The plasticity of stem cells in response to environmental change is critical for multicellular organisms. Here, we show that MYB3R-like directly activates the key plant stem-cell regulator WUSCHEL (WUS) by recruiting the methyltransferase ROOT INITIATION DEFECTIVE 2 (RID2), which functions in m7G methylation of the 5′ cap of WUS mRNA to protect it from degradation. Transcriptomic and molecular analyses showed that protein-folding genes are repressed by WUS to maintain precise protein synthesis in stem cells by preventing the reuse of misfolded proteins. Interestingly, we found that upon heat stress, the MYB3R-like/RID2 module is repressed to reduce WUS transcript abundance through decapping of nascent WUS mRNA. This releases the inhibition of protein-folding capacity in stem cells and protects them from heat shock by eliminating misfolded protein aggregation. Taken together, our results reveal a strategic trade-off whereby plants reduce the accuracy of protein synthesis in exchange for the survival of stem cells at high temperatures.

中文翻译：

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热应激诱导的 WUSCHEL mRNA 加帽增强了拟南芥中干细胞的耐热性


干细胞响应环境变化的可塑性对于多细胞生物至关重要。在这里，我们表明 MYB3R 样通过募集甲基转移酶 ROOT INITIATION DEFECTIVE 2 （RID2） 直接激活关键的植物干细胞调节因子 WUSCHEL （WUS），该酶在 WUS mRNA 的 5' 帽的 m7G 甲基化中发挥作用，以保护其免受降解。转录组学和分子分析表明，蛋白质折叠基因被 WUS 抑制，通过防止错误折叠蛋白质的再利用来维持干细胞中精确的蛋白质合成。有趣的是，我们发现在热应激下，MYB3R 样/RID2 模块被抑制，通过脱帽新生的 WUS mRNA 来减少 WUS 转录本的丰度。这释放了干细胞中蛋白质折叠能力的抑制，并通过消除错误折叠的蛋白质聚集来保护它们免受热休克。综上所述，我们的结果揭示了一种战略权衡，即植物降低蛋白质合成的准确性以换取干细胞在高温下的存活。