Zhou Sa, Luo Qiuling, Nie Zhiyan, Wang Changhui, Zhu Wenkang, Hong Yingxiang, Zhao Jun, Pei Baolei, Ma Wenjian
Key Laboratory of Industrial Fermentation Microbiology of the Ministry of Education, College of Biotechnology, Tianjin University of Science and Technology, Tianjin 300457, China.
State Key Laboratory of Plant Physiology and Biochemistry, College of Biological Sciences, China Agricultural University, Beijing 100193, China.
Plants (Basel). 2023 Mar 12;12(6):1285. doi: 10.3390/plants12061285.
The pivotal role of cysteine-rich receptor-like kinases (CRKs) in modulating growth, development, and responses to stress has been widely acknowledged in . However, the function and regulation of has remained unclear. In this study, we demonstrate that is critical for modulating microtubule depolymerization in response to salt stress. The mutant exhibited increased tolerance, while overexpression of led to hypersensitivity to salt. Further analysis revealed that CRK41 interacts directly with the MAP kinase3 (MPK3), but not with MPK6. Inactivation of either MPK3 or MPK6 could abrogate the salt tolerance of the mutant. Upon NaCl treatment, microtubule depolymerization was heightened in the mutant, yet alleviated in the and double mutants, indicating that suppresses MAPK-mediated microtubule depolymerizations. Collectively, these results reveal that plays a crucial role in regulating microtubule depolymerization triggered by salt stress through coordination with MPK3/MPK6 signalling pathways, which are key factors in maintaining microtubule stability and conferring salt stress resistance in plants.
富含半胱氨酸的类受体激酶(CRKs)在调节生长、发育以及对胁迫的响应中所起的关键作用已在[具体领域]中得到广泛认可。然而,[具体内容]的功能和调控仍不清楚。在本研究中,我们证明[具体内容]对于响应盐胁迫调节微管解聚至关重要。[具体内容]突变体表现出耐受性增强,而[具体内容]的过表达导致对盐超敏。进一步分析表明,CRK41直接与促分裂原活化蛋白激酶3(MPK3)相互作用,但不与MPK6相互作用。MPK3或MPK6的失活均可消除[具体内容]突变体的耐盐性。在NaCl处理后,[具体内容]突变体中的微管解聚加剧,但在[具体内容]和[具体内容]双突变体中减轻,表明[具体内容]抑制MAPK介导的微管解聚。总体而言,这些结果表明,[具体内容]通过与MPK3/MPK6信号通路协调,在调节盐胁迫引发的微管解聚中起关键作用,而MPK3/MPK6信号通路是维持微管稳定性和赋予植物耐盐性的关键因素。