Huang Chien-Yu, Rangel Diana Sánchez, Qin Xiaobo, Bui Christine, Li Ruidong, Jia Zhenyu, Cui Xinping, Jin Hailing
Department of Microbiology & Plant Pathology, Institute for Integrative Genome Biology, University of California, Riverside, CA 92521-0122, USA.
Department of Microbiology & Plant Pathology, Institute for Integrative Genome Biology, University of California, Riverside, CA 92521-0122, USA; Cátedra CONACyT en la red de Estudios Moleculares Avanzados del Instituto de Ecología A.C. (INECOL), Carretera antigua a Coatepec 351, El Haya, Xalapa, Veracruz 91070, México.
Cell Host Microbe. 2021 Mar 10;29(3):425-434.e4. doi: 10.1016/j.chom.2021.01.005. Epub 2021 Feb 5.
In both plant and animal innate immune responses, surveillance of pathogen infection is mediated by membrane-associated receptors and intracellular nucleotide-binding domain and leucine-rich-repeat receptors (NLRs). Homeostasis of NLRs is under tight multilayered regulation to avoid over-accumulation or over-activation, which often leads to autoimmune responses that have detrimental effects on growth and development. How NLRs are regulated epigenetically at the chromatin level remains unclear. Here, we report that SWP73A, an ortholog of the mammalian switch/sucrose nonfermentable (SWI/SNF) chromatin-remodeling protein BAF60, suppresses the expression of NLRs either directly by binding to the NLR promoters or indirectly by affecting the alternative splicing of some NLRs through the suppression of cell division cycle 5 (CDC5), a key regulator of RNA splicing. Upon infection, bacteria-induced small RNAs silence SWP73A to activate a group of NLRs and trigger robust immune responses. SWP73A may function as a H3K9me2 reader to enhance transcription suppression.
在植物和动物的固有免疫反应中，对病原体感染的监测是由膜相关受体以及细胞内核苷酸结合结构域和富含亮氨酸重复序列的受体（NLRs）介导的。NLRs的稳态受到严格的多层调控，以避免过度积累或过度激活，过度积累或激活通常会导致自身免疫反应，对生长和发育产生不利影响。NLRs在染色质水平上如何进行表观遗传调控仍不清楚。在此，我们报道，SWP73A是哺乳动物开关/蔗糖非发酵（SWI/SNF）染色质重塑蛋白BAF60的直系同源物，它通过与NLR启动子结合直接抑制NLRs的表达，或者通过抑制RNA剪接的关键调节因子细胞分裂周期5（CDC5）来影响一些NLRs的可变剪接，从而间接抑制NLRs的表达。受到感染时，细菌诱导的小RNA使SWP73A沉默，从而激活一组NLRs并触发强烈的免疫反应。SWP73A可能作为H3K9me2的读取器来增强转录抑制作用。
