 so were short despite having Le
  2. chose lele plant which was short due to absence of Le gene so they lack enzyme converting GA -20 to GA-1
  3. grafter and joined the two plants
  4. plant grew really tall as the lele plant now had the enzyme that converted GA-20 to GA-1 from the mutated LeLe plant
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26
Q 
What are the heights of:
-LeLe 
-lele
-mutated LeLe
and why?
A
  • LeLe = tall as Le causes production of enzymes converting GA-20 to GA-1
  • lele = short as the lack of Le means no production of GA-1 so cant get tall
  • mutated LeLe = short as conversion of ent kaurene to GA-12 aldehyde is blocked so GA-1 is never produced despite still having everything else that’s needed
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27
Q

Where does plant growth occur/

A

Plant growth occurs in meristmatic tissue as the cell wall limits the cells ability to divide and expand

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28
Q

Where is the meristematic tissue?

A

Meristems:

  • Apical meristems at the tips of plants (roots and shoots)
  • Lateral bud meristems found in side buds
  • Intercalary meristems at internodes. this is responsible for shoots getting longer
  • Lateral meristems are in cylinders and are responsible for shots and roots getting wider
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29
Q

What are 3 things you need in an inverstigation?

A
  1. dependent variable
  2. independent variable
  3. control condition
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30
Q

Whats a basic investigation into phototropisms?

A

Phototropiusm investigation:

  • positive control condition where plant is illuminated from all sides
  • Experimental condition has illumination from one side only
  • mark roots and shoots every 2mm before start
  • side away from light has elongated gaps
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31
Q

Whats a basic investigation into geotropisms?

A

Investigation into geotropisms:

  • Control condition has klinostat rotating so gravity is exerted equally on the plant so shoots and roots grow horizontal
  • Experimental condition has the klinostat turned off so that gravity is only acting on one part of the plant and roots bend down and shoots bend up
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32
Q

What part of the plant is elongation faster in?

A

Elongation is faster in cells on the outside of the bend, the side away from light

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33
Q

What was darwin’s investigation into plant hormones?

A

Role of the tip in phototropism:
-control with plant left alone BENT
-plant tip cut off DID NOT BEND
-tip covered by opaque cover DID NOT BEND
-tip covered by transparent cover BENT
-base covered by opaque cover BENT
All had light coming from the same direction and he concluded shoot tip is responsible for phototropism

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34
Q

What did boysen jensen add to darwins investigation into the role of the tip in phototropism?

A

Role of the tip in phototropism (boysen jensen)
-Tip separated by gelatin block (permeable) BENT
-tip separated by mica that’s impermeable to water and solutes DID NOT BEND
Concluded water and solutes needed to move from the tip back down the plant for phototropism to occur

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35
Q

What was Went’s investigation?

A

Went used blocks infused with different concentrations of auxin and found shoot curvature proportional to the concentration of auxin in the block

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36
Q

Describe the mechanisms of auxins effect.

A

Mechanism if auxin:

  1. light causes auxin to transport towards the shaded side of the plant
  2. auxin causes active transport of H+ into the cell wall by ATPase
  3. pH of cell wall drops causing disruption to H bonds in cellulose and an optimum pH for expansins enzymes which loosen cell walls by digesting it slightly
  4. wall becomes less rigid allowing cells to elongate as they take up water
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37
Q

How is it thought auxins move?

A

Auxin movement:

  1. phototropin 1 and phototropin 2 are promoted by blue light which is in sunlight. They are therefore more active on the light side (allowing auxin to move to shaded side)
  2. These influence pinoid proteins which control pin proteins
  3. Pin proteins are channels used to auxin to get through the plasma membrane and these pin can be distributed differently
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38
Q

Discuss auxins in geotropisms

A

Auxins and geotropism:
-Gravity causes auxin t accumulate on the lower side of the SHOOT causes cell elongation here so it bends upwards
-auxin inhibits cell elongation in roots so they bend down
Cells in the roots and shoots are specialised to respond to auxins concentrations differently

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39
Q

What can auxins be use for as a commercial use>

A

Commercial use of auxins:

  • prevent fruit and leaf drop
  • promote flowering
  • make cutting grow
  • parthenocarpy (seedless fruit)
  • use as herbicides to over elongate stems until they buckle
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40
Q

What are the commercial uses of cytokinins?

A

Commercial use of cytokinins:

  • prevent yellowing of lettuce leaves
  • plant mass production by promoting bud and shoot growth
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41
Q

What are the commercial uses of gibberllins?

A 
Commercial uses of gibberllins:
-delay senescence of citrus fruits
-elongate apples
-make less compact grape stalks
-Brewing
-Sugar procuction
-plant breeding 
Inhibitors keep plants short and stocky
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42
Q

Explain brewing, sugar production and plant breeding by gibberellins?

A

Gibberelins:

  • Brewing= amylase breaks down starch into maltose
  • sugar production stimulates growth between nodes
  • plant breeding= induces seed formation on young trees before they naturally would and induce seed formation on binneal plants
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43
Q

What are the uses of ethene?

A

Commercial uses of ethene:

  • speeds up ripening of apples tomatoes and citrus fruits
  • promotes fruit drop on cotton cherry and walnut
  • Reduces self pollination in cucumbers by promoting female sex expression so they do not taste bitter
  • promote lateral growth making a compact flowering stem
44
Q

Hoe can restricting ethene be useful?

A

Restricting ethene:
Use low oxygen levels, high carbon dioxide levels and a low temperature
Silver salts also inhibit ethene action

45
Q

How is the central nervous system divided up?

A

Central nevrous system:

  • Brain = mainly relay nerurones and non myelinated
  • spinal cord = mainly relay neruones and has some grey matter and some white
46
Q

What is white matter?

A

White matter is where there are myelinated neurones present and as they are fatty they make the matter look white

47
Q

How is the peripheral nervous system divided up?

A

Peripheral nervous system:
-sensory system (receptors—cns)

-motor system (cns—-effectors)
Somatic nervous system
Autonomic nerovus system —- sympathetic and parasympathatic

48
Q

What does the somatic and autonomic nervous system do?

A

Somatic:
Voluntary, conscious movement. It has myelinated neurones and 1 single motor neurone connecting the cns to the effector

Autonomic:
Effectors bnot under voluntary control like glands. They are non myelinated as they do not need to be rapid and there is at least 2 neurons connecting cns to effector

49
Q

What is the main role of sympathetic and parasympathetic systems?

A

Sympathetic prepares the body for activity whilst the parasympathetic conserves energy

50
Q

What are the structural features of the sympathetic system?

A

Sympathetic system:

  • many nerves lead to CNS to an effector
  • ganglia are outside of the cns
  • long post ganglionic neurones
  • short pre ganglionic neurones
51
Q

What are the structural features of the parasympathetic system?

A

Parasympathetic:

  • few nerves lead out of cns and divide to different effectors
  • ganglia in effector tissue
  • short post ganglionic neurones
  • long pre ganglionic neurones
52
Q

What are the differences in function of sympathetic and parasympathetic?

A

Sympathetic:

  • noradrenaline
  • in times of stress
  • increase in heart rate and ventilation, dilation of pupils

Parasympathetic

  • acetylcholine
  • times of relaxtion
  • decrease in ventilation, heart rate and reduction in pupils
53
Q

Describe the cerebrum

A

The CEREBRUM is all around the top of the brain and has two cerebral hemispheres connected by the corpus callosum. The outermost layer is called the CEREBRAL CORTEX which has lots of nerves and has 3 components; sensory, motor and association areas

54
Q

What are the roles of the cerebrum

A

The CEREBRUM:

  • concious thought and actions
  • emotions
  • reasoning
  • factual memory
55
Q

Describe the cerebellum and its role

A

The CEREBELLUM contains more thna 50% of the neurones in the brain. It is the mini brain lik bit attched at the back and is connected to the CEREBRUM by the PONS

  • balance
  • fine movement
  • store of motor processes after learning them
56
Q

What are the roles of the hypothalamus?

A

HYPOTHALAMUS is in the middle of the brain:

  • temperature regulation
  • osmoregulation by osmoreceptors
57
Q

Describe the pituitary gland and its complex with hypothalamus

A

PITUITARY GLAND is connected to the HYPOTHALAMUS by NEUROSECRETORY CELLS. It is split into two:

  • ANTERIOR releases its own hormones in response to releasing factors from the hypothalamus
  • POSTERIOR releases hormones made by the hypothalamus. They pass from there down neurosecretory cells to be released
58
Q

Describe the medulla oblongatas roles.

A

The MEDULLA OBLONGATA is below the PONS and controls non skeletal muscle through the autonomic nervous system. It contains:

  • Cardiac centre
  • Vasomotor centre regulates circulation and blood presure
  • respiratory centre which controls rate and depth of breathing
59
Q

How can the blinking relfex be described?

A

Blinking relfelx is a CRANIAL relflex meaning the singla passes through the barin without processing. It is also a REFLEX ARC meaning the receptor and efffector are in the same place

60
Q

What is a reflex action?

A

REFLEX ACTIONS are not processed by the brain and have a short pathway in order to be quick. Thye have a sensory—relay—-motor.

61
Q

Describe the corneal reflex without inhibition.

A

CORNEAL RELFEX:

  1. Pressure on eye is detected by sensory receptors in cornea
  2. Signal passes down sensory neurone to the pons
  3. pons is connected by a non myelinated neurone to a motor neruone
  4. motor neurone causes contraction of muscles above and below the eye to blink
62
Q

Describe the corenal relfex with inhibtion

A

CORNEAL RELFEX with INHIBITION:

  1. Pressure on eye is detected by sensory receptors in cornea
  2. Signal passes down sensory neurone to the pons
  3. pons is connected by a non myelinated neurone to a motor neruone AND * a myelinated neruone
  4. signal travels down the myelinated neurone to sensory region of cerebral cortex to tell the brain its been touched
  5. myelinated inhibitory neurone travels to motor neurone to prevent formation of action potential to override the reflex by conscious control *
63
Q

What is the optical reflex?

A

Optical reflex protects light sensitive cells of the retina from damage. Stimuli is detected by the retina and signal travels to the optical centre in the cerebral cortex. It is slower than the corneal reflex

64
Q

What type of reflex is a knee jerk reflex?

A

A knee jerk reflex is a spinal reflex as it doesn’t pass through the brain

65
Q

Describe what happens when the hammer hits the knee cap

A

Knee jerk reflex:

  • hammer hits patella tendon which connects the quadriceps to the lower leg so tapping here deforms the tendon pulling the muscle
    2. Stretch receptors (muscle spindles) detect the stretch sending a signal via a sensory neurone to the spinal cord.
    3. Goes down a motor neurone causing contraction of quadriceps lifting the leg
66
Q

Which is the knee jerk response rapid and cannot be inhibited?

A

The knee jerk reaction is rapid as there is no interneurone and it cant be inhibited because there are only 2 neurones

67
Q

What does the knee jerk reflex help us do?

A

The knee jerk reflex helps us maintain our balance and helps us bend the knee when walking etc

68
Q

How does the body detect a threat?

A

Detecting a threat:

  1. various inputs from the peripheral nervous system
  2. sensory centres in the cerebrum
  3. signal passes to association centres in the cerebrum
69
Q

How 2 responses does he hypothalamus have immediately after a threat is etected?

A

Hypothalamus after threat:

  • activates the sympathetic nervous system
  • secretes CRH and TRH (releasing hormones) to stimulate the anterior pituitary
70
Q

When responding to a threat what happens when the sympathetic nervous syetm is stimulated?

A

Hypothalamus:

  1. activation of smooth muscle and glands
  2. activation of adrenal medulla which releases adrenaline into the blood stream
71
Q

When responding to a threat what happens when the hypothalamus releases releasing factors?

A

Hypothalamus:
-Releases CRH which causes secretion of ACTH, causing the adrenal cortex to release corticoid hormones into the bloodstream
-Releases TRH causing release of TSH making the thyroid gland release thyroxine into the blood stream
Combination of NEURAL ACTIVITY and HORMONES is the FIGHT OR FLIGHT response.

72
Q

Describe the mechanism of adrenaline action

A

Mechanism of adrenaline action:

  1. Binds to COMPLIMENTARY and SPECIFIC recepetor on plasma membrane
  2. G PROTEIN activated
  3. G protein stimulates ADENYL CYCLASE which cinverts ATP to cAMP
  4. cAMP is SECOND MESSENGER
  5. cAMP activates enzyme action
73
Q

In the action of adrenaline what is adrenaline?

A

Adrenaline is the first messenger and is an amino acid derivative

74
Q

What do CRH and TRH stand for? Overall what do they do?

A

CRH is corticotropin releasing hormone
TRH is thyrotropin releasing hormone
These stimulate the release of tropic hormones from the anterior pituitary

75
Q

What do the releasing hormones travel down to get to the anterior pituitary?

A

Releasing hormones from hypothalamus travel down a portal vessel to the anterior pituitary

76
Q

What does CRH do? (corticotropin releasing hormone)

A

CRH causes ACTH (ardrenocorticotropic hormone) release which acts on the ADRENAL MEDULLA causing CORTICOSTERIODS to be released. These REGULATE CARBOHYDRATE METABOLISM (more glucose)

77
Q

What does TRH do? (thyrotropin releasing hormone)

A

TRH causes release of TSH (thyroid stimulating hormone) causing the release of THYROXINE which INCREASES METABOLIC RATE and INCREASES SENSITIVITY TO ADRENALINE. Thyroxine acts on nearly every cell in the body

78
Q

Why does the heafrt rate ned tpo be changed?

A

The heart rate needs to be able to meet changing demands of tissues

79
Q

How can the heart be changed to meet demands of tissues?

A

Changing demands:

  • alter heart rate
  • force of contractions
  • alter stroke volume
80
Q

Discuss some features of the heart and its heart rate.

A

-The heart is MYOGENIC.
-it has its own PACEMAKER, SAN.
-Atria have a higher myogenic rate
T-issue between atria and ventricles is insulating so impulse travels to AVN then down purkyne fibres to apex of the heart
-adrenaline directly affects the heart it increases heart rate

81
Q

How is ehart controlled at rest? What is its resting beat?

A

At rest the heart is controlled by the SAN and it has a resting rate of 60-80bpm

82
Q

How can frequency of excitation waves be altered in the heart?

A

Frequency of excitation can be altered by the cardio vascular centre in the medulla oblongata. Nerves from here (accelerans and vagus) supply the AVN.

83
Q

Describe the action of 2 nerves supplying the SAN

A
  • Accelerans nerve is sympathetic and so causes the release of noradrenaline at the SAN causing heart rate to increase
  • Vagus nerve is parasympathetic so releases acetylcholine to the SAN to decrease heart rate
84
Q

What are some sensory inputs to the cardiovascular system in the medulla oblongata?

A

Sensory inputs to the cardiovascular centre:

  • muscle stretch receptors increase heart rate when stretched
  • chemoreceptors in carotid arteries, aorta and brain monitor pH of blood. Low pH increases heart rate
  • Stretch receptors in wall of carotid sinus (swelling in carotid artery) monitors blood pressure so heart rate decrease if BP is too high
85
Q

What are 2 ways of artificially controlling heart rate?

A

Artificial control of heart rate:

  • connect pace maker directly to SAN
  • connect pacemaker directly to ventricle muscle
86
Q

What are three types of muscle?

A

Types of muscle:

  • Smooth (involuntary)
  • Skeletal (voluntary/striated)
87
Q

Discuss the features of skeletal muscle

A

Skeletal muscle:

  • occurs at joints at skeleton in antagonistic pairs
  • sarcolemma (plasma membrane)
  • sarcoplasm (cytoplasm)
  • sarcoplasmic reticulum
  • cells are multinucleate
  • many mitochondria
88
Q

What sort of ability does skeletal muscle have?

A

Skeletal muscle is quick and powerful to contract but is easily fatigued

89
Q

Discuss cardiac muscle

A

Cardiac muscle:

  • power and will not fatigue. It is myogenic
  • intercalated discs
  • gap junctions to allow free diffusion of ions
  • cross bridges to spread excitation evenly
  • branching
90
Q

Discuss smooth (involuntary muscle)

A

Smooth muscle:

  • slow to contract but slow to tire and is controlled by the autonomic system
  • it has longitudinal layers and circular layers which oppose each other. they are a tapered shape
  • it is found in tubular structures like the intestines
  • 500um long and 5um wide
91
Q

What is a neuromuscular junction?

A

A neuromuscular junction is the section between the end of the nervous system and the start of the muscle

92
Q

What is a motor unit?

A

Motor unit is multiple muscle fibres supplied by the same motor neurone

93
Q

Describe the action at a neuromuscular junction

A

Neuromuscular junction:1. action potential causes voltage change which opens the voltage gated Ca2+ channels

  1. calcium diffuses to axon tip causing vesicles to fuse with the plasma membrane
  2. acetylcholine is released from vesicles across the gap and binds to receptors on the muscle
  3. Na+ channels open and Na+ enter the muscles causing depolarisation which passes along sarcolemma and down transverse tubules.
  4. calcium is released into muscle fibre
94
Q

Describe the structure of actin

A

Actin:

  • 2 chains of actin wound around each other
  • binding sites for myosin
  • tropomyosin protein wound around the actin blocking the myosin binding sites
  • troponin protein is attached to tropomyosin and holds the tropomyosin and actin together. 3 binding sites: one for actin, one for tropomyosin and one for Ca2+ ions
95
Q

Describe the structure of myosin

A

Myosin:

-2 protruding heads stick out the end of the molecule and these can stick to the actin

96
Q

What are 2 requirements for muscle contraction?

A

Requirements for muscle contraction:

  • move tropomyosin to expose myosin binding sites
  • get myosin moving
97
Q

Describe the sliding filament hypothesis

A

Sliding filament hypothesis:

  1. depolarisastion (neuromuscular junction) causes the release of calcium ions from the sarcoplasmic reticulum into sarcoplasm
  2. Ca2+ binds to troponin causing conformational change which moves tropomyosin exposing myosin binding sites
  3. myosin head binds to actin forming cross bridges
  4. myossin head moves pulling the actin past the myosin
  5. myosin heads detaches and binds further down
98
Q

Describe ATP action for muscle contraction

A

ATP action of muscle contraction:

  1. ATP attaches to myosin head
  2. ATP is hydrolysed into ADP and Pi which energizes the myosin head causing it to flip backwards- a high energy conformation
  3. myosin head attaches to actin with cross bridge
  4. The myosin head snaps forward releasing ADP and Pi and this is the POWER STROKE
  5. new molecule of ATP binds causing old cross bridge to detach
99
Q

How does the muscle contraction end?

A

Once completed Ca2+ is quickly pumped back into the sarcoplasmic reticulum so it no longer binds to troponin, making it back to its inactive state, bringing the tropomyosin back up to cover the myosin binding sites this is an active process

100
Q

Describe the areas of a sarcomere

A

Sarcomere:

  • H zone between ends of the thin filaments where there is only thick filament
  • z lines at end of each sarcomere
  • I band is the distance between each thick filament (only light band)
  • A band is the length of the myosin filament
  • light band = thin filaments (actin)
  • dark band = thick filaments (myosin)
101
Q

What happens to each section of the sarcomere during muscle contraction?

A

Sarcomere during contraction:

  • A band stays the same length
  • I band shortens
  • H zone shortens/disappears
  • Z lines get shorter = sarcomere gets shorter
102
Q

What are two events in muscle contractions that need ATP?

A

Muscle contraction ATP:

  • movement of myosin heads
  • active pumping of Ca2+ back into sarcoplasmic reticulum
103
Q

What are 3 processes that supply ATP for muscle contraction?

A

Supply of ATP for muscle contraction:

  • aerobic respiration
  • anaerobic respiration
  • creatine phosphate/phosphocreatine
104
Q

How does aerobic and anaerobic respiration supply atp for muscle contraction?

A

Supply of ATP for muscle contraction

  • Aerobic respiration by mitochondria produces atp and is limited by oxygen delivery
  • Anaerobic respiration produces lactic acid which is toxic and causes fatigue but it produces a few extra atp and gives a few extra seconds of muscle movement
105
Q

How does creatine phosphate act as an atp supply?

A

Supply of ATP for muscle contraction
-creatine phosphate in the sarcoplasm acts a reserve supply of phosphates which can combine with adp to make atp with the help of phosphotransferase. This produces an extra 2-4 secs of movement

BIOLOGY REVISION (21 decks)

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