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2019年度 国際バイオ特論A (4062)

授業科目基本情報

科目区分 専門科目 教職科目 指定なし
単位数 1 選択・必修・自由 選択
授業形態 講義 主な使用言語 英語
開講時期 履修登録システム 【使用しない】
履修登録期間 履修取消期限

教育プログラム別の履修区分

プログラム名 IS CB BS BN MS CP DS
履修区分
コア科目
履修方法 ・基盤科目及び専門科目から12単位以上履修すること。

授業科目概要

担当責任教員 塩﨑 一裕
担当教員 真木智子
教育目的/授業目標 海外から招聘した講師による英語による集中講義を通じて、特定の専門分野の基礎的な知識および最先端の研究内容について学ぶ。積極的に質問を行い議論に参加することを通して科学の現場での英語でのコミュニケーション能力や国際感覚の育成を図る。
指導方針 講義に内容に関連する英語論文を事前に読解。学習し。キーワードやキーコンセプトを理解したうえで講義に臨ませる。少人数クラスのゼミ形式の講義と議論に対して主体的で積極的な取り組みを奨励する。

クラス情報



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授業計画

[1限目 9:20-10:50] [2限目 11:00-12:30] [3限目 13:30-15:00] [4限目 15:10-16:40] [5限目 16:50-18:20] [6限目 18:30-20:00]
回数 日付 [時間] テーマ 内容
1 12/12 [2] Lecture 1: Overview and principles of cell signaling
Dr. Ted Powers, Department of Molecular and Cellular Biology, College of Biological Sciences, University of California Davis
We will discuss fundamental aspects of cellular signaling, including a description of common components of the majority of signal transduction pathways, including Protein Kinases, GTP-binding proteins (GTPases) and their regulators, as well as role of protein scaffolds. We will discuss a number of well-defined examples of signaling modules, including the role of two-component systems in bacterial chemotaxis and the function of scaffolds in the mitogen activated protein kinase (MAPK) cascade. Finally, we will discuss approaches used to explore the architecture and function of signaling pathways, including genetic, biochemical, proteomic, bioinformatic, and novel single cell-based approaches.
2 12/12 [3] Lecture 2 Inter-organelle communication and the role of membrane-contacts in signaling
Dr. Ted Powers, Department of Molecular and Cellular Biology, College of Biological Sciences, University of California Davis
We will discuss the advantages and obstacles that eukaryotic cells encounter due to the presence of internal membrane-bound compartments for controlling cellular homeostasis. We will explore in depth one major mode of communication between the endoplasmic reticulum (ER) and the nucleus, termed the unfolded protein response (UPR), as well as understand how the UPR is part of a larger integrated cellular stress response pathway. We will examine how the accumulation of unfolded proteins in the ER initiate the UPR as well as how this pathway is coupled to other stress-related processes such as autophagy and apoptosis. We will also discuss how the ER is involved in physical contacts with several other organelles within cells and how these contacts can modulate growth and stress-related signaling pathways.
3 12/13 [2] Lecture 3 Nutrient sensing and cell growth control
Dr. Ted Powers, Department of Molecular and Cellular Biology, College of Biological Sciences, University of California Davis
We will discuss how metabolic needs of the cell are controlled and signaled through specific signaling pathways. Emphasis will be placed on the rapamycin-sensitive mTOR pathway, which will form a focal point for understanding the interplay between glucose, amino acid, and lipid metabolism during growth and proliferation. Experiments will be described that led to the identification and characterization of the two major TOR-kinase containing complexes, mTORC1 and mTORC2 in mammalian cells, as well as how these complexes collaborate and are regulated to control downstream processes essential for cell growth. We will see how mTOR activity is coupled to other important cell signaling proteins such as AMP-regulated protein kinase (AMPK) and AKT, as well as how the mTORC1/2 complexes are influenced by organelle dynamics within cells. Finally, we will discuss how alterations in the mTOR network can lead to dysregulated cell growth in cancer as well as contribute to metabolic disorders.
4 12/13 [3] Seminar
TOR Signaling Network: Balancing Growth and Stress
Dr. Ted Powers, Department of Molecular and Cellular Biology, College of Biological Sciences, University of California Davis
Regulation of cell proliferation requires a balanced response to both growth and stress-related cues. The ability of eukaryotic organisms to coordinate these cues occurs, in part, through the evolutionarily conserved TOR kinase-signaling network. TOR functions as part of two distinct protein complexes, TOR Complexes 1 and 2 (TORC1 and TORC2), where TORC1 is uniquely inhibited by rapamycin. TORC1 and TORC2 function, in part, by phosphorylating distinct members of the AGC kinase family of protein kinases. In S. cerevisiae, TORC2 recognizes YPK1 and YPK2, orthologs of mammalian AKT. Following activation, YPK1/2 carry out a majority of activities attributable to TORC2, where YPK1 is the most predominant functionally. Because TORC2 is not inhibited by rapamycin, our understanding of its role within cells is not as complete in comparison to TORC1. In this lecture, I will describe two novel functions we have identified regarding TORC2-YPK1 signaling. First, we have determined that these components suppress intracellular levels of reactive oxygen species (ROS). This is important because unregulated production of ROS is deleterious to cells and contributes to aging and disease. Second, we have discovered that TORC2-YPK1 signaling also acts as a novel positive regulator of autophagy that is induced specifically following amino acid starvation. Autophagy facilitates cellular adaptation to stress and has also been linked to aging and disease. Remarkably, we have found that both of these cellular activities downstream of TORC2-Ypk1 intersect with both the vacuole/lysosome as well as mitochondrial function to regulate cellular homeostasis. In addition to these functional studies, I will also describe our recent experiments aimed at understanding the physical basis for the assembly of TOR into distinct multi-protein complexes that contain overlapping yet distinct binding partners. Together our studies have increased our understanding of the architecture and function of this essential signaling network.
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授業日程

[1限目 9:20-10:50] [2限目 11:00-12:30] [3限目 13:30-15:00] [4限目 15:10-16:40] [5限目 16:50-18:20] [6限目 18:30-20:00]
回数 日付 時間 講義室 備考
1 12/12 2 L13
2 12/12 3 L13
3 12/13 2 L13
4 12/13 3 L13

テキスト・参考書

テキスト 講師よりあらかじめ指定される学術論文4-5報
参考書 特になし

その他

履修条件 講師が指定する論文等を講義前に読解・学習しておくこと。
オフィスアワー Eメールで連絡の上、日時を決める
成績評価の方法と基準 ・5段階(秀・優・良・可・不可)で評価する。
・講義への取り組み(70%)および受講後のレポート(30%)で評価する。
・当該分野の基本概念と研究アプローチの理解、および英語による論理的な議論の技能を基準とする。
関連科目 特になし
関連学位 バイオサイエンス
注意事項 集中講義の日程、テーマ、および内容については、当該年度に海外から招聘する講師と打ち合わせの上、Eメール等で告知する。

授業関連URL



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配布資料



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