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3224 FINAL
| Question | Answer |
|---|---|
| what is the main difference in plant and animal receptors? | plants have RK and animals have GPL |
| how do plants respond to light ? | shade avoidance, development, chloroplast position, stomatal opening |
| what are the 3 main plant photoreceptors? | -> phytochromes, cytochromes, phototropins / LOV domain proteins |
| what do phytochromes do? | uses chromophore to absorbs R-FR -> conformational change. -sense Red/Far-Red / much in shade they are. important for seed germination, gravitropism, circadian clock. |
| what do cryptochromes do? | uses FAD +BLUE LIGHT & has protein tail autoinhibited -> conformational change -> active w half detached tail. CRY sequesters ubiquitinators and allows HY5 to transcribe hypocotyl genes |
| what does phototropism do? | uses FMN flavin mononucleotide plasma membrane localized kinase domain receptor - NOT receptor kinases. BLUE light. controls: tropsim (growth 2 light), chloroplast location (high light= chloro move out of way, dark = move to top of cells / leaf & stomata |
| what do photoreceptors do? | perceive specific wavelengths for different processes and undergo conformational change |
| 3 main light sensing mechanisms in plants? | - incidence / intensity (shade avoidance / grow towards sun) - duration / period (circadian rhythm) - wavelength (UVB via far red) |
| where do plants and animals differ in light sensing? | plants do it multicellularly and across various tissues, humans only have retinal tissue to perceive light |
| how do phytochromes alter plant behaviour? | When sensing FR, the conformationally changed protein enters the nucleus as a transcription factor and activates specific genes. When no more R -> FR, the protein reverts and exits nuc |
| what induces blue light stomatal opening? | phototropins via receptor activation -> inc solute in guard cell, water follows, inc tugor pressure -> stomata open |
| what is N-myristoylation? | amide linked, relatively stable, short 14:0 FA - myristic fatty acid |
| what is S-Acylation? | thioESTER bond, readily hydrolyzed, 16C FA, palmitic acid |
| what is prenylation? | thioETHER bond, stable, huge lipid group attached @ C-terminus |
| LEC recording 13 and ON ------------------ lec 11 slide 30 | -------------------------------------------------------------------- |
| what does BIK1 do? | main downstream RLCK of the FLG2/BAK1 LRR-RK receptor complex. BECOMES PHOSPHORYLATED AND further phosphorylates other proteins in downstream signalling |
| what happens when you knock BIK1 out? | compromised ROS production and Ca2+ signaling, even upon flg2 perception - MORE SUSCEPTABLE TO PATHOGENS |
| what does callose do? | a polysaccharide BARRIER! typically induced by a pathogen COMES FROM THE GOLGI! |
| what happens when you lose a PRR like flg2? | plant shows a decrease in pathogen resistance |
| what is the TTSS? | type three secretion system, a syringe formed by bacteria to insert effectors into plant cells |
| what is ETS? | effector triggered susceptibility- where effectors block PTI signals |
| what does ETS typically target in plants? | BIK1 - TTSS released effectors are proteins that cleave the genetic sequence or directly block translation of this RLCK. |
| how do pathogens fight back against stomatal closure by plants a as a form of resistance? | pathogens secrete CORONATINE (COR) which is a mimic of JA, causing the stomata to open again because JA promotes opening |
| how can COR bind the JA receptor COI1 ? | COR actually has a HIGHER affinity to the JA receptor than JA-ile that plants actually use |
| what is Flor's GENE-4-GENE model of immunity? | historical finding that plant resistance and pathogen virulence are in a 1:1 genetic ratio, where plants have 1 gene for resistance (R) of that pathogen, and pathogen has 1 gene (Avr) to overcome plant gene. sometimes the plant wins and sometimes bacteria |
| what happens when effectors (Avr) are NOT recognized by plant R (resistant) genes? | the effectors are virulent factors -> suppress PTI / facilitate infection |
| what happens when effectors (Avr) ARE recognized by plant R (resistant) genes? | the effectors are avirulent factors -> triggers ETI! |
| what do the R (resistant) genes in plants encode? | NLR proteins (nucleotide-binding leucine-rich repeat proteins). - receptors for the 2nd layer of immunity |
| what are the 3 segments of NLR proteins? | VARIABLE signaling domain (CC/TIR) - N-Terminus NB/ARC domain - BINDS NUCLEOTIDES LRR domain (for protein/protein interaction) - C-Terminus |
| what are NLR proteins ? | - the receptors for the second layer of plant immunity - Nucleotide binding Leucine rich Repeats BOUND TO: ADP = INACTIVE, ATP=ACTIVE |
| how do NLR recognize effectors? | directly or indirectly |
| what happens w/ direct effector binding on a R gene ? | the effector directly binds to the LRR portion of the R gene, activating the gene |
| what happens w/ indirect effector binding on a R gene? | by using either guardee proteins or decoy guardee proteins, these proteins activate the R gene -> NLR protein. the guard proteins are someplace for effectors to stick to, reducing virulence and guarding a commonly targeted ETI gene |
| how do ETI and PTI signals vary? | they are similar in the TYPE of response (ROS, Ca2+, MAPK, genes) but ETI is MUCH stronger (more!!! amplified signal!!) |
| what is hyper-sensitive response (HR) ? | accompanies ETI and is essentially programmed cell death @ site of infection- works great for everything other than necrotrophs |
| what do NLR proteins do after activation from ADP -> ATP? | they oligomerize into RESISTOMES, conjugating @ the C-terminus, forms PORES allowing ion and cellular content transduction & cell DEATH |
| what is ZAR1? | a CC-NLR protein that aggregates to forms a resistome, creating a Ca2+ PORE in plasma membrane -> HR |
| how does ZAR1 sense its effectors? | PBL2, a decoy protein RLCK, catches a effector and brings it to the _______CC-NLR protein, exchanging ADP-> ATP, aggregates with other activated NLR proteins form resistome -> HR |
| what are TIR C-terminus NLR proteins? | the other N-terminus variation other than CC-NLR. aggregates into holoenzyme that uses NADH to form signaling molecules to recruit resistome pores |
| how do TIR and CC N-terminus resistomes differ? | one forms calcium pores, one doesn't. it forms a holoenzyme that produces signaling molecules and recruits resistome pores |
| how do animal and plant NLR pore structures differ? | both assemble into large, multisubunit ring structure BUT different downstream mechanisms! |
| what is the ''evolutionary arms race'' perspective of plant immunity? | due to constant pathogens, we can see a multi level defense against pathogens, starting with pattern trig imm -> effector trigg susceptibility -> effector trigg IMMUNITY via NLR |
| what is the zig zag model? | we can see a zigzag of pathogen population vs plant population until one outsmarts the other and dominates ! *PTI -> ETS -> ETI ***************************** |
| how many NLR genes do plants have? | TONS! evolved for many years to have an arsenal like this -arabid = 149, rice has over 400!) |
| are PTI and ETI interconnected? | YES! have mutual potentiation = both systems can prime / boost each other = both required for full function |
| what are 3 plant microbe interactions? | - root nodule symbiosis - mycorrhizal fungi - the microbiome |
| what plants have the most root symbiosis? | legumes because they associate with Rhizobia OR Frankia bacteria -> nodule organ formation |
| what are the steps to symbiosis | plants release flavonoids under low N stress -> rhizobia produce NOD factor -> plant preps for nodule formation |
| what is NOD and why do bacteria release it for the plant to sense? | after plants release flavonoids they enter bacteria and induce transcription of NOD gene which create NOD factors |
| what are NOD factors? | a variable fatty acid (LCO's) that can have many strucutres allowing for wide variety of hosts for the bacteria releasing this factor |
| why are NOD factors similar to PAMPS? | both have chitin which could trigger immune response but DOESNT - activates SYM pathway |
| how are NOD factors perceived? | via NFR - nod factor receptor kinase @ plasma membrane |
| what downstream pathway is signaled upon NOD and NFR binding? | the NFR is activated, signaling another RK (SYMRK) -> 2nd mess. relay signal into nuc where gene expression occurs. nuclear CALCIUM SPIKING ALSO OCCURS ! |
| why is the calcium spiking upon NOD perception important? | these spikes allow for creation of a symbiotic relationship - also seen in symbiotic fungal associations |
| unlike Rhizobia (legume) bacteria, Frankia (actinorhizal) bacteria uses what? | NO NOD, uses something else "Frankia factor? but we DEF know it still uses the SYM pathway to create nodules! |
| what is the most common mycorrhizal fungus? | AM - arbuscular mycorrhizal fungus - gives plant P and gets sugar AND LIPIDS! |
| do fungus also use the SYM pathway and thus calcium spiking? | YES! |
| steps to fungal symbiosis? (AM) | plant secretes stringalactones -> fungus produces MYC factor -> plant allows fungus in to create its arbuscule (hijacked by Striga!) |
| are MYC factors also LCO's? | YES THEY ARE |
| what do plants form to prep for AM symbiosis? | epidermal cells form pre-penetration apparatus - HELPING THE FUNGUS GET INTO THE PLANT CELL! |
| what do strigalactones cause the AM fungus to do? | hyphae branches and forms arbuscule INSIDE INNER CORTEX CELLS |
| what membrane surrounds the AM fungus? | the peri-arbuscular membrane - full of transporters to facilitate symbiotic exchange |
| What are the 3 microbiomes plants have where they interact with non-pathogenic species? | - phyllosphere (shoot surface) - rhizosphere (root surface) - endosphere (internal tissues) |
| what are the 3 ways plants respond to mechanical sensation? | - thigmorphogenesis - thigmotropism - thigmonasty |
| what is thigmorphogenesis? | long term physiological changes in response to mechanical stimuli - like a tree growing bent over due to constant wind |
| what is thigmotropism? | directional, differential growth in response to mech. stim. used by parasitic climbing plants to weave around a host OR ROOT TO GET AROUND A ROCK |
| what is thigmonasty? | rapid, dynamic movement in response to mech. stim. *driven by changes in turgor/elasticity/ growth***** |
| how is mechanical stimulus sensed inside a plant? | calcium signaling ! repeated long term stimulation causes reduced growth due to constant 'stress' |
| how do plants respond to herbivores? | JASMONIC ACID! key defense - removes gene repressor (BRAKE), activating genes related to producing proteins and other defence compounds |
| what is the long distance signalling in herbivory? | glutamate like receptors that bind glutamate (GLR) -> propagate ROS/Ca2+ ion signal thru plant to induce antiherbivory (JA) |
| what does glutamate act as ? | mechanical wounding causes the release of this molecule and it acts as a DAMP |
| what else can plants do against herbivores? | release VOC! (volatile organic compound) - can call predators of the herbivore - enemy of my enemy is my friend or PRIME immune responses in neighboring plants - cut grass smell!! |
| what is HIPV? | herbivore-induced plant VOC |
| what is an example of thigmonasty? | Mimosa folding plant that uses Ca2+ signaling to fold closed against herbivores or Venus Flytrap closing around a fly |
| how does the Venus Flytrap snap shut? | to stay open = stored kinetic energy and then when triggered, this turns into kinetic energy snapping it closed |
| what mechanosensitive channels initiate trigger hair electrical signals? | FLYCATCHERS (FLYCs) - expressed in trigger hairs and when the hair is pulled, the plasma membrane is also pulled and allows for Ca2+ to trigger Action Potential |
| why does CWI signaling have to occur? | cell wall must be monitored to ensure proper growth and NO mechanical failure |
| the cell wall is both a site of ____ and a reservoir of ____? | sensors and signals !!!!!!!!!!!! |
| what kind of sensors does the cell wall have? | - mechanosensitive channels (OSCA, FLYC) - receptor kinases (FER = Ferionia!) - others (LRX, GPI anchored protiens that stick to PM on 1 side) |
| what does the FER receptor sense? | signals such as RALF proteins which are secreted by cell wall upon damage |
| Where else are RALF proteins perceived? | at FER + LRX co-receptor complex (cell wall anchored). also @ GPI-anchored proteins (LLG) and FER-RK complex (PM anchor). |
| what do RALFs do? | act as integrators of CW and RK signaling- important for many processes and stress responses |
| what are some signals cell walls contain? | - peptides (RALF protiens) - cell wall breakdown products (DAMP/ oligosaccharides) |
| what kind of down stream signalling occurs after RALF perception? | ROS, Ca2+, MAPK, GTPase, classic relay signals but TRIGGER CHANGE IN PHYTOHRMN LVL AND ALTERED GENE EXPRSN |
| how can CWI sensing help with BIOTIC stress response? | when pathogens secrete CW degrading/modifying enzymes, plants have evolved receptors to both the enzyme AND breakdown products of the plant iself. TRIGGERS PTI!!! |
| how can abiotic stress affect cell wall? | alters pectin and protien content. Also high SALINITY (Na+) can soften wall |
| how can CWI sensing help with ABIOTIC stress response? | FER, sensing the cell wall conditions, signals when there are changes such as high Na+ and soft walls, allowing for RECOVERY |
| what happens to plants that have FER receptor knocked out under high salt? | are UNABLE to repair and burst because there was NO sensor ! |
| how can stress be signaled around the cell? | various organelles sense perturbations in environmental conditions and GENERATE SIGNALS TO REGULATE GENE EXPRESSION -> to restore cellular homeostasis |
| what specific signaling pathway does stress usually trigger? | ROS and Ca2+ signals. Ca2+ as a signal is useful and common in most plants as [Ca2+] cannot be high in the cell |
| how do abiotic stresses interact? | can interact negatively (additive-double harm) or positively (interfering-reduce the burden of the other) |
| what structure is most important for transpiration and gas exchange in plants? | stomata!- sun energy DRIVES this system! |
| what are byrophytes? | desiccation tolerant plants descended from early land colonizers. like the resurrection plants |
| what are xerophytes ? | desiccation sensitive plants that live in arid environments and have adapted via 4 mechanisms |
| what are the 4 mechanisms xerophytes adapted to their arid envirnoment? | phenological (evade/quiescent), anatomical (THICK cuticle) morphological (deep roots / succulent storage) biochemical (CAM metabolism where stomata open @ night) |
| what are the 2 major drought effects? | -ROS accumulation due to lack of photosynthesis but constant light energy input -CELL DEHYDRATION |
| what are mesophytes? | MOST PLANTS- desiccation SENSITIVE and |
| what are the 3 effects of water deficit? | perception, signaling, and responses |
| how does perception of water deficit occur? | cell loses turgor, transmembrane proteins detect changes, ROS increases |
| what is the phytohormone that signals drought? | ABA! this causes STOMATA to close ! but there are ABA independent pathways for drought too |
| how do cells adapt to low water? | increase ion conc. in vacuoles and solutes in cytosol, lower water potential and doesn't disrupt metabolic functions |
| what functions do LEAs have? | sequesters ions/small molecules, associates with membrane to preserve fluidity upon stress, acts like HSP and protects other proteins |
| what does the cell upregulate at drought exposure>? | ABA, aquaporins, ROS detox pathways, LEAs |
| ABA levels are tightly controlled by _____ & ______ & _________? | synthesis, conjugation, and degradation |
| how does ABA signaling occur? | binds to negative regulator protein (PP2CA) releasing the SnRK2 kinase ->phosphorylation of TF's + ion channels to CLOSE STOMATA via loss of ions and therefore water pressure |
| what happens to mutants that have no ABA? | NO stomatal closure upon heat stress and wilts easily |
| how can plant morphology change in response to drought? | ROOTS grow towards water / nutrient and adaption type varies on severity and genotype capabilities. can go deeper, left, right, lateral. INCREASE # of XYLEM |
| plant responses to water deficit are _____, complex and context dependent, includes an ______, _______, and _______&____. | PLEIOTROPIC, increase in root growth, decrease in shoot growth, decrease in transpiration & photosynthesis. |
| what are the 2 types of methods to see Ca2+ signalling? | fluorescent dyes loaded into the plant that pick up Ca2+ and glow, OR GECI luminescent or fluorescent protiens! genetically encoded Ca2+ indicators! most common method now cuz endogenous ! |
| what do luminescent GEIC proteins do? | the binding of Ca2+ causes an emission of light |
| what do fluorescent GEIC proteins do? | needs a light source to activate the protein first and then emits back at a longer wavelength. 2 TYPES |
| what are intensometric (single wavelength) fluorescent GEIC proteins? | qualitative, single light is emitted when Ca2+ binds. not very precise |
| what are radiometric fluorescent (dual wavelength) GEIC proteins? | emits 2 wavelengths of light (like FRET) and can even tell you the concentration of Ca2+. QUANTITATIVE |
| why is GECI useful? | we can see Ca2+ signals from a variety of stimuli, touch or cold or cut or pathogens |
| what the paradigm of calcium signalling? | encoding, decoding, and response |
| what is calcium encoding? | generation of signal via influx (channels) or efflux (pumps, antiporters, exchangers) |
| what is calcium decoding? | sending of the signal / elevated Ca2+ levels |
| what is calcium response? | downstream signaling that induces transcriptional reprogramming and altered metabolism -> gene expression change! |
| do plants and animals have similar calcium channels? | NO, plants do not have VGCC, IP3 receptors, or TRPs |
| what kind of calcium channels are found in plants? | ligand gated and mechanosensitive |
| what are some ligand gated calcium channels? | glutamate-receptor-like channels (GLRs) or cyclic nucleotide gated channels (CNGCs) |
| what are some mechanosensitive calcium channels? | OSCA and MSL - require physical deformation |
| what is another type of calcium channel in plants? | the ZAR1 protein LRR that forms a resistome- pore! |
| how are calcium ions sensed in the cell? | a binding motif of EF (fingergun), each binding motif holds one Ca2+ and 2 alpha helixes |
| what are the 4 main calcium sensors plants employ? | - CaM, CML, CBL, and CPK - Calmodulin, CaM like, calcineurin-B like, calcium-dependant protien kinases |
| what is CaM? | binds 4 Ca2+ w cooperativity like hemoglobin. like Q-tip and can wrap around target proteins -> CLOSED (w/o Ca2+)= APO-CaM. ->OPEN (w/Ca2+)= Ca2+CaM |
| what is CML? | we don't know much about these other than they are CaM-Like. not all bind Ca2+, plant specific, maybe do same things as CaM? |
| what is CBL-CIPK complex? | calcineurin B-like proteins that target SPECIFIC CBL- interacting protein kinases (CIPK). most precise machinery than CaM |
| what is CPK or CDPK? | calcium dependent protein kinases. with Ca2+ present, they have kinase activity, involved in stress response and immunity |
| how is specificity attained w a broad signal like Ca2+? | encoded within the signature - large magnitude or short duration or kinetics. vice versa too. |
| which 2 Ca2+ sensing proteins are the main "sensor" that binds and activates downstream proteins + regulating their function ? | CaM's and CML's |
| which 2 Ca2+ sensor proteins are the sensor/responders that have catalytic activity regulated by Ca2+ binding? | CBL-CIPKs and CPKs |
| are human and plant CaM similar? | humans only have CaM Ca2+ sensing protiens, and plant to human CaM is 95% similar! |
| what does CaM binding do to a protien? | can affect target activity, localization, conformational state etc. |
| what kind of proteins can CaM regualte? | development, reproduction, abiotic stress response, immunity, symbiosis, etc. |
| what do CBL-CIPK complexes do? | upon Ca2+ activation, these complexes regulate ion transport and are usually near the PM anyways as they are N-Mirosylated |
| how does ROS come about the cell? | dysregulated aerobic photosynthesis (baseline level ROS) and ENDOGENOUSLY (enzymes in cell wall) produce 2nd messengers |
| how is ROS produced enzymatically? | RBOH protiens in the cell wall that uses FAD and NADPH to reduce oxygen to superoxide |
| do humans have RBOH proteins? | YES- theyre called NOX and produce free radicals (ROS) |
| why is RBOH not a problem even though its producing harmful ROS? | the ROS scavenging (SOD) quickly changes the superoxide to hydrogen peroxide to b used as signal molecule that can pass PM |
| what is the known ROS receptor? | HPCA1 = receptor kinase that has sulfur bonds that allows the ROS to activate it and open Ca2+ pore nearby |
| what are the 2 types of ROS scavenging systems? | enzymatic and nonenzymatic |
| how are ROS and Ca2+ signals interconnected? | calcium triggers ROS via activation of RBOH via CPKs and ROS triggers Ca2+ influx via HPCA1 sensor. ROS/Ca2+ WAVE! |
| how do cyclic nucleotide monophosphates appear in humans? | TONS!!! |
| how do cyclic nucleotide monophosphates appear in plants? | NONE! we cant find much of the cNMP mahcinery in plants, seems like Ca2+ pathways took off more during evolution |
| what kind of cNMP machinery can we find in plants? | we only find CNGCs! cyclic nucleotide gated channels that allow calcium through! we cant find much of other machinery |
| how else can CNGC calcium channels be modulated? | not only cyclic nucleotides but also calmodulin and phosphorylation |
| how are cyclic nucleotide monophosphate signals generated and attenuated by plants? | we dont know! dont produce the same pathway molecules like ours |
| what do we know cNMP triggers? | CALCIUM SIGNALLING! |
| what are membrane lipid derivative secondary messengers? | membrane phospholipids cleaved by phospholipases to become a different structure and thus signal recognized by other cells |
| what are the 2 common PLANT membrane lipid derived 2nd messengers? | IP6, and PA |
| what do phytohormones helps plants do? | helps adjust plant processes in response to environment, can initiate response and also be a RESULT of the response. |
| what else can produce phytohormones? | plant associated microbes! they can produce either the same compound or mimics to invade/evade the plant |
| what is polar auxin transport? | this hormone travels from the TIP OF SHOOT to TIP OF ROOT and then travels back up along the sides BASIPETALLY |
| how can auxin change charge to move between cells? | inside the cell, ___ is charged and membrane impermeable until it is released by the basal channel. when it leaves the cell it gains a proton and is neutral and can cross the PM- loses proton again |
| what is the influx auxin channel? | AUX1/LAX allows IAAH into the cell passively |
| what are the 2 auxin efflux channels? | PIN (@ the bottom) and ABCB (@sides) to allow dynamic auxin release like forming an organ |
| auxin controls developmental patterning as a ______ and _______? | morphogen and trigger! |
| how does auxin act as a morphogen? | the concentration of this hormone drives growth, which regulates tissue patterning. low A= elongate/ differentiate. medium= divide frequently. high= no growth, QUIESCENT |
| how does auxin act as a trigger? | synthesis of this hormone in just ONE cell is sufficient to TRIGGER lateral root formation, specifies fate of cell and initiates organogenesis |
| how does auxin trigger changes at the plasma membrane? | receptor kinase TMK1 rapidly senses this hormone and causes ion fluxes and downstream protein phosphorylation - rapid changes that we knew were not genetic yet |
| what are the 3 steps (2-component) to cytokinin signaling? | CK binds to PM receptor, HK receptor phosphorylates, passes P to histidine phosphotransfer proteins (HPT) then transfer P to RR (response regulators) that carry out diff functions |
| what are the 3 steps (2-component) to cytokinin signaling in ACRONYMS? | CK + HK =HK+P -> P+ HPT-> HPT + P -> RR -> transcription factor or inhibition of other phytohormones (auxin) |
| how can CK signaling get specific? | the types of downstream RR (response regulators) that it activates, either gene expression or inhibitors of CK signaling |
| how many receptors does CK have? | there is both a plasma membrane and endoplasmic reticulum (ER&PM) |
| what is the broad scope of what CK does? | 2 receptor spots, triggers RR (response regulators) that trigger transcriptional change, then downstream cellular/physiological responses |
| what is the nature of the relationship between CK and AUX? | they are antagonistic! auxin moves basipetally (root2shoot), and CK acropetally (top down). concentration of each determines development |
| how can CK generate organs via organogenesis? | can create ROOT formation but too much = stem cells |
| how can Auxin generate organs via organogenesis? | can promote SHOOT formation but too much = stem cells |
| what does GA interact with? | ABA! abscisic acid and gibberellins act antagonistically to either stay dormant (ABA) or germinate (gibberellins) |
| what does abiotic stress cause in plants? | an accumulation of ABA |
| what are the transcriptional responses of ABA? | synthesis of osmoprotectants, ROS/2nd messenger, movement of water, membrane stabilization, STOMATAL CLOSURE |
| how does ABA regulate the stomata? | 1. ABA binds receptor. 2. ABA+receptor SEQUESTER inhibitor. 3. uninhibited kinase now phosph. RBOH (ROS) and ion channels, pumping ions OUT of guard cells. water follows. |
| does ABA just close the stomata? | no it actively inhibits the opening of K+ pores that would trigger influx |
| what is ethylene? | gas used for ripening derrived from stress (wounding/smoke)-- MORE specific uses unlike other hormones |
| what hormone actually controls leaf abscission? | ethylene! suprise! not ABA |
| where does ethylene come from? | methionine -> ACC -> ethylene. ASC ASO = enzymes used to regulate eth formation |
| what type of activation pathway does ethylene have? | a very simple one - wounding -> MAPKKK -> increase in ASC and ASO (ACC synthase + oxidase) -> ethylene |
| what are the 3 plant responses to ethylene during germination? | - reduced elongation - hypocotyl swelling - apical hook exaggeration |
| what is the receptor for ethylene? | ETR1 - first phytohormone receptor found- MEMBRANE LOCALIZED |
| how is ethylene perception different than other phytohormones? | in the absence, the transcription factors are phosphorylated and DEGRADED by CTR1.w/ hormone, receptors inactivate CRT1 and allow TF's (EINs) to transcribe the specific genes . |
| what are Strigolactones used for? | interactions w fungal symbionts and PARASITIC plant interactions |
| what are the 3 main things SL phytohormone promote? | inhibited shoot branching, AM fungus association, and parasitic plant germination. also has internal effects like development and root growth |
| how are SL percieved? | D14 (receptor+enzyme) attaches to hormone and then degrades repressor (SMXL)! |
| what primarily induces jasmonates? | necrotrophic pathogens, wounding/herbivory. less involved in development more for PROTECTION |
| how is JA synthesixed? | LIPID DERRIVED from PM, it gets broken down into JA-Ile in the cytoplasm by JAR1 |
| where is JA percieved? | in the nucleus! |
| how is JA percieved? | JAZ repressor is bound, JA + COI1 receptor degrade repressor and allow transcription |
| what 2 receptors are similar in plant hormones? | JA and Auxin! similar structure and mechanism- likely evolved from common ancestor |
| what is special about the JAZ + COI1 interaction? | the repressor and receptor act as a complex that has an affinity for JA 100x greater than either alone |
| what is the initial place of SA syntehsis? | in the plasmid |
| what range of effects does SA have? | local and systemic responses- primes the whole plant |
| what does SA induce? | causes cell death - not good for defense against necrotrophs |
| what is the receptor for SA? | NPR. not so much receptor, but proteins controlled by SA. theres 2 kinds, monomer (outside nuc, TF) and complex (in nuc, repressors) |
| how does SA perception turn into signalling? | the monomer is always baseline present but in SA presence, more monomer that gets into nuc and activates genes. SA binds to repressor and allows transcription of those genes too |
| what kind of genes does SA induce? | PR genes - pathogenesis related genes for fighting off pathogens-ONLY BIOTIC THO! NOT NECROTROPHS (JA+ET INSTEAD) |
| what do BR do to the plant? | causes cell and stem elongation |
| what does BR do to the plant cell? | loosens the cell wall, allowing for growth and expansion. DOES THIS AT THE EXPENSE OF IMMUNE SYSTEM. suppresses it to allow for growth! |
| where is the BR receptor? | BRI1 is located at the plasma membrane and is a RK with a LRR. requires the hormone to join to bring co-receptor BAK1 and glue them together |
| what kind of BR mutants can be saved via exogenous application? | only biosynthesis mutants, NOT receptor mutants because they cant downstream signal anyways |
| what are the steps to BR signalling? | BAK1 and BRI1 come together (repressor on BRI1 removed) and then BIN2 gets dephosphorylated and degraded, allowing for BES1 to get to nucleus and transcribe genes. no BIN2 dephosph= BES1 is phosphorylated and degraded=no TF |
| what are the 4 proteins that are the HUBS of cross talk between hormones? | DELLA, JA, BIN2, and BES1. |
| what is the main diff btwn proteins as hormones and other hormones? | one requires synthesis from biochemical reactions and the other is genetically encoded |
| what processes do peptide hormones signal? | nearly all of them but we dont know cuz they such a small chunk of DNA compared to the whole genome. BUT USED FOR IMMUNITY!!!!!!!!!!!!!!!!!!!!!!! MAINLY |
| what other non hormonal roles do peptides play? | anti microbial (disrupts membranes) OR protease blockers (cant cleave proteins!) |
| what was the first protein hormone discovered? | systemin - like insulin in humans but also active at low conc so hard to detect! |
| what are protein hormones key for? | long-distance signaling -> transported in xylem or phloem |
| what are the 4 similarities btwn protein hormones and other phytohormones? | - low conc to regulate -long distance acting -may req PTM - requires a receptor for recognition |
| what are the 2 ways protein hormones are classified? | primary sequence and post translational modifications |
| what are the stages of peptide development into mature? | mRNA -> prepropeptide -> propeptide -> peptide (mature) (ALL OCCURS IN CYTOSOL outside of nuc) |
| proteins that are supposed to be secreted out of cell and not kept inside must have WHAT signal? | N-terminal signal that targets it outside of cell (for long distance!) |
| is peptide processing REQUIRED for its function? | plants with no proteases cannot produce functional proteins |
| what are the 5 peptide classes? | -functional, precursor derived (chunk off another large functioning 1) -PTM peptides (ENZYMATIC!)-cysteine rich (NONENZYM.) -unmodified (forms own structure) -nonprecursor derived |
| 3 methods of peptide signaling attenuation? | -endocytosis of receptor -antagonistic ligands block receptor binding site -nonactive receptors sequester active proteins |
| what are some PTM used on protiens? | proper folding (non enzymatic) and hydroxylation or sulfonation (enzymatic!) |
| what are the 4 large roles of peptide hormones? | development, reproduction, abiotic stress, and immunity |
| what are immune-modulating protein hormones called? | phytocytokines - actively secreted |
| where are peptide hormones percieved? | like BR, at the cell surface and with a similar RK receptor fomation! |
| how does peptide signaling occur? | receptor (HAE) w/ LRR binds protein & co-receptor (SERK1) and -> downstream signaling |
| what are the 2 receptor types plants have? | LIGAND GATES ION CHANNELS RECEPTOR KINASES |
| what's the diff between plants and animal RK? | animals have RTK (tyrosine) and plants have RK (no Tyr) |
| how are plant RK able to have diversity? | the extracell domain (LRR) can have different proteins and shapes allowing for specificity. can bind peptides, carbs, steroids, lipid derived compounds |
| what is the structure of LRRs? | beta sheet strand, turn , alpha helix then this repeats many times |
| what is the common activation seen in LRR RKs? | ligand binds, co repressor binds, downstream signaling occurs |
| what is a common family of Co-Receptors>? | BAK1 and SERK - used in many other RK complexes but its the RK LRR that determines specificity |
| what are RP receptor protiens? | like LRR RKs but no kinase domain, complexes with adapter kinase AND co-receptor. 3 part combination. |
| how is LRR-RK similar in plants and animals? | animals have another protein before receptor activates kinases, but plants it goes LRRRK -> kinase -> substrates |
| what are regulatory RKs? | complex with co-receptors to ensure no false activation |
| what are the 3 types of LRR-RK receptors we looked at in plants? | - LRR RK, -LRR Receptor Protien+ adapter, -Regulatory RK *******ALL HAVE CO-RECEPTORS********** |
| what is an RRK example? | BIRs - sequester BAK1/SERK |
| what are the effects of activated RK complexes ? | some RK are kinase but mostly its the co-receptor with the catalytic activity and is DUAL SPECIFICITY (can phosph all 3 amino!) |
| what is the ultimate downstream effects of RK complexes? | downstream signals (CDPK, MAPK, RLCK, ROS out) ->TF phosphorylation and change in gene expression |
| the protein IDA controls what specific mechanism? | floral organ abscission, induces RK + coRK complex, can be seen w Western blot to see proteins. GOF mutants without co-RK ARE NOT stunted |
| how can plants use peptide hormones to signal low N? | deficient side CEP peptide moves from root -> shoot, perceived by CEPR -> downstream shoot -> root signal (CEPD) then increases N uptake |
| what are the 2 receptors RALF is recognized by? | NOT LRR! LLG (gpi outer PM linked), LRX (cell wall anchor) |
| what are the 3 biotic interactions? | pests/pathogens, other plants (parasitic or competitive) and lastly mutualistic/ symbiotic |
| what is the disease triangle? | the 3 requirements for plants to be overcome w disease. 1.HOST, 2. ENVIRONMENT 3. PATHOGEN |
| how do environmental conditions affect plant disease? | can favor growth, dispersal, and virulence of pathogens. can also affect host plant condition |
| what can plants do morphologically to avoid pathogens? | waxy cuticle and cell wall. pathogens must overcome this |
| how do pathogens usually invade plants? | CELL WALL DEGRADING ENZYMES (CWDE) of which plants have formed receptors for ! |
| what kind of immunity do plants have? | only innate that is induced by pathogen detection |
| plants can ______ and _______ to potential pathogens? | sense and respond |
| what are elicitors sensed by? | RK or RPs |
| what are PRRs? | pattern recognition receptors - receptors of PTI that are either RK or RP only. (both w LRR) |
| how is PTI triggered? | pathogens are sensed, RK and ligand and co-receptor (BAK1/SERK co-r) complex forms-> kinases activated ->PTI |
| what are some effects of PTI? | JA/SA/ET production, ROS, MAPK, TF/genes, CELLULOSE DEPOSITION, and PA production (more ROS) and toxic 2nd metabolites |
| what is the temporal/ sequential PTI signaling? | immediately, 2nd mess are triggered RLCK, Ca2+, after few hours ET, callose, stomata close ABA/noABA. LONG TERM= growth inhibition |
| what are the 2 stresses that salinity induces? | OSMOTIC AND IONIC |
| how does salinity induce osmotic stress? | causes decrease of water potential OUTSIDE the cell relative to inside, making it harder to pull up water |
| how does salinity induce ionic stress? | toxicity of Na+ salt ions due to loss of ion homeostasis |
| why is Na+ a dangerous ion? | it mimic the essential K+ ion and disrupts homeostasis |
| what is salinization? | the excessive accumulation of salt |
| how can soil salinization occur? | too little water, high evaporation, poor drainage, fertilizer |
| what are salt tolerate plants called? | halophytes |
| what are not salt tolerant plant called? | glycophytes |
| what are halophytes similar to? | xerophytes that survive in arid conditions |
| what kind of mechanisms do halophytes employ to tolerate stress? | similar cellular functions (sequestration in vacuole) or physiological like salt glands and denser stomata. others r succulents |
| what kind of responses do plants have to osmotic stress? | like water deficit- ABA/no ABA pathways, transcriptional responses, and accumulation of solutes |
| what kind of responses do plants have to ionic stress? | calcium triggered SOS pathway to remove/sequester/exclusion of ions |
| what does salt trigger in plants? | rapid calcium signaling and over long distances! |
| what is the SOS salt overly sensitive pathway? (3->1) | calcium sensor -> CBLK -> phosphorylates Na+/H+ exchanger |
| what is the PM salt sensor? | MOCA1! |
| what does moca1 do? | it is actually a lipid in the membrane in the outer leaflet that triggers downstream Ca2+ signal? that activates SOS pathway |
| what is the current model for salt sensing? | direct sensing of Na+ in apoplast by LIPID sensor |
| nitrogen stress is sensed how? | proteins! the CEP -CEPR - CEPD causes more N uptake and increase in HIGH AFFINITY channels |
| what are plant N deficiency responses? | increased uptake via expression of high affinity transporters (HATs) and decreased production of molecules containing N |
| what happens when there's lots of N? | plants dont grow roots as long! only grow roots in nutrient containing places - dynamic ! |
| what are the 2 types of transporters expressed by N deficient plants? | HATs and LATs (high and low affinity transporters) |
| how is N sensed? | directly by proteins that then activate and become TF to N assimilation genes - called NLP7! |
| what local and systemic responses does low P induce? | more root hairs to inc surface area, and then P transport and homeostasis |
| how are phosphate levels sensed? | SPX domains - group of binding domains - multiple "types" of sensors. these domains attach and sequester TF unless no P |
| what is the PSR? | phosphate starvation response |
| how is PSR triggered? | triggered by genes expressed by SPX domain bound TF. increases P transporters to increase uptake |
| why wont PSR be triggered under low N too? | N is the most crucial - builds proteins to survive. NO N= no life |
| how do abiotic and biotic stresses interact? | nutrient deficiency and symbiosis effort by plants are correlated, either fungus or bacteria is preferred under P stress/abundance |
| what is the current model for P starvation ? | sufficient P= bacteria sym promoted (N) insufficient P = antibacterial, goes for fungus symbiosis |
| what effects does severe cold stress induce? | cellular dehydration and rupture - DEPENDS ON TYPE OF PLANT- cold acclimated try fighting the cold induced stuff more |
| what do ice binding protiens do? (IBP) | proteins that surround ice to inhibit RECRYSTALLLIZATION into larger crystals |
| how do plants sense cold? | unknown - could be RKs, channels, or multi-transmembrane proteins that sense membrane fluidity |
| what are cold signaling outputs? | CALCIUM SIGNALING!!!!!!!! then downstream TF |
| how does heat stress alter plant morphology? | hyponastic growth and INCREASED HYPOCOTYL LENGTH |
| how is heat stress sensed and signaled? | sensed by membrane fluidity likely and also triggers calcium signaling -> HSP / chaperone and ROS scavenging systems |
| what role can proteins play as thermosensors? | ELF3 - at high temp, it condensates and allows transcription of genes |
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