BIOL2210 Plant cell signalling

animal vs plant development

dvelop from single celled zygote

cell division and differentiation

extensive cell mitration vs no cell migration

most cell types terminally differentiated, and germ lime segregated early in development vs meristems retain stem cell character thru life of adult plant

meristem

region of plant tissue at tips of shoots and roots, where cell division occurs

(shoot apical meristem and root apical meristem)

(axillary meristems (where leaves attach to plant) norm inactive as repressed by SAM)

maintain capacity to maintain by cell division and to differentiate

how do plants vs animals interact with environment

animals interact with environ by behaviour (animal development is predom genetically determined)

plants respond to environ by adaptation at biochemical, physiological and developmental level (development is genetically det. but is also plastic)

are plants inactive

no, are immobile but not inactive

do plants have a central processor like animals e.g. CNS

No, but still respond to environ stimuli

diff responses to environmental stimuli

elelctrochemical (v fast)

or respond via change in gene expression (slower)

do plant hormones and their signalling interact like in humans

yes

reg growth and development in response to genetic and environ factors

are plant hormones produced in specialised areas like glands in humans

no, everywhere in plant prod

target local and distant targets

effect dep on combo of hormones

regulated locally (no CNS)

what are jasmonates

fatty acid derived signal molecules

analogous to prostaglandins in animal cells

biotic vs abiotic stress responses

respond to microbes, insects etc

respond to e.g. UV, ozone

are jasmonates produced in response to biotic stress

yes,

xause change in gene expresson

e.g. upreg of protease inhibitors (block insect digestion)

or production of volatiles (prime defense of nearby plants or attract parasitoids)

jasmonate biosynthesis

starts in chloroplast, where cleave alpha-linolenic acid (18:3) from chloroplast phospholipids

cont. in peroxisome where beta oxidation of alpha-linolenic acid prod jasmonic acid

role of JASSY

transporter that exports OPDA (prod from alpha-linolenic acid) from chloroplast

in outer envelop of chloroplast

forms a pore

effects of JASSY mutants

more sus. to pathogens and cold

dont activate JA mediated gene expression as cant syth them (req b-ox in perox)

how does OPDA get into peroxisome

JASSY pore transp OPDA from chloroplast

active transp of OPDA by comatose (ABC transporter) in perox memb req ATP

or diffuses across perox memb in reduced form, get ox (lose H+) in high pH 8.2 of perox,

red form cant diffuse as readily back, therefore ION TRAPPING

if try stim jasmonic acid synth via wounding plants, do comatose mutants still prod some jasmonic acid

yes, as OPDA can still enter perox by ion trapping, but signif reduction in jasmonates synth

where does JA conjugation occur

in cytoplasm, to prod jasmonate derivatives (oxylipins)

often conjugate to aa’s

how do JA deficient mutants differ (cant synth JA)

male sterile

suseptible to disease and cold

rescued by application of JA

explain the coi1 mutant

are male sterile, sus to attack

but cant be rescued by JA application (can make JA but cant respond to it)

res to effects of coronatine (bact. metab that mimics effect of jasmonates)

encodes an F box protein (part of E3 ligase) (req for ubiquitination for protein degredation) req for substrate binding

role of JAZ proteins

are transc repressors

inhib JA response genes

by binding TFs

how do jasmonates activate JA response genes

JA-Ile promotes int. between JAZ proteins and E3 ligase (SCF (which coi is part of))

therefore ub med degred JAZ, allow exp by TF

is auxin essential

yes, no mutants taht lack auxin are known

are there natural and sythetic auxins

yes, nat = IAA

sythetic are more stable and used experimentally

how are natural auxins e.g. IAA made

synth from tryptophan

req beta oxidation in peroxisomes

how is auxin (IAA) activity modulated

by conjugation

e.g. add sugars, forming inactive storage form

(IAA not too stable so gets degraded quite fast)

how is auxin transported

fast nonpolar transport in vascular system up and down plant

slow cell-cell polar transport

explain polar auxin transport

unique to auxin in plants, when move from cell-cell

gives rise to conc grads that shape cell responses,

movement therefore driven by chemiosmotic force

are ATP pumps that pump it in (AUX1) and also proton pumps that pump H+ out, so reduced form of IAA diffuse in to cell (lose H+) so ION TRAPPING

are efflux pumps too (PIN)

all help achieve asymmetric distribution of auxins (by asymmetric distribution of influx and efflux proteins)

how is the presence of auxin detected

use auxin responsive promoters e.g. DR5, linked to GFP seq

what does PIN protein localisation changing in response to developmental and environ stimuli cause

change in auxin distribution

how does auxin regulate tropisms e.g. phototropism and gravitropism

starch granules in e.g. root cap sense gravity by sedimenting

PIN proteins relocate, changing auxin distribution (accumulate on lower side of root)

inhibs growth, so get asymmetric growth = downward bending

how is PIN protein localisation changed

they constitutively cycle between PM and endosomes, so direct to where want by regulating site of vesicle fusion

control rate of export to memb, rate of internalisation, recycling and degredation

how are auxin responsive genes activated

req degredation of AUX/IAA repressors (bound to TFs)

bound by SCF (E3 ligase complex) that ub AUX/IAA repressor, so degrade

SCF recognise repressor via TIR1 protein (like coi1 Fbox protein in SCF for JAZ proteins)

do gibberellins also use Fbox proteins to regulate repressor degradation

yes

ub-proteasome system central to plant signalling