Arabidopsis (Arabidopsis thaliana) PROTEIN ARGININE METHYLTRANSFERASE5 (PRMT5) post-translationally modifies RNA-binding proteins by arginine (R) methylation. However, the impact of this modification on the regulation of RNA processing is largely unknown. We used the spliceosome component, SM-LIKE PROTEIN 4 (LSM4), as a paradigm to study the role of R-methylation in RNA processing. We found that LSM4 regulates alternative splicing (AS) of a suite of its in vivo targets identified here. The lsm4 and prmt5 mutants show a considerable overlap of genes with altered AS raising the possibility that splicing of those genes could be regulated by PRMT5-dependent LSM4 methylation. Indeed, LSM4 methylation impacts AS, particularly of genes linked with stress response. Wild-type LSM4 and an unmethylable version complement the lsm4-1 mutant, suggesting that methylation is not critical for growth in normal environments. However, LSM4 methylation increases with abscisic acid and is necessary for plants to grow under abiotic stress. Conversely, bacterial infection reduces LSM4 methylation, and plants that express unmethylable-LSM4 are more resistant to Pseudomonas than those expressing wild-type LSM4. This tolerance correlates with decreased intron retention of immune-response genes upon infection. Taken together, this provides direct evidence that R-methylation adjusts LSM4 function on pre-mRNA splicing in an antagonistic manner in response to biotic and abiotic stress.

中文翻译：

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SM 样蛋白 4 的精氨酸甲基化拮抗地影响拟南芥应激反应期间的选择性剪接

拟南芥 (Arabidopsis thaliana) 蛋白精氨酸甲基转移酶 5 (PRMT5) 通过精氨酸 (R) 甲基化进行翻译后修饰 RNA 结合蛋白。然而，这种修饰对 RNA 加工调节的影响尚不清楚。我们使用剪接体成分 SM 样蛋白 4 (LSM4) 作为范例来研究 R 甲基化在 RNA 加工中的作用。我们发现 LSM4 调节此处确定的一组体内靶标的选择性剪接 (AS)。 lsm4 和 prmt5 突变体显示出具有改变的 AS 的基因相当大的重叠，这提高了这些基因的剪接可能受到 PRMT5 依赖性 LSM4 甲基化调节的可能性。事实上，LSM4 甲基化会影响 AS，尤其是与应激反应相关的基因。野生型 LSM4 和不可甲基化版本与 lsm4-1 突变体互补，表明甲基化对于正常环境中的生长并不重要。然而，LSM4 甲基化随着脱落酸的增加而增加，并且是植物在非生物胁迫下生长所必需的。相反，细菌感染会降低LSM4甲基化，表达不可甲基化LSM4的植物比表达野生型LSM4的植物对假单胞菌具有更强的抵抗力。这种耐受性与感染后免疫反应基因的内含子保留减少相关。总而言之，这提供了直接证据，表明 R-甲基化以拮抗方式调整前 mRNA 剪接上的 LSM4 功能，以响应生物和非生物胁迫。