Regulation of developmental robustness by cell death signaling

2015 Fiscal Year Final Research Report

• Project/Area Number: 23229002
• Research Category: Grant-in-Aid for Scientific Research (S)
• Allocation Type: Single-year Grants
• Research Field: General medical chemistry
• Research Institution: The University of Tokyo
• Principal Investigator: Miura Masayuki 東京大学, 薬学研究科(研究院), 教授 (50202338)
• Project Period (FY): 2011-04-01 – 2016-03-31
• Keywords: カスパーゼ / 細胞死 / エピジェネティクス / 神経発生 / 代謝 / 頑強性

Outline of Final Research Achievements

Selection of sensory organ precursor (SOP) by cell death occurs in the early stage of neural development in Drosophila. SOP cell number is regulated by non-apoptotic caspase activity. We identified the histone methyltransferase eggless/SETDB1 that can synergistically regulate SOP cell number with caspase, suggesting epigenetic histone modification can regulate the robust control of SOP cell number collaborating with non-apoptotic caspase function. For robust tissue regeneration, we found that imaginal disc injury systemically control the methionine metabolism in fat body. Changes of methionine metabolism in fat body then remotely control the imaginal disc regeneration, suggesting that cell death controls tissue regeneration systemically. In mammalian neural development, we found that apoptosis precisely controlled the size and elimination of FGF8 signaling center, thereby actively regulating signal center activity for establishment of robust patterning of brain development.

Free Research Field

発生遺伝学