Plants are sessile organisms and constantly encounter a myriad of pathogens;
therefore, they rely on highly effective defense system for their survival. Our
understanding of how plant immunity is triggered and regulated has seen
tremendous progress over the last two decades, with many important players
identified in the model systems, Arabidopsis thaliana. Mitogen activated protein
kinases play a central role in signal transduction in biotic and abiotic stresses.
MAPK pathways are regulated by three-interlinked protein kinases (MAPKKK,
MAPKK, MAPK), which are sequentially activated by phosphorylation. The
activation of the three MAPKs MPK3, MPK4 and MPK6 is one of the earliest
cellular responses following pathogen attack leading to the phosphorylation of
appropriate cytosolic or nuclear targets to regulate cellular processes. However,
only few targets of MPK3, MPK4 and MPK6 have been identified and validated
so far and many MAPK substrates remain to be discovered. We performed largescale
phosphoproteomics on mock treated and flg22 treated WT and the three
loss-of-function mutants mpk3, mpk4 and mpk6 to identify novel MAPKs
substrates and their cellular functions in response to pathogen attack. We identify
and validated some of the differentially phosphorylated cytosolic and chromatin
targets of MPK3, MPK4 and MPK6.
DEK2, a nuclear protein involved in multiple chromatin-related processes, was
identified in the phosphoproteomics screen as an in vivo target of MPK6 and it
interacts in planta and is phosphorylated in vitro by the three immune MAPKs.
dek2 loss-of-function mutants were susceptible to bacterial as well as fungal
pathogens. Additionally, transcriptome data of the dek2-1 mutant show that
DEK2 is a transcriptional repressor inclusive of defense related genes and
hormone synthesis and signaling genes. We determined that DEK2 is a reader of
the histone mark, H3K9me1, by Microscale thermophoresis. From ChIP-Seq
analysis, DEK2 was found to be enriched at class I TCP binding motif regions.
We further need to determine whether DEK2 binds to TCP transcription factors
directly or indirectly. Finally, based on our data we postulate a hypothetical
working model for the function of DEK2 as a transcriptional repressor and a
reader of H3K9me1 mark.
|Date of Award||Apr 2019|
|Original language||English (US)|
- Biological, Environmental Science and Engineering
|Supervisor||Heribert Hirt (Supervisor)|
- MAPK Signaling