What is the probable mechanism of WRKY Transcription factor or the pathway in which wrky plays a major role against biotic stress. Please provide references.
Please have a look at this thesis: Role of WRKY Transcription Factors in Arabidopsis Development and Stress Responses. Jing li, 2014
Out paper on defense against Botrytis in Arabidopsis discusses the action of WRKYs. http://www.plantcell.org/content/24/9/3530.long
The pathway in Arabidopsis involves a MAP kinase (MAPK) pathway consisting of a MAP kinase kinase kinase (MEKK), a MAP kinase kinase (MKK), and a MAP kinase (MPK). In barley (right), MAMP or PAMP are perceived by receptors that initiate signalling via intracellular MAPK cascades. This stimulates the induction of unknown WRKY transcriptional activators (red) and HvWRKY1/2 repressors (blue). The WRKY repressors may prevent chronic defence gene activation. Autorepressed MLA receptors are folded by RAR1, SGT1 and cytosolic HSP90 and the result is basal defence. Upon coactivation of one or several MAMP or
PAMP receptors and MLA by cognate Blumeria graminis f. sp. hordei (powdery mildew) effectors (in this case AVRA), an integrated MAMP or PAMP and MLA-triggered immune response is triggered. Activated MLA stimulates nuclear association with the WRKY1/2 repressors, thereby de-repressing MAMP-triggered immunity. Derepression of basal defence responses is thought to amplify the expression of defence-related genes. In Arabidopsis, the MEKK1–MKK1/2–MPK4 module is activated by MAMP or PAMP. This leads to nuclear dissociation of the MPK4–MKS1–WRKY33 complex and release of WRKY33 and MKS1. WRKY33 enhances the expression of PAD3. PAD3 is required for the synthesis of the antimicrobial camalexin.
Dear all,
Why is Mr. Lilly asking other researchers to do the literature review that he himself should do as a PhD student? He can perfectly search on e.g. google scholar and then ask specific questions.
Regards,
Ruben
Dear all,
Many of you would agree with me when I say that Mr. Fernandez has pointed out something which applies to many at “Research Gate” but at the same time you would also agree that this site is open to both questions and answers.
Asking a question depends upon an individual’s interest and whether to answer it or not depends on the other. You have every right not to answer such questions which one can easily get through any literature search and that is why people though knowing an answer, prefer not to answer. So it depends on what scientifically literate people think about it at times.
We scientifically literates may lazily (sometimes) do what Mr. Fernandez has pointed out but according to me such questions are usually put up only to come across publications which gets burried with time or the ones which one doesnot have acess to.
Regards
Jimmy
A simple answer is - they are transcription factors - they activate expression of genes involved in biotic stress response when they are upregulated or not, when they are low :). Many WRKY factors are SA dependent and can regulate PR1 expression as well as interact with ET/JA pathways (not always in inhibitory way).
An honest answer to this question would be: We don't know.
Maybe, we identify one or the other WRKY or MAPK-signaling in the context of pathogenicity or biotic interaction, but we also see that there are many WRKYs doing other, very basal things on gene expression.
I think, we still miss a lot on the mechanistics side.
In addition, we should not forget about the following:
1) We have recently shown that the binding motif for WRKYs is rather small and that DNA-shape readout is a probable mechanism (Brand et al. Nucl. Acids Res. 2013).
So, how does a WRKY identify its target gene with specificity then, if the binding motif is very short? - This probably requires many more than only a WRKY
2) Turck et al., Plant Cell 2004 already showed that WRKY proteins are bound to their target promotors already BEFORE a biotic signal was applied.
So, where does the specificity of a biotic response come from? - Again, probably other factors are required
3) Several WRKY factors have been linked with development and patterning.
So, what makes them different from those who apparently seem to function in stress responses? As there are not so many differences on sequence level, we must asume different mechanistics that make a different
4) The AtGenExpress data revealed that many of the WRKY genes are expressed in overlapping expression domains - irrespective of a given signal.
Again, where and who is involved in the targeting to achieve specificity in gene expression? - Other factors must be involved, that we do not know at the moment.
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