Signaling networks have a crucial role in every aspect of plant communication with the environment. There is significant interest in identifying signal transduction pathways governing CW homeostasis in interactions with pathogens and symbionts. In previous work, our lab has demonstrated that the RAF-like Integrin-Linked Kinase 1 (ILK1) is a negative regulator of FLS2 (Flagellin Sensing2)-mediated signaling, required for defense against a low-virulence P. syringae T3SS-mutant, and modulating cellular ion homeostasis through functional interactions with Ca2+ sensor CML9 and HAK5 K+ transporter (Brauer et al., 2016). In this work we revealed that ILK1 homologs, ILK4 and ILK5, are required for plant response to PAMPs (elf18) and plant damage-associated molecules (pep1) but not flg22. Specifically, we found that ilk4 and ilk5 were unable to undergo priming for Pattern-Triggered Immunity (PTI) with elf18 and pep1 and showed increased susceptibility to virulent P.syringae pv.tomato DC3000. A global transcriptomic analysis revealed the role of ILK1 in modulating the temporal dynamics and range of Arabidopsis transcriptional re-programming postlg22 treatment. In the absence of the PAMP challenge, ilk1-1 showed derepression of a sector of PTI, osmotic and ionic stress, and iron starvation transcriptional programs. Postlg22 challenge, genes for innate immunity, microtubule (MT) structure and movement, CW biosynthesis, and plant growth were differentially regulated in ilk1-1 compared to wt. Phenotyping of ilk1-1 alongside ilk4, ilk5, and OE-ILK5 mutant lines revealed significant de-regulation of induction of defense genes, upregulation of auxin (SAURs) genes, and repression of tubulins and MT-motor protein genes. Moreover, the mutants showed abnormal insensitivity to MT-depolymerizing treatments and defective root growth and displayed CW-specific defects (i.e., ectopic lignin accumulation in the xylem and defects in the pectin-rich seed mucilage). We postulate that ILKs are components of a CW-integrity signaling pathway that suppresses PTI and facilitates CW biosynthesis during normal growth, whereas post-pathogen challenge this pathway is required for defensive re-modeling of the CW and MT cytoskeleton and resumption of plant growth.
| Identifer | oai:union.ndltd.org:MSSTATE/oai:scholarsjunction.msstate.edu:td-3768 |
| Date | 07 August 2020 |
| Creators | Dimlioglu, Gizem |
| Publisher | Scholars Junction |
| Source Sets | Mississippi State University |
| Detected Language | English |
| Type | text |
| Format | application/pdf |
| Source | Theses and Dissertations |
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