Department of Horticulture and Crop Science, The Ohio State University, Columbus, OH 43210.
Department of Molecular Genetics, The Ohio State University, Columbus, OH 43210.
Proc Natl Acad Sci U S A. 2020 Dec 1;117(48):30805-30815. doi: 10.1073/pnas.2016049117. Epub 2020 Nov 16.
Transcriptional regulation is a complex and pivotal process in living cells. HOS15 is a transcriptional corepressor. Although transcriptional repressors generally have been associated with inactive genes, increasing evidence indicates that, through poorly understood mechanisms, transcriptional corepressors also associate with actively transcribed genes. Here, we show that HOS15 is the substrate receptor for an SCF/CUL1 E3 ubiquitin ligase complex (SCF) that negatively regulates plant immunity by destabilizing transcriptional activation complexes containing NPR1 and associated transcriptional activators. In unchallenged conditions, HOS15 continuously eliminates NPR1 to prevent inappropriate defense gene expression. Upon defense activation, HOS15 preferentially associates with phosphorylated NPR1 to stimulate rapid degradation of transcriptionally active NPR1 and thus limit the extent of defense gene expression. Our findings indicate that HOS15-mediated ubiquitination and elimination of NPR1 produce effects contrary to those of CUL3-containing ubiquitin ligase that coactivate defense gene expression. Thus, HOS15 plays a key role in the dynamic regulation of pre- and postactivation host defense.
转录调控是活细胞中一个复杂而关键的过程。HOS15 是一个转录共抑制因子。尽管转录抑制剂通常与非活性基因相关联,但越来越多的证据表明,通过尚未完全了解的机制,转录共抑制因子也与转录活跃的基因相关联。在这里,我们表明 HOS15 是一个 SCF/CUL1 E3 泛素连接酶复合物(SCF)的底物受体,该复合物通过使包含 NPR1 和相关转录激活因子的转录激活复合物不稳定,从而负调控植物免疫。在未受挑战的条件下,HOS15 持续消除 NPR1 以防止防御基因的不当表达。在防御激活时,HOS15 优先与磷酸化的 NPR1 结合,从而刺激转录活性的 NPR1 的快速降解,从而限制防御基因表达的程度。我们的研究结果表明,HOS15 介导的 NPR1 的泛素化和消除产生了与包含 CUL3 的泛素连接酶相反的效果,后者共同激活防御基因的表达。因此,HOS15 在宿主防御的预激活和激活后的动态调控中发挥着关键作用。