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热胁迫诱导的WUSCHEL mRNA脱帽增强了拟南芥干细胞的耐热性。

Heat stress-induced decapping of WUSCHEL mRNA enhances stem cell thermotolerance in Arabidopsis.

作者信息

Liu Sumei, Wu Haijun, Zhao Zhong

机构信息

MOE Key Laboratory for Cellular Dynamics, Hefei National Research Center for Physical Sciences at the Microscale, The First Affiliated Hospital of University of Science and Technology of China, School of Life Sciences, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei 230027, China.

Ministry of Education Key Laboratory of Cell Activities and Stress Adaptations, Gansu Province Key Laboratory of Gene Editing for Breeding, School of Life Sciences, Lanzhou University, Lanzhou 730000, China.

出版信息

Mol Plant. 2024 Dec 2;17(12):1820-1832. doi: 10.1016/j.molp.2024.10.011. Epub 2024 Oct 28.

Abstract

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.

摘要

干细胞对环境变化作出反应的可塑性对多细胞生物至关重要。在此,我们表明,类MYB3R通过招募甲基转移酶ROOT INITIATION DEFECTIVE 2(RID2)直接激活关键的植物干细胞调节因子WUSCHEL(WUS),RID2在WUS mRNA的5'帽的m7G甲基化中发挥作用,以保护其不被降解。转录组学和分子分析表明,蛋白质折叠基因受到WUS的抑制,以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,在热胁迫下,类MYB3R/RID2模块受到抑制,通过新生WUS mRNA的脱帽来降低WUS转录本丰度。这解除了对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策略性权衡,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。

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