Michael Smith Laboratories, University of British Columbia, Vancouver, BC V6T 1Z4, Canada.
Plant J. 2012 Jun;70(6):916-28. doi: 10.1111/j.1365-313X.2012.04906.x.
Plant resistance (R) proteins protect cells from infections through recognizing effector molecules produced by pathogens and initiating downstream defense cascades. To mount proper immune responses, the expression of R genes has to be tightly controlled transcriptionally and post-transcriptionally. Intriguingly, alternative splicing of the R genes of the nucleotide binding leucine-rich repeat (NB-LRR) type was observed in different plant species, but its regulatory mechanism remains elusive. Here, we report the positional cloning and functional analysis of modifier of snc1,12 (mos12-1), a partial loss-of-function mutant that can suppress the constitutive defense responses conferred by the gain-of-function R gene mutant suppressor of npr1-1 constitutive 1 (snc1). MOS12 encodes an arginine-rich protein that is homologous to human cyclin L. A null allele of mos12-2 is lethal, suggesting it has a vital role in plant growth and development. MOS12 localizes to the nucleus, and the mos12-1 mutation results in altered splicing patterns of SNC1 and RPS4, indicating that MOS12 is required for the proper splicing of target R genes. MOS12 co-immunoprecipitates with MOS4, indicating that MOS12 associates with the MOS4-associated complex (MAC). Accordingly, splicing patterns of SNC1 and RPS4 are changed in most MAC core mutants. Our study highlights the contribution of MOS12 and the MAC in the alternative splicing of R genes, providing regulatory details on how alternative splicing is used to fine-tune R gene expression in plant immunity.
植物抗性（R）蛋白通过识别病原体产生的效应分子并启动下游防御级联反应来保护细胞免受感染。为了产生适当的免疫反应，R 基因的表达必须在转录和转录后水平受到严格控制。有趣的是，核苷酸结合富含亮氨酸重复（NB-LRR）型 R 基因的可变剪接在不同植物物种中都有观察到，但它的调控机制仍不清楚。在这里，我们报道了 snc1,12（mos12-1）的位置克隆和功能分析，mos12-1 是一个部分功能丧失的突变体，可以抑制 gain-of-function R 基因突变体 suppressor of npr1-1 constitutive 1（snc1）赋予的组成型防御反应。MOS12 编码一种富含精氨酸的蛋白质，与人类细胞周期蛋白 L 同源。mos12-2 的 null 等位基因是致死的，这表明它在植物生长和发育中具有重要作用。MOS12 定位于细胞核，mos12-1 突变导致 SNC1 和 RPS4 的剪接模式发生改变，表明 MOS12 是靶 R 基因正确剪接所必需的。MOS12 与 MOS4 共免疫沉淀，表明 MOS12 与 MOS4 相关复合物（MAC）相关。因此，大多数 MAC 核心突变体中 SNC1 和 RPS4 的剪接模式都发生了改变。我们的研究强调了 MOS12 和 MAC 在 R 基因可变剪接中的作用，为如何利用可变剪接来精细调节植物免疫中 R 基因的表达提供了调控细节。
