Role and localization of Polycomb-mediated histone H2A ubiquitination

• Project/Area Number: 25871129
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Genome biology; Cell biology
• Research Institution: The Institute of Physical and Chemical Research
• Principal Investigator: ENDOH Mitsuhiro 独立行政法人理化学研究所, 統合生命医科学研究センター, 客員研究員 (40391883)
• Project Period (FY): 2013-04-01 – 2015-03-31
• Project Status: Completed (Fiscal Year 2014)
• Budget Amount: ¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000); Fiscal Year 2014: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000); Fiscal Year 2013: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
• Keywords: エピジェネティクス / ヒストン修飾 / クロマチン / 転写制御 / 遺伝子発現 / 胚性幹細胞 / 転写 / 発生 / 分化 / 減数分裂

Outline of Final Research Achievements

It is still unclear how Polycomb group proteins Ring1A/B, E3 ubiquitin ligases for histone H2A, recognize and bind to their target genes. In this study, we focused on Polycomb Repressive Complex 1 (PRC1) and MBLR complex, both of with include Ring1A/B. We found that the physical interaction of Ring1B with chromo-domain proteins Cbx2/7, which have an affinity for PRC2-mediated trimethylated histone H3-K27, is essential for PRC1 recruitment to the developmental regulator genes. On the other hand, MBLR complexes recognize and bind to genes related to meiosis dependently on transcription factors Max/Mga, and repress those target genes through Ring1A/B-mediated H2A monoubiquitination.

Research Products

• [Journal Article] Gene regulation. Transcribed enhancers lead waves of coordinated transcription in transitioning mammalian cells (2015)
  • Author(s): Arner E, Daub CO, Vitting-Seerup K, Andersson R, Lilje B, Drabløs F, Lennartsson A, Rönnerblad M, Hrydziuszko O, Vitezic M, Freeman TC, Alhendi AM, Arner P, Axton R, Baillie JK, Beckhouse A, Bodega B, Briggs J, Brombacher F, Davis M, Detmar M, Ehrlund A, Endoh M, Eslami A, Fagiolini M, et al.
  • Journal Title: Science Volume: 347 Issue: 6225 Pages: 1010-1014
  • DOI: 10.1126/science.1259418
  • Peer Reviewed / Open Access / Acknowledgement Compliant
• [Presentation] MBLR-PRC1ポリコーム複合体による減数分裂遺伝子のエピジェネティック制御 (2014)
  • Author(s): 遠藤充浩、信賀順、遠藤高帆、古関明彦
  • Organizer: 第37回日本分子生物学会年会
  • Place of Presentation: パシフィコ横浜（神奈川県横浜市）
  • Year and Date: 2014-11-27
• [Presentation] Role of an atypical Polycomb Repressive Complex 1 (PRC1) involving MBLR and Mga/Max in repressing meiosis-related genes in mouse ES cells (2014)
  • Author(s): 遠藤充浩、信賀順、遠藤高帆、古関明彦
  • Organizer: 第12回幹細胞シンポジウム
  • Place of Presentation: 九州大学医学部百年講堂（福岡県福岡市）
  • Year and Date: 2014-05-30 – 2014-05-31
• [Presentation] MBLR-assembled atypical Polycomb Repressive Complex 1 (PRC1) is directed to meiosis-related genes by Max/Mga and drives PRC2 recruitment (2014)
  • Author(s): 遠藤充浩、信賀順、遠藤高帆、古関明彦
  • Organizer: 第8回日本エピジェネティクス研究会年会
  • Place of Presentation: 伊藤国際学術研究センター（東京都文京区）
  • Year and Date: 2014-05-25 – 2014-05-27
• [Presentation] MBLRポリコーム複合体による減数分裂遺伝子のエピジェネティック制御 (2014)
  • Author(s): 遠藤充浩
  • Organizer: 第8回日本エピジェネティクス研究年会
  • Place of Presentation: 伊藤国際学術研究センター（東京大学）
• [Presentation] Role of an atypical Polycomb Repressive Complex 1 (PRC1) involving MBLR and Mga/Max in repressing meiosis-related genes in mouse ES cells (2014)
  • Author(s): 遠藤充浩
  • Organizer: 第12回幹細胞シンポジウム
  • Place of Presentation: 九州大学医学部 百年講堂
• [Presentation] Polycomb group protein Pcgf6 assembles atypical PRC1 and recruits PRC2 to repress germ cell-related genes in mouse ES cells (2013)
  • Author(s): 遠藤充浩
  • Organizer: The 61st NIBB Conference "Cellular Community in Mammalian Embryogenesis"
  • Place of Presentation: NINS 岡崎コンファレンスセンター
• [Presentation] Max-Pcgf6 axis assembles atypical Polycomb Repressive Complex 1 (PRC1) and recruits PRC2 to repress germ cell-related genes in mouse ES cells (2013)
  • Author(s): 遠藤充浩
  • Organizer: NGS現場の会 第三回研究会
  • Place of Presentation: 神戸国際会議場
• [Presentation] ヒトiPS細胞を用いた低線量放射線影響の研究
  • Author(s): 遠藤充浩
  • Organizer: 第148回 原医研セミナー
  • Place of Presentation: 広島大学原爆放射線医科学研究所
  • Invited