Chromatine Modification Related Genes HUB1and CHR5and Transcription Factor Myb44Regulate Immunity Responses In Arabidopsis

Due to their sessile lifestyle, plants are in constant conflict with pathogens throughout their life cycles. In order to fend off a wide range of microbial pathogen attacks, plants have developed sophisticated immunity system to defend themselves. Plant immunity responses against pathogen infection largely depend on the plant’s capacity to reprogram rapidly and specifically the transcription of a large number of the host genes. In a pathogen stress type-dependent manner, external signals are trans-located into the nucleus to activate transcription factors, resulting in the increased expression of particular sets of defense-related genes. Among mechanisms of transcriptional regulation, transcription factors and chromatin modification accomplished through the activity of histone-modifying enzymes and ATP dependent chromatin-remodeling complexes are emerging as two key processes in the orchestration of plant immunity responses.1. Regulation of disease resistance gene expression by H2B monoubiquitination in ArabidopsisRegulation of disease resistance (R) genes is one key event in plant immunity response. Here we show that two Arabidopsis E3ubiquitin ligase genes HUB1(HISTONE MONOUBIQUITINATION1) and HUB2are involved in the regulation of the R gene SNC1(SUPPRESSOR OFnpr1-1, CONSTITUTIVE1) in the autoimmune mutant bon1. The SNC1gene is up-regulated in bon1and the SNC1locus has a higher monoubiquitination of H2B. The loss of HUB1or HUB2function largely suppresses the autoimmune phenotypes in bon1. Thus the up-expression of SNC1in bon1is dependent on H2B modification at the SNC1locus. Furthermore, the expression of SNC1and HUB1are moderately up-regulated by pathogen infection and H2B monoubiquitination at SNC1is enhanced by pathogen infection. Together, this study indicates that H2B monoubiquitination is critical for R gene up-regulation in autoimmune mutants and it might also contribute to R gene regulation during immune responses.2. Characterize and function studies of one plant helicase-like domain (CHD) chromatin remodeling factor chromatin remodeling5(CHR5) in Arabidopsis innate immunityATP-dependent chromatin remodeling complexes use the energy of ATP hydrolysis to alter the structure of chromatin, which is an important mechanism in the regulation of eukaryotic gene expression. In this study, we characterized the function of chromatin remodeling5(CHR5), a member of plant helicase-like domain(CHD) chromatin remodeling factor, in Arabidopsis innate immunity. We found that knock out CHR5gene can largely suppress the autoimmunity in bon1-1by a genetic screen of the potential suppressor of the autoimmunity mutant bon1-1.The constitutively expression of the SNC1and PR1gene and the accumulation of SA in bon1-1were all largely suppressed by CHR5mutation. And the constitutively pathogen resistance in bon1-1was also disappeared in the chr5bon1-1double mutants.While chr5single mutants exhibit defects in basal resistance against the bacterial pathogen P. syringae pv.maculicola ES4326(Psm E4326). Furthermore, we approved that CHR5may regulate the expression of SNC1in a locus specific manner. After RNAseq data analysis, we found that the expression many important defense response genes were significantly changed in chr5mutants. Our study indicates that CHR5is a negative regulator of plant immunity and may regulate gene expression at chromatin level.3. AtMYB44positively modulates disease resistance to Pseudomonas syringae through the salicylic acid signalling pathway in ArabidopsisAtMYB44which belongs to sub-group22of the R2R3MYB transcription factor family is one well known stress response related gene. Here, we found that the expression of AtMYB44is sensitive to the phytophormone salicylic acid (SA) treatment and the hemibiotrophic pathogen Pseudomonas syringae pv. tomato DC3000(Pst DC3000) infection. And the induction expression of AtMYB44by Pst DC3000requires both the SA accumulation and the NPR1gene. AtMYB44over-expression up-regulated PR genes induction expression and ROS accumulation by Pst DC3000, leading to enhanced resistance to the Pst DC3000. While the knockout mutant atmyb44shows opposite effects. Induction of PR1by Pst DC3000is reduced in atmyb44mutants. AtMYB44over-expression phenotypes, such as retarded growth, up-regelated PR1and resistance to Pst DC3000are reversed by SA depletion and NPR1mutation. Thus, AtMYB44positive regulates Arabidopsis defense response against Pst DC3000through SA signaling pathway.