第83回 アイセムスセミナー / CeMI セミナーシリーズ 25: Profs. Kai Simons, Mikael Simons, Ludger Johannes, Robert Parton
CeMI：Center for Meso-Bio Single-Molecule Imaging
How do membrane proteins become raftophilic?
(Prof. Kai Simons)
The study of lipid rafts as a membrane compartmentalization principle has been fraught with problems! Now the situation has changed by the discovery that plasma membranes can phase separate. These membrane systems are convenient models to study the basics of lipid-protein collectives. In this seminar, Prof. Kai Simons will discuss these newer developments of raft studies.
Molecular mechanisms of myelination in the central nervous system
(Prof. Mikael Simons)
The myelin sheath is one of the most abundant membrane structures in the vertebrate nervous system. It is produced by two types of specialized glial cells, oligodendrocytes in the central nervous system, and Schwanncells in the peripheral nervous system. The myelin sheath is formed by the spiral wrapping of glial plasma membrane extensions around the axons, followed by the extrusion of cytoplasm and the compaction of the stacked membrane bilayers. These tightly packed membrane stacks provide electrical insulation around the axons and maximize their conduction velocity. Axonal insulation by myelin not only facilitates rapid nerve conduction but also regulates axonal transport and protects against axonal degeneration. Damage to the myelin sheath, as it for example occurs in multiple sclerosis (MS) results therefore in severe neurological disability also as a result of neurodegeneration. The main goal of Prof. Mika Simons is to come up with new approaches of how to promote remyelination in demyelinating diseases such as MS. To realize this goal, he and his colleagues try to understand how myelin is formed during normal development. He will talk about his new progress in this front.
Mechanisms of membrane bending and scission in clathrin-independent endocytosis
(Prof. Ludger Johannes)
Several endocytic processes exist that do not require the activity of clathrin, and it has been a conundrum how the plasma membrane would be bent in the apparent absence of membrane coats. Recent studies by Prof. Ludger Johannes and his colleagues have uncovered a novel mechanism through which nanodomain construction by glycosphingolipid-binding Shiga and cholera toxins or polyoma viruses (SV40) induces membrane curvature changes and drives the coat-independent formation of endocytic plasma membrane invaginations. They could show that actin polymerization on Shiga toxin-induced tubule membranes alone is sufficient to induce scission in a process that requires membrane reorganization and domain formation. Their data suggest that tubule membranes are poised to undergo actin induced demixing, thereby generating domain boundary forces that trigger line tension-driven squeezing of the tubules membranes leading to scission. Prof. Johannes will present these results as well as newer data, showing that cellular proteins that like the toxins use glycosphingolipids for membrane bending, thereby regulating the cell surface dynamics of various markers with critical roles in cellular processes such as cell migration.
New insights into the formation and function of caveolae
(Prof. Robert G. Parton)
One of the most abundant and characteristic surface microdomains of mammalian cells are surface pits termed caveolae. Despite their abundance the exact functions of caveolae remain elusive. Over the last ten years, the research by Prof. Rob Parton and his colleagues has focussed on the fine ultrastructure of caveolae, the major components of caveolae, and their specific cellular functions. Their recent studies, utilising a range of systems including mouse models, cultured cells, and the zebrafish embryo, have identified a new family of coat proteins which work with membrane proteins called caveolins to regulate caveola formation. PTRF-cavin family members regulate association of caveolin with caveolae and identify a cellular mechanism to regulate caveolar and non-caveolar functions of caveolins. In this seminar, Prof. Parton will speak about the results of these studies, which are providing insights into a novel role for caveolae as mechanosensory organelles.
| 講演者 演題 |
Prof. Kai Simons マックス・プランク分子細胞生物学・遺伝学研究所（MPI-CBG） ドイツ ドレスデン 演題：How do membrane proteins become raftophilic? Prof. Mikael Simons Max Planck Institute for Experimental Medicine (Göttingen) Department of Neurology ドイツ ゲッティンゲン大学 演題：Molecular mechanisms of myelination in the central nervous system Prof. Ludger Johannes フランス キュリー研究所 演題：Mechanisms of membrane bending and scission in clathrin-independent endocytosis Prof. Robert G. Parton Institute for Molecular Bioscience オーストラリア クィーンズランド大学 演題：New insights into the formation and function of caveolae |
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| 日時 | 2011年6月27日（月）9:00-12:20 |
| 場所 | 京都大学 iCeMSコンプレックス1 本館 2階 セミナールーム (A207) アクセスマップ |
| フライヤー |  PDF (131KB) |
| 主催 | 京都大学 物質－細胞統合システム拠点（iCeMS＝アイセムス） |
| 共催 | 京都大学医学研究科グローバルCOEプログラム「生命原理の解明を基とする医学研究教育拠点」 |
| 連絡先 | iCeMS 楠見明弘 / Fax: 075-751-4113 akusumi@frontier.kyoto-u.ac.jp |