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Abstract
背景回顾：Drought is a major environmental stress threatening plant growth and productivity. Calcium-dependent protein kinases (CPKs) are plant-specific Ca2+ sensors with multifaceted roles in signaling drought responses.
提出问题：Nonetheless, the mechanisms underpinning how CPKs transmit downstream drought signaling remain unresolved. Through genetic investigations,
结果1-CPK27正调控耐旱性：our study unveiled that knocking out CPK27 reduces drought tolerance in tomato (Solanum lycopersicum) plants and impairs abscisic acid (ABA)-orchestrated plant response to drought stress.
结果2-CPK27磷酸化的蛋白与糖代谢有关：Proteomics and phosphoproteomics revealed that CPK27-dependent drought-induced proteins were highly associated with the sugar metabolism pathway, which was further verified by reduced soluble sugar content in the cpk27 mutant under drought conditions.
结果3-CPK27互作蛋白TST2：Using protein-protein interaction assays and phosphorylation assessments, we demonstrated that CPK27 directly interacts with and phosphorylates Tonoplast Sugar Transporter 2 (TST2), promoting intercellular soluble sugar accumulation during drought stress. Furthermore, Ca2+ and ABA enhanced CPK27-mediated interaction and phosphorylation of TST2, thus revealing a role of TST2 in tomato plant drought tolerance.
摘 要
干旱是个威胁植物生长和产量的一个主要环境胁迫因子。钙调蛋白依赖性蛋白激酶（CPKs）是植物特有的钙离子感受器，其在干旱胁迫响应的信号转导中发挥重要作用。然而，有关CPKs如何将干旱信号往下游转导还不清楚。本文中，作者通过遗传学研究发现敲除CPK27基因会导致番茄植株的干旱耐受性降低，并且脱落酸（ABA）介导的植物干旱响应出现缺陷。蛋白组学和蛋白磷酸化组显示，依赖于CPK27的干旱诱导蛋白显著富集在糖代谢途径，干旱条件下cpk27突变体的可溶性糖含量测定也符合这一结果。利用蛋白互作分析和磷酸化测定，作者发现CPK27能够与糖转运蛋白TST2互作并磷酸化TST2，从而促进干旱胁迫下细胞间的可溶性糖积累。此外，钙离子和ABA能够增强CPK27介导的TST2互作和磷酸化，从而揭示了TST2在番茄植株干旱耐受性中的作用。本文的研究结果拓展了植物干旱抗性改良的可用基因资源，即可通过操纵CPK27介导的可溶性糖积累来提高植物的耐旱性，从而以应对多变的气候环境。
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个人简介：
2008-2012年，浙江大学，学士；
2012-2018年, 浙江大学，博士；
2018-2020年，浙江大学，博士后；
2021-2023年，浙江大学，助理研究员；
2024年-至今，浙江大学，副研究员。
研究方向：设施蔬菜环境逆境机制解析。
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