DRL Exam 2

What are the steps of signal transduction

1. perception of stimulus

2. transduction

3. response

4. attenuation

Spatially, what are the two types of respionses

cell autonomous (same cell sense signal and responded)

non cell autnomous (response un distant cells/tissue/organs)

Name some protein receptors

membrane receptors: lipophobic ligands for faster responses

nuclear receptors: lipophilic ligands for slower and gene expression

name types of receptors that exist

protein kinases

F-Box proteins (TIR1 for auxin)

Mechanosensitive ion channels

Nucleotide bidning receptors (R-gene)

LRR-RK (leucine rich repeats receptor kinases for MAMPS)

What does it mean when a receptor is disrupted

loss of sensitivity

disruption of photophatse

constitutive signaling

what is the primary type of signal transduction that triggers sig amplification

phosphorylation is key!

• activate enzyme activity

• conformational changes

• protein to protein interactions

protein kinase: transfer terminal phosphate of ATP ot hydroxyl

Protein phophatase: removes phosphate by hydrolysis & is reversible

what are the effects if phosphorylation

alter enzyme activity

conformational change

enables protein-protein interactions

transcription factors can interact with transcriptional complex

What is MAPK

mitogen-activiated protein kinase cacasdes

• amplify environ & developmental signals

What do second messengers do

amplify the inital signal to trigger a potent response

Name the fast & small second messengers

Ca++ ions

action potentials (ion potentials)

ROS

H+

Nitric Oxide (NO)

Name slow second messgers

lipids

carbs

small peptides

flavonoids

sRNA

What does Ca do as an universal messenger

• binds to CaM (Calmodulin) = conformational change to explose non-polar ends for CaM to target proteins and activate downstream responses

  • can be decoded differently for diff responses

What are action potentials similar to in terms of signaling

endocrine system

fast and long distance signaling

• uses glutamate-like receptors and Ca++

  • CLV3-WUS is key signaling pathway for controlling meristem status in this way

What are hormones

secondary messengers that control physiological and developmental processes

Name the modes of hormone action

• autocrine/intracrine: hormone acts on same cell that produces it (ABA, GA)

• paracrine: act on neighboring cells (auxins)

• endocrine: acts on distant cells via transport in phloem (CK, Auxin, ABA)

Primary function of auxin

organ growth

proliferation

cell specification

plar transport drives tropisms

Primary function of cytokinin

cell division/proliferation

differentiation

breaks apical dominance

Primary function of gibberellin

germination

cell elongation

reproduction

flowering time

green revolution gene

Primary function of ethylene

cell elongation

fruit ripening/senescence

stress response

triple response in dark

Primary function of brassinosteriods

cell elongation

fertility

stress response

cell wall loosening

Primary function of ABA

inhibits growth

promotes dormancy

drought stress response

stomatal closure

Primary function of strigolactones

inhibits shoot branching

mycorrhizal symbiosis

parastiic plant germination

Primary function of jasmonic acid

insect hervivory response

necrotrophic pathogen defense

trichome development

Primary function of salicylic acid

biotrophic pathogen defense

system acquired resistance

Primary function of peptide hormones

flowering

stem cell homeostasis (CLV3)

cell differenciation (systemin)

what is the result of hormone signal transduction and repressor proteins working together

proteasomal degragation

What is the general hormone pathway for auxin

auxin → membrane TIR1 (F-box) → AUX/IAA repressors degraded → ARF transcription → activate gene expression

What is the general hormone pathway for cytokinin

cytokinin → histidine kinase receptor → phospho-relay with HPt → ARR response → gene expression

What is the general hormone pathway for GA

GA → GID1 (F-box) receptor → DELLA repressors degraded → PIF and growth genes activated

What is the general hormone pathway for ABA

ABA → cytoplastmic PYR receptor → PP2C phosphatase inhibit → SnRK2 kin autophosphorylates → ABF transcription

What is the general hormone pathway for brassinosteriods

BRI1 LRR at membrane → SERK co receptor → phosphorylation cascade → BES1 active

What is the general hormone pathway for ethylene

ERS receptors (ER BOUND) → ethylene binding → inhibits receptor → CTR1 inactive → EIN2 active

What is the general hormone pathway for JA

JA → COI1 (f-box) receptor → JAZ repressors degraded → MYC2 transcription factors active

What is the general hormone pathway for SL

SL → D14 receptor → conformational change → D3 MAX Box degrade repressors → PHR active

What is the general hormone pathway for SA

SA → NPR1 receptor → TGA transcription factors interaction → Pathogenesis related gene expression

Types of plant interactions with plant and environment

Mutualism (both benefit)

Commensalism (one benefits, other unaffected)

Parasitism (one benefits, other harmed)

Predation/Herbivory

Allelopathy (competition)

What is the first line of defense for plants against pathogens and herbivores

physical and mechanical barriers

• thorns, spines, prickles, trichomes, wax

How are trichomes developed

Jasmonates control (as well as secondary metabolite in trichomes like the ones with glands and chemical compounds)

Example of plant using chemical to defend itself

glucosinolates (mustard bomb) and protease inhibitors to block insect gut digestion

What is the active form of JA

JA-Ile from fatty acids

Functions of JA for defense

1. induction of anti-herbivory responses

2. production of herbivore induced volatiles (HIPVs)

3. response to necrotrophic pathogens

   1. induce systemic response to herbivory (SYSTEMIN)

Components of disease triangle

susceptible host

virulent pathogen

conducitve environemnt

What must a pathogen do to be considered successful

find host

penetrate defenses

avoid defense repsinses

grow and reproduce

spread and proliferate

What are the different lifestyles of pathogens

biotrophic (steal)

necrotrophic (kill & feed)

hemibiotroph (both)

entry of wounds, haustora, degrading enzymes to get into place

What is the zig-zag mofel

model of arms race of plant and pathogen

PTI → plants learn to recognize MAMP

ETS → pathogen effectors suppress PTI

ETI → R-proteins recognize effectors and have stronger response

pathogen evolves to avoid R-protein detection

What are MAMPs

microbe associated molecular patterns

what are DAMPs

damage assocated molecular patterns

what are PRRs

pattern recognition receptors with LRR-RK proteins to recognize MAMPS

What are some PTI responses

phytoalexins

ROS release

callose deposition

stomata closure

restrict nutrient transport

programmed cell death

What is the pathway for ETI

R-proteins find effectors → RESISTOSOMES form → stronger immune response

What is HR

programmed cell death of infected cells to seal biotrophic pathogen

What is gene-for-gene resistance

interaction bt specific pathogen effector and mathcing plant R-gene

What are some hormones that are induced after pathogen recogition

SA, JA, ET

SA and JA control response types tradeoffs in defense

SA: SAR, HR to fight biotrophic

JA: phytoalexin and fights necrotrophic

SA & JA are antagonistic (suppress each other)

JA triggers ISR from symbionts to prime defenses tho

Who sense strigolactones

mycorrhizal fungi to initate symbiosis with roots

Who manipulates SL sensing in roots

parasitic plants germinate near host roots and form haustoria

what do plants perceive in terms of photoreceptors

light quality

quantity

duration

What are photoreceptors

multi-domain proteins that bind chromophores

DIMERS

What is the wavelength and function of PhyA-E

R&FR (660-730 nm)

photomorphogensis

germination

shade avoidance

flowering

What is the wavelength and function of cryptochrome

UV-A/Blue (320-500nm)

Hypocotyl elongation

circadian rhythms

flowering

What is the wavelength and function of phototropin (PHOT)

Blue (320-500nm)

phototropism

chloroplast movement

stomata open

What is the wavelength and function of UVR8

UB-B (280-315nm)

circadian thythms

flowering time

What type of photoconversion does phytochrome go through

Pr (inactive and reads R) ←> Pfr (active and reads FR)

How does phytochrome signaling move

Pfr enters nucelus → inhibits COP1 → photomorphogenesis

How does COP1 work

DARK: suppress photomorphogenesis

LIGHT: inhibited by UVR8 → photomorphogenesis

What are PIFs

phytochrome interacting factors

they are negative regulators to promote elongated FR growth

What are the fluence classes

VLFR (phyA) → LFR (phyB) → HIR (phyA)

What are CRY1 and CRY2 features

CRY1: light stable, in cytoplasm and nucelus, low fluence, hypocotyl inhibitation

CRY2: degrades in light, nucleus only, high fluence, cotyledon expansion, flowering

what is the pathway for CRY activation

blue light → phosphorylatoin → CRY2 degrades COP1 → HY5 active → photomorphogensis

What are the PHOT1 and PHOT2 responsibilities

PHOT1: receptor for low f& high blue light fluence (phototrophism)

PHOT2: receptor for high light; chloroplast avoidance

What is the phototroph (PHOT) mechanism for phototrophism

blue light → PHOT1 autophosphorylates → blocks auxin transport on light side → auxin redistrubuted to shaded side → shaded cells elongate → plant bend towards the light

PHOT2 active to move chloroplast to walls → prevent photoinihibition

What is UVR8

plant specific UV-B receptor

inactive dimer → UV-B → monomer active to go to nucleus with COP1 → HY5 active → flavonoid production

what is flavonoid

sunscreen to absorb UV to protect DNA

3 parts of seeds

embryo

food storage (endosperm w/ aleurone&scutellum or cotyledons)

seed coat

what about seed dormancy makes it not germ even in good conditions

exogenius barrier or endogenus with hormones

What changes of the ABA:GA results in what

ABA>GA = dormancy

ABA<GA = germination

how does ABA in seed accumulate

during late seed development → dormancy + desiccation tolerance

Water uptake phases in seeds

1. rapid imbibition → metabolic repair → translation of stored mRNAs

2. plateau → cell wall loosening with metabolic activation → radical emergence and germination

3. water uptake resumes → makor reserve mobilization with new mRNA transcription for seedling growth

In cereals, how does GA and nutrient movement pathway look like

Embryo → GA → aleurone cells → a-amylase + hydrolases → starch breakdown → scutellum absorb → embryo growth

What breaks seed dormancy in terms of hormones and light

photoblasty (phytochrome promotoes GA buildup to germ)

stratification uses cold and wet for ROS and GA buildup

Name the 4 tropisms, their sensors, and mechanism

What is there to note for polar auxin transport

it is INDEPENDENT of gravity

directed by PIN and AUX1 and LAX influx carriers

What is the acid growth hypothesis

Auxin → H+ ATPase → apoplast acidification → expansin activation → cell wall loosening → cell elongation

What is the ethylene tripe response

hook + hypocotyl thicken + reduced elongation

ethylene reorients the microtubles in walls to transverse to longitudinal

How do plants develop organs post embro phase

maintaining stem cell populations in meristems

Name all meristems, their location in the plant, and the control/products of each

What are the root zones (from tip to base)

root cap → meristematic zone (QC + inital cells) → elongation zone → maturation zone

What is the quiescent center

only a few cells near root cap

low division rate, but maintain RAM with WOX5 and PLETHORA gradients

What is the pathway for QC vs in the elongation zone

QC: AUXIN + cytokinin → WOX5 + PLETHORA expression = meristemic

Elongation: CYTOKININ + ARR + less PLETHORA = elongation and differenciation

WOX5 movement between cell is important in meristem activity regulation

what are the SAM regions

Central zone (slow division)

Peripheral zone (fast division for leaf primoridia)

Rib Zone (generate stem tissue)

What are the SAM cell layers

L1 - epidermis, single cell thick (anticlinal growth)

L2 - internal tissue (anticlinal growth)

L3 - internal tissue and flowers

What is the CLV3-WUS feedback loop

WUS promotes stem cell activity in QC cells

CLV3: peptides from QC cells bind to CLV1 receptor → repress WUS → limit meristem size

more QC cells → more CLV3 → less QC cells created → less CLV3 → more WUS → more QC cells

In SAM, what are needed for meristem identity

SHOOTMERTISTEMLESS and cytokinins

What are the SAM hormone domains

HIGH CK + low auxin → meristem

HIGH AUXIN + low ck → organ differentiation

HIGH AUXIN → more GA + BR → organ development

Where does leaf initation occue in SAM

sites of localized AUXIN concentration in peripheral zone of sam (BOUNDARY)

What defines leaf polarity in the SAM/development?

adaxial: HD-ZIP II genes

abaxial: YABBY genes

What defines somata development in leavs

meristemoid cells

make asymmetric division → meristemoid → guard mother cell → symmetric division → guard cell pair

EPF1 peptides force stomatal spacing

What regulates the vein formation in stems

AUXIN and PIN1 that is directed with auxin flow from tip down

define a phytomer

basic module of shoot organization

What makes up a phytomer

internode + node + leaf + axillary bud