International Forefront in BioscienceⅡ【230302】 International Forefront in BioscienceⅡ【230302】


科目区分 International Course 単位数 1
選択・必修 選択 授業形態 講義
開講時期 December 18 & 19, 2017 講義室 Dec.18 L12, Dec.19 L12 & Large seminar room


担当教員筆頭者名 Dr. Keith Baar, Department of Neurobiology, Physiology and Behavior, University of California Davis
担当教員 Dr. Keith Baar, Department of Neurobiology, Physiology and Behavior, University of California Davis
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。To acquire knowledge in current topics in biological sciences, To acquire skills in scientific discussion in English
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。これらを通じて、英語でのコミュニケーション能力の向上と国際性の涵養を図る。Two-day intensive course comprosing three lectures and one research seminar by lecturers from universities abroad


備考 回数 テーマ 内容
1回 Lecture 1:  Regulation of mTORC1 by growth factors/loading
2回 Lecture 2:  Nutritional regulation of mTORC1
3回 Lecture 3:  Role of muscle force transfer in strength across the lifespan
4回 Research Seminar: MicroRNA-31 and Aging: Impact on the force transfer apparatus in skeletal muscle
In very old animals, lateral force transmission in skeletal muscle is severely impaired. The dystrophin-glycoprotein (DGC) and integrin/focal adhesion complexes are important in promoting interactions between the cytoskeleton, membrane, and extracellular matrix within skeletal muscle. Thus as animals age their muscles become more prone to contraction-induced injury (Hughes et al., 2016). A specific microRNA, miR-31, binds to the 3' untranslated region (UTR) of the dystrophin mRNA and decreases its rate of translation. MiR-31 is increased >70-fold and >20-fold in skeletal muscle of mdx mice and muscular dystrophy patients respectively (Greco et al., 2009), as well as being elevated >6-fold in aged rat muscle (29-months), possibly contributing to the lower dystrophin protein in these muscles (Hughes et al., 2016). Thus we investigated miR-31 expression across the lifespan and manipulated its expression in young muscle to determine its impact on the cytoskeleton network. Male C57BL/6 mice (8 weeks-old) were subjected to in vivo electroporation of a mouse specific miR-31 plasmid (5ug) in the tibialis anterior (TA) muscle with the contralateral leg serving as a vector control (pmR-Cherry). Western blotting was performed to determine DGC complex, β-1 integrin, and α-actinin protein levels in the transfected TA muscles. Treatment comparisons were made using a paired students’ t-test. We observed a 70-fold increase in miR-31 expression levels in the transfected TA muscle compared to the contralateral control leg. The overexpression of miR-31 lead to a 22% reduction in dystrophin protein content (P=0.02) after just 7 days. Interestingly, surrounding cytoskeleton proteins such as α-sarcoglycan, sarcospan and β1-Integrin were all significantly elevated within the miR-31 transfected TA muscle. A similar adaptive response in surrounding cytoskeleton proteins has been observed in aged skeletal TA muscle (Hughes et al., 2016). Future studies will seek to investigate the functional significance of the miR-31 induced dystrophin loss on skeletal muscle.


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 4 to 5 scienfic papers disgnated by the lecturer


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。Students must read disignated papers before the course starts.
成績評価の方法と基準 講義への取り組み(70%)および受講後のレポート(30%)により評価する。
Evaluation will be made based on attendance and active participation in the classes (70%) and the report to be submitted afterwards (30%).
注意事項 各講義科目のテーマ及び開講日時は別にE-メールで通知する。履修手続きはそのメールに返信することで完了。
Registration is completed upon responding to the email announcing the opening of the course.