时 间:2023年10月11日 (星期三) 12:30-13:30
地 点:农生学院创新楼(B楼)104会议室
主办单位:农生学院学科与科技办、农生学院青年教师联谊会
报告题目:植物高渗胁迫早期信号转导机制的研究
报告摘要:
干旱是农作物减产最主要的环境因素。干旱胁迫的本质是由于缺水导致植物细胞的高渗透胁迫。基于植物生理、生化等的研究发现响应高渗透胁迫,植物细胞会产生瞬时、特异的钙震荡,并迅速激活SnRK2家族蛋白激酶。根据这些现象,研究组开展了相关研究,包括植物细胞调节特异性钙信号的分子机制,SnRK2家族蛋白激酶的活性调控方式。本期学术沙龙将介绍如何开展这些研究及目前团队对渗透胁迫早期的信号网络的理解。
报告人简介:
【所在学科研究组研究方向】:
1 植物感受盐、渗透胁迫的信号调控网络。
2 植物根向水性生长的分子机制。
3 脱落酸信号转导途径及其在叶绿体发育和叶片衰老过程中的调节作用。
【代表性著作】:
1. Fan, W., Liao, X.L., Tan, Y.Q., Wang, X.R., Schroeder, J.I., Li, Z.* Arabidopsis PLANT U-BOX44 down-regulates osmotic stress signaling by mediating Ca2+-DEPENDENT PROTEIN KINASE4 degradation. Plant Cell. (2023). doi: 10.1093/plcell/koad173.
2. Li, Z., Takahashi, Y., Scavo, A., Brandt, B., Nguyen, D., Schroeder, J.I. Abscisic acid-induced degradation of guanine nucleotide exchange factor requires calcium-dependent protein kinases. PNAS. (2018). https:// doi.org/10.1073/pnas.1719659115. (F1000 Recommended).
3. Hauser, F., Li, Z., Waadt, R., Schroeder, J.I. SnapShot: Abscisic Acid Signaling. Cell. 171(7):1708-1708.e0. doi: 10.1016/j.cell.2017.11.045. (2017)
4. Li, Z., Waadt, R. & Schroeder, J. I. Release of GTP Exchange Factor Mediated Down-Regulation of Abscisic Acid Signal Transduction through ABA-Induced Rapid Degradation of RopGEFs. PLoS Biol 14, e1002461, doi:10.1371/journal.pbio.1002461 (2016).
ACADEMIC SALON (XLII)
SPEAKER: Zixing Li
Associate Professor, Department of Plant Science, SAB
TIME :12:30-13:30 October 11th, 2023 (Wed)
VENUE:Room 104, Building B, SAB
ORGANIZER:Office of Discipline and Science & Technology, SAB;
Young Teachers Association, SAB
TITLE: Studies on early signaling events in the plant hyperosmotic stress
ABSTRACT:
Drought is the largest contributor to world-wide crop yield losses. Drought stress, by nature results from hyperosmotic stress to plant cell produced by water deficiency. Different from the small molecule recognition by ligand-receptor binding like phytohormone auxin, ABA etc, the molecular mechanisms by which plant cells sense hyperosmotic stress still remain elusive. Physiological observation and biochemical assays demonstrated that hyperosmotic stress elicits transient and rapid cytosolic calcium oscillation, and activates SnRK2 family protein kinases. Based on these physiological effects, we set out to investigate the mechanisms of specific calcium signals induced by hyperosmotic stress and also explore the regulatory mechanisms for controlling the kinase activities of SnRK2 family protein kinases. We will present our research procedures, conclusions and discuss the current progress on early osmotic stress signaling.
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