| Plants are constantly challenged by pathogens. Studies from several plant-pathosystems indicate that manipulation of host cell fate might be a common strategy that pathogens use to succeed in their attacks. Genetic perturbation of the key defense signaling mediated by salicylic acid (SA) is also known to lead to altered cell fate in some Arabidopsis mutants. One of such mutants is accelerated cell death 6 (acd6-1), which demonstrates aberrant cell death coupled with cell growth, constitutive defense, and extreme dwarf phenotypes. However, the mechanism by which cell fate is determined during pathogen infection and in some defense mutants has not been well understood.;I hypothesize that precise regulation of cell fate is intimately linked to plant disease resistance. I tested this hypothesis during my PhD research. I have found that: 1) There are dynamic, quantitative, and qualitative differences in the accumulation of the defense signaling molecule salicylic acid, expression of the defense marker gene PR1, cell death formation, and H2O 2 accumulation during Arabidopsis-P. syringae interactions. The differences between PTI, ETS, and ETI are dosage and strains dependent. Interestingly later during the infection, P. syringae induces the formation of tumor-like growths on the back of the leaves. The HrcC- strain lacking TTSS induced more large cells in comparison to the virulent DG3 and the avirulent DG34 strains. The enlarged cells have increased DNA content, suggesting a possible activation of endoreduplication. I also found that treating Col-0 plants with the PTI elicitor flg22 activates the formation of the abnormal cell growth. These data suggest that PTI plays a major role in regulating cell growth. Additionally SA is necessary but not sufficient to induce this phenotype. 2) The SIM and SMR1 genes contribute synergistically to regulate cell ploidy in both leaf cells and trichomes. Additionally I found that the cell cycle regulators, SMR1 and CYCD genes, are involved in plant basal defense responses against P. syringae by acting upstream of SA. Furthermore cell ploidy analysis by flow cytometry with SA mutants and plants treated with an SA activator revealed that SA signaling is necessary but not sufficient to alter cell cycle progression. 3) Arabidopsis-conferred Ewa resistance requires SA signaling but not ET and JA signaling. On the other hand, Ewa-induced callose deposition is independent of SA, ET, and JA pathways but requires a functional callose synthase PMR4. Furthermore callose deposition is required for Ewa resistance. Finally I found that Ewa induces tumor-like growths in Arabidopsis, which contain enlarged cells with increased nuclear content. Deletion of Ewa effectors reduces significantly Ewa virulence in Col-0, but it did not affect the formation of the abnormal growths in Arabidopsis.;In summary, my work strongly supports the importance of cell fate control in plant innate immunity and reveals potential novel defense genes that play a role in cell fate control. Information from this study advances our understanding of plant defense mechanisms, and ultimately facilitates the development of better strategies to improve disease resistance in economically important crop plants. |
