拟南芥PUB30介导的HB24泛素化降解途径参与盐胁迫诱导的根生长调控的机制研究

植物在应对逆境胁迫时往往会采用“sacrifice-for-survival”策略，通过适度地抑制生长来合理分配能量，有效地平衡生长发育和抵御逆境的需求，以便更好的生存。然而相关的信号转导和分子调控机制却鲜有报道。申请人前期研究发现一个功能未知的转录因子HB24是盐诱导的主根生长抑制途径中的重要负调控因子，并且盐胁迫诱导的HB24蛋白降解对于植株的生存至关重要。初步研究还发现HB24能与E3泛素连接酶PUB30结合。在此基础上，本研究拟深入解析HB24参与盐胁迫下主根生长调控的作用机制，并阐释植物响应盐胁迫，通过PUB30介导的泛素-26S蛋白酶体途径降解HB24，从而适度抑制生长以利于植株生存的分子机制。本研究拟揭示植物响应盐胁迫，通过泛素-蛋白酶体降解途径对关键转录因子蛋白稳定性的调控，施行适度抑制生长以利生存的策略，在植物响应逆境、蛋白稳定性调控等研究领域具有重要的科学理论意义。

In response to stresses, a trade-off between plant growth and stress tolerance is required for plants to survive and accomplish the reproduction. However, the regulatory mechanisms underlying this “sacrifice-for-survival” strategy is largely unknown. Previous studies reveal a root growth inhibition induced by salt stress, however, the physiological function and key regulators of this process need to be further illustrated. Our preliminary research demonstrated that HB24, a member of ZF-HD transcription factor subfamily in Arabidopsis, acted as a key transcription factor and negatively regulated the salt-induced root-growth-inhibition. Loss function of HB24 led to shorter roots under 125 mM NaCl treatment, whereas a better survival of seedlings under 200 mM NaCl. We also found that salt stress triggered the degradation of HB24, likely through the ubiquitin-proteasome system. Moreover, we identified a U-box type E3 ubiquitin ligase PUB30 that directly interacted with HB24. In this study, we will investigate how does HB24 negatively regulate the salt-induced root growth inhibition. Furthermore, we will also demonstrate that in response to salt stress, PUB30-involved ubquintin-proteasome system mediates the salt-induced HB24 degradation for plants to adopt “sacrifice-for-survival” strategy. Our study will provide new insight in the regulatory mechanisms of plant tolerance to salt stress, and is helpful for better understanding the “sacrifice-for-survival” strategy for trade-off between plant growth and stress tolerance.