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SKLBE学术论坛

SKLBE学术论坛

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第540次SKLBE学术论坛

作者: 发布时间:2021-07-08 08:07:00

  目:线粒体rRNA甲基化修饰及线粒体基因表观遗传调控机理研究

报告人:中国科技大学教授、中国科学院院士施蕴渝

  间:2021-07-08(周四) 14:00-15:00

  逸夫楼演讲厅

540SKLBE学术论坛

  1Molecular delineation of EB1 code in mitosis

报告人:教育部长江学者、国家杰青获得者、国家基金委创新群体负责人、中国科技大学教授姚雪彪

  间:2021-07-08(周四) 15:00-16:00

  逸夫楼演讲厅

  2Adhesion molecules organize trans-synaptic nanocolumn and tune synaptic transmission

报告人:青千计划获得者、中国科技大学教授唐爱辉

  间:2021-7-8 (周四 16:00-17:0 0

  点:逸夫楼演讲厅

主持人:杨弋教授

施蕴渝简介:生物物理学与结构生物学家。1997年当选为中国科学院院士,博士生导师。2009年当选为发展中国家科学院院士。中国科学技术大学生命科学学院教授。1965年毕业于中国科学技术大学物理系生物物理专业。1965-1970年卫生部中医研究院实习研究员。1970-至今年中国科学技术大学助教,讲师,副教授,教授。合肥微尺度物质科学国家实验室(筹)研究员。1979-1981年意大利罗马大学化学系,CNRS结构化学实验室进修。曾作为访问学者在荷兰格罗宁根大学物理化学系,法国CNRS酶学与结构生物学实验室,法国理论化学实验室进修或合作研究。

报告摘要:Mitochondria are essential molecular machinery for the maintenance of cellular energy supply by the oxidative phosphorylation system (OXPHOS). Mitochondrial transcription factor B1 (TFB1M) is a dimethyltransferase that maintains mitochondrial homeostasis by catalyzing dimethylation of two adjacent adenines located in helix45 (h45) of 12S rRNA. This m62A modification is indispensable for the assembly and maturation of human mitochondrial ribosomes. However, both the mechanism of TFB1M catalysis and the precise function of TFB1M in mitochondrial homeostasis are unknown. Here we report the crystal structures of a ternary complex of human (hs) TFB1M–h45–S-adenosyl-methionine and a binary complex hsTFB1M–h45. The structures revealed a distinct mode of hsTFB1M interaction with its rRNA substrate andwith the initial enzymatic state involved in m62A modification. The suppression of hsTFB1M protein level or the overexpression of inactive hsTFB1M mutants resulted in decreased ATP production and reduced expression of components of the mitochondrial OXPHOS without affecting transcription of the corresponding genes and their localization to the mitochondria. Therefore, hsTFB1M regulated the translation of mitochondrial genes rather than their transcription via m6 2A modification in h45

姚雪彪简介:博士,国家自然科学基金委“杰出青年基金”获得者,国家自然科学基金委“着丝粒动态组装与调控”创新群体负责人,无膜细胞器与细胞动力学教育部重点实验室主任。主要从事细胞器动力学及细胞命运可塑性调控机制研究,其研究工作发表在CellNatureAnnual Reviews等顶级学术期刊,作为通讯作者在Cancer CellNat Rev Mol Cell Biol, Nat Chem Biol, GastroenterologyCell ResearchPNASNat CommunCancer Research等国际学术期刊发表论文100 余篇。

1995年美国加州大学伯克利分校获细胞分子生物学博士学位,1997年受聘为美国威斯康星州医学院生理系助理教授。1999年入选“国家自然科学杰出青年基金”、教育部“长江学者”,任中国科学技术大学教授,创建首个细胞动力学重点实验室。作为项目首席科学家主持了973 项目“调控细胞增殖重要蛋白质作用网络的研究”。作为项目首席科学家主持国家重点研发计划“着丝粒蛋白质机器调控细胞命运抉择的分子机制”。曾/并担任国际期刊J Biol ChemCell DiscoveryCell Research编委,J Mol Cell BiolBMC Cell Biology副主编。任美国Keystone Symposia 科学咨询委员会委员。美国细胞生物学学会国际事务委员会主席。中国细胞生物学会外事委员会主任、细胞结构与细胞行为分会会长。

报告摘要:Mitotic spindle orientation is essential for cell fate determination and tissue morphogenesis. Early studies indicate the essential role of the evolutionarily conserved Gαi/LGN/NuMA network in spindle positioning. However, the regulatory mechanisms that couple astral microtubules dynamics to the spindle orientation remain elusive. Here we delineated a novel mitosis-specific crotonylation-regulated astral microtubule-EB1-NuMA interaction in mitosis. Biochemical characterization demonstrated that EB1 is a bona fide substrate of TIP60, and the crotonylation of Lys66 by TIP60 tunes astral microtubule binding for spindle positioning. Importantly, this crotonylation-elicited regulation of EB1 binding to astral microtubule promotes accuracy of spindle positioning. Modeling crotonylation of Lys66 in 3D gastric organoids from mice with knock-in of hyperactive TIP60, or with genetically crotonylated EB1 in HeLa cells, confirms the importance of crotonylation dynamics for accurate control of metaphase-anaphase transition. These findings delineate a general signaling cascade that integrates protein crotonylation with accurate spindle positioning for genomic stability in mitosis.

唐爱辉简介:教授,“青年千人计划”获得者。分别于2002年和2008年在北京大学生命科学学院获得理学学士和生物物理学博士学位,从事心肌细胞钙动态及功能研究;后在美国马里兰大学医学院先后以博后、副研和研究助理教授身份从事神经生物学研究;于2018年起任中国科学技术大学生命科学学院特任教授。近年来聚焦于单分子超高分辨显微成像技术的开发和在神经生物学中的应用,并在神经生理和病理学领域取得多项重要发现,在Nature, NeuronPNAS,  Journal of Neuroscience, 等国际学术期刊上发表过多篇文章。获得Brain&Behavior FoundationYoung Investigator Grants.

报告摘要:Synaptic transmission is maintained by a delicate, subsynaptic molecular architecture. Even mild alterations in synapse structure drive functional changes during experience-dependent plasticity and pathological disorder. Key to this architecture is how the distribution of presynaptic vesicle fusion sites corresponds to the position of receptors in the postsynaptic density. Using multiple super-resolution imaging techniques, we find that key proteins mediating vesicle priming and fusion form mutually-enriched nanoclusters within the presynaptic active zone, and action-potential-evoked fusion is guided by this protein gradient and occurs preferentially around these subregions. More importantly, these presynaptic RIM nanoclusters closely align with concentrated postsynaptic AMPARs and scaffolding proteins, forming a trans-synaptic molecular ‘nanocolumn’. Moreover, using engineered, rapid proteolysis, we find that acutely disruption of an adhesion molecule, LRRTM2, leads quickly to nanoscale de-clustering of AMPARs away from release sites without prompting their escape from synapses. This remodeling of AMPAR position produce significant deficits in evoked, but not spontaneous, postsynaptic receptor activation. These findings suggest the nano-positioning of synaptic proteins is a new mechanism that modulates synaptic efficiency, and support the novel concept that adhesion molecules acutely position AMPA receptors to dynamically control synaptic strength.