时间：2022年7月1日（星期五）8:30-10:30
会议号：腾讯会议955 445 618
主办：www.bob.com、湖北洪山实验室、动物育种与健康养殖前沿科学中心
承办：动物科学技术学院、动物医学院
报告人1：张磊（8:30-9:30）
题目:结核杆菌的铁摄取机制：铁载体分泌是一个致命弱点
Iron acquisition by Mycobacterium tuberculosis: siderophore secretion is an Achilles’ heel
摘要：结核杆菌是人畜共患传染病结核病的病原体。铁元素对于结核杆菌在宿主体内存活是必需的。我们通过转座子插入测序技术，鉴定出结核杆菌中160多个基因参与铁的利用。我们发现结核杆菌在利用铁载体和血红素这两种铁源时展现出了几乎截然相反的遗传需求，还发现结核杆菌的VII型分泌系统ESX-3在铁采集的过程中扮演了核心角色。进一步地，我们发现Rv0455c蛋白对结核杆菌的铁载体分泌和致病性是必需的。该蛋白的缺失导致结核杆菌分泌铁载体严重受阻，细菌毒力衰减，同时对多种抗结核药物极为易感。这项研究验证了结核杆菌的铁载体分泌途径可以作为一种新的药物靶标。
Mycobacterium tuberculosis (Mtb) is the causative agent of tuberculosis, a zoonotic infectious disease. Iron is essential for the survival of Mtb in the host. We identified more than 160 genes involved in iron utilization in Mtb via transposon insertion sequencing (TnSeq). We found that Mtb exhibited nearly opposite genetic requirements in utilizing iron from siderophore and heme, and that ESX-3, the type VII secretion system of Mtb, played a central role in iron acquisition. Further, we found that Rv0455c protein is required for siderophore secretion and pathogenicity of Mtb. The loss of rv0455c results in a severe defect on siderophore secretion by Mtb, attenuation of bacterial virulence, and high susceptibility to a variety of anti-tuberculosis drugs. This study validated the siderophore secretion pathway of Mtb as a novel drug target.
报告人2：严国楷（9:30-10:30）
题目：mTORC1感应营养物质的分子机制
Molecular mechanism of how mTORC1 senses nutrients
摘要： mTORC1通路是细胞协调营养物质信号及调节生长代谢的中心之一。营养物质尤其是氨基酸通过感受体蛋白将其含量信号经过一系列的信号转导过程传递至溶酶体表面，进而调控mTORC1的活化。揭示营养物质的信号转导过程，能为我们理解mTORC1感应营养物质的分子机制提供理论基础，同时也能为后续以mTORC1活性异常相关的疾病-如癌症和老化-的药物开发提供候选靶点。
The mechanistic target of rapamycin complex 1 (mTORC1) is an essential hub that integrates nutrient signals and coordinates metabolism to control cell growth. Nutrients, especially amino acids, are signaled by sensor proteins and relayed to a series of signal transduction nodes to control lysosomal localization of mTORC1. Dissection of the process of signal transduction will provide a basis for understanding the molecular mechanisms of how mTORC1 senses nutrients, and will highlight potential clinical targets for dealing with mTORC1-related diseases, such as cancer and aging.