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homeostasis
internal conditions maintained in dynamic equilibrium within its limit
why does core temp need to be maintained
maintain rate of enzyme reactions
why does blood pH need to be maintained
maintain rate of enzyme reactions
why does water potential need to be maintained
prevent osmotic lysis
negative feedback
self regulatory
return the internal environment to optium if there is change
positive feedback
a fluctuation triggers change which results in greater change from normal
what are hormones
proteins secreted by endocrine glands and transported in blood stream
specific tertiary structure so only complementary to certain cell receptors
stage of negative feedback pt 1
receptors detect deviation
stage of negative feedback pt 2
coordinator
stage of negative feedback pt 3
corrective mechanism by effector
stage of negative feedback pt 4
receptors detect that conditions have returned to normal
why separate feedback systems control fluctuations in different directions
provides more control
stops overcorrection
why is there a time lag between hormone production and response by effector
produce hormone
transport hormone in blood
cause required change to protein
mode of action of adrenaline pt 1
hormone receptor complex forms
mode of action of adrenaline pt 2
conformational change to receptor activates g- protein
mode of action of adrenaline pt 3
activates adenylate cyclase which converts ATP to cyclic AMP
mode of action of adrenaline pt 4
cAMP activates protein kinase A pathway
mode of action of adrenaline pt 5
results in glycogenolysis
mode of action of estrogen pt 1
steroid hormone diffuses through cell membrane
mode of action of estrogen pt 2
forms hormone receptor complex with ER receptor in cytoplasm
mode of action of estrogen pt 3
complex enters nucleus and acts as transcription factor
3 groups of plant growth factors
auxins
cytokinins
gibberellins
functions of auxins
involved in trophic responses
controls cell elongation
supresseslateral buds to maintain apical domiance
promote root growth
how do auxins cause cell elongation acid growth hypothesis pt 1
IAA causes active transport of H+ ions into cell wall
how do auxins cause cell elongation acid growth hypothesis pt 2
disruption to H- bonds between cellulose molecules and action of expansins make cell more permeable to water
how do auxins cause cell elongation acid growth hypothesis pt 3
cells with higher turgor pressure elongate faster
functions of gibberellins
stimulates germination
elongation at cell internodes
fruit growth
rapid growth
how is germination stimulated pt 1
seeds absorbs water activating embryo to secrete gibberellins
how is germination stimulated pt 2
gibberellins diffuse to aleurone layer which produces amylase
how is germination stimulated pt 3
amylase diffuses to endosperm layer to hydrolyse starch
how is germination stimulated pt 4
hexose sugars act as respiratory substrate to produce ATP
functions of cytokinins
stimulate development of lateral buds by promoting cell division at apical meristems
how does plant growth hormones interact
synergistically
antagonistically
synergistically
to achieve same effect
antahonistically
with inverse effects eg auxins and cytokinins
phytochrome
plant photoreceptor with bilin chromophore group
phytochrome 2 forms - inactive
biologically inactive Pr absorbs red light
phytochrome 2 forms - active
biologically active Pfr absorbs far- red light
when are phytochromes abundant- darkness
Pr abundant
when are phytochromes abundant- aunlight
Pfr abundant
how does phytochrome control flowering
Pr absorbs red light and converts it to Pfr which stimulate flowering as it signifies that light intensity is high enough for photosynthesis
what is photomorphogenesis
pattern of plant growth and development determined by light intensity
how does phytochrome control photomorphogenesis
the transition from Pr to Pfr
localisation of proteins within cells
transcription of certain genes
phosphorlyation of proteins
how does phytochrome control photomorphogenesis - affects
germination
circadian rhythm
flowering