Xiao Fei, Li Xiaochuan, He Jiaxian, Zhao Jinfeng, Wu Guochun, Gong Qianyuan, Zhou Huapeng, Lin Honghui
Key Laboratory of Bio-Resource and Eco-Environment of Ministry of Education, College of Life Sciences, Sichuan University, Chengdu, 610064, People's Republic of China.
National Key Facility for Crop Gene Resources and Genetic Improvement, Institute of Crop Science, Chinese Academy of Agricultural Sciences, Beijing, 100081, China.
Plant Mol Biol. 2021 Apr;105(6):685-696. doi: 10.1007/s11103-021-01120-4. Epub 2021 Feb 4.
This work demonstrates that PpCIPK1, a putative protein kinase, participates in regulating plant salt tolerance in moss Physcomitrella patens. Calcineurin B-Like protein (CBL)-interacting protein kinases (CIPKs) have been reported to be involved in multiple signaling networks and function in plant growth and stress responses, however, their biological functions in non-seed plants have not been well characterized. In this study, we report that PpCIPK1, a putative protein kinase, participates in regulating plant salt tolerance in moss Physcomitrella patens (P. patens). Phylogenetic analysis revealed that PpCIPK1 shared high similarity with its homologs in higher plants. PpCIPK1 transcription level was induced upon salt stress in P. patens. Using homologous recombination, we constructed PpCIPK1 knockout mutant lines (PpCIPK1 KO). Salt sensitivity analysis showed that independent PpCIPK1 KO plants exhibited severe growth inhibition and developmental deficiency of gametophytes under salt stress condition compared to that of wild-type P. patens (WT). Consistently, ionic homeostasis was disrupted in plants due to PpCIPK1 deletion, and high level of HO was accumulated in PpCIPK1 KO than that in WT. Furthermore, PpCIPK1 functions in regulating photosynthetic activity in response to salt stress. Interestingly, we observed that PpCIPK1 could completely rescue the salt-sensitive phenotype of sos2-1 to WT level in Arabidopsis, indicating that AtSOS2 and PpCIPK1 are functionally conserved. In conclusion, our work provides evidence that PpCIPK1 participates in salt tolerance regulation in P. patens.
这项研究表明，假定的蛋白激酶PpCIPK1参与调控小立碗藓的植物耐盐性。据报道，类钙调神经磷酸酶B蛋白（CBL）互作蛋白激酶（CIPK）参与多个信号网络，并在植物生长和胁迫响应中发挥作用，然而，它们在非种子植物中的生物学功能尚未得到充分表征。在本研究中，我们报道了假定的蛋白激酶PpCIPK1参与调控小立碗藓（P. patens）的植物耐盐性。系统发育分析表明，PpCIPK1与其在高等植物中的同源物具有高度相似性。盐胁迫下，小立碗藓中PpCIPK1的转录水平被诱导。利用同源重组，我们构建了PpCIPK1基因敲除突变株系（PpCIPK1 KO）。盐敏感性分析表明，与野生型小立碗藓（WT）相比，独立的PpCIPK1 KO植株在盐胁迫条件下表现出严重的生长抑制和配子体发育缺陷。一致地，由于PpCIPK1缺失，植物中的离子稳态被破坏，PpCIPK1 KO中积累的H2O2水平高于WT。此外，PpCIPK1在响应盐胁迫时调节光合活性。有趣的是，我们观察到PpCIPK1可以将拟南芥中sos2-1的盐敏感表型完全恢复到WT水平，表明AtSOS2和PpCIPK1在功能上是保守的。总之，我们的研究提供了证据，证明PpCIPK1参与小立碗藓的耐盐性调控。
