Recognizing Plant Physiology author Guichen Li

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Guichen Li, first author of Mitochondrial Heat Shock Cognate Protein 70 Contributes to Auxin-mediated Embryo Development

Current Position: Ph.D. candidate, College of Life Sciences, Nankai University

Education: 2012/09-2016/07: Bachelor in College of Life Sciences, Lanzhou University; Since 2016/09: Master and Ph.D. in College of Life Sciences, Nankai University

Non-scientific interests: Badminton and cooking

Brief bio: I joined the College of Life Sciences, Nankai University in 2016 and studied for a master’s degree under the guidance of Professor Shuzhen Men. In 2019, I became a PhD student in Men Lab. During this period, we focused on the biological function of the mitochondrial heat shock protein mtHSC70 in Arabidopsis. Under the guidance of my advisor, we found that mtHSC70-1 deficiency leads to defective embryo development, and the embryo defect was associated with reduced or ectopic expression of auxin responsive reporter DR5rev:GFP. On the other hand, mitochondrial retrograde regulation (MRR) was enhanced in mthsc70-1, and treatment with an inhibitor which activates mitochondrial retrograde signaling reduced the expression level of auxin biosynthesis and polar auxin transport genes and induces similar phenotypes as that in the mthsc70-1b. Taken together, our data reveal that loss of function of mtHSC70-1 induces MRR, which inhibited auxin biosynthesis and polar auxin transport, leading to abnormal auxin gradients and defective embryo development. This finding shedding light on the underlying mechanism of mtHSC70 regulated reproductive development in Arabidopsis.

姓名：李桂忱

目前职位：南开大学生命科学学院在读博士研究生

教育背景：2012/09-2016/07 兰州大学，生命科学学院，学士

2016/09至今 南开大学，生命科学学院，硕士和博士

兴趣爱好：羽毛球和烹饪

个人简介：我于2016年加入南开大学生命科学学院，在门淑珍教授的指导下攻读硕士学位，2019年转为博士。在此期间主要研究拟南芥线粒体定位的热激蛋白mtHSC70的生物学功能。在导师的悉心指导下，我们发现mtHSC70-1缺失会导致胚胎发育缺陷，且胚胎的异常型态与生长素报告基因DR5rev:GFP的减少或异位表达有关，与此一致，在mthsc70-1中生长素的合成和极性运输基因的表达发生了明显的变化。另外，我们发现mtHSC70-1缺失后线粒体逆行信号调节会增强，并且用激活线粒体逆行信号的抑制剂处理会降低生长素合成和极性运输相关基因的表达，并诱导出与mthsc70-1b相似的表型。据此，我们认为mtHSC70-1的功能缺失会诱导线粒体逆行信号增强，从而抑制植物生长素的合成和极性运输，从而导致植物生长素梯度异常和胚胎发育缺陷。这一发现，为理解mtHSC70在植物生殖发育过程中的功能提供了新的线索