Kyoto University · Biochemistry, Genetics and Molecular Biology
Professor Tatsushi Igaki's research lab focuses on the molecular mechanisms underlying cell competition, apoptosis, and tumor suppression in Drosophila, with a particular emphasis on how cellular fitness, endoplasmic reticulum stress, and intercellular communication govern tissue homeostasis and tumor suppression. The lab investigates key regulators such as Xrp1, DIAP1, and Drob-1, exploring their roles in cell death, proteostasis, and non-autonomous signaling in epithelial tissues. By integrating genetic screens, cell biological analyses, and molecular dissection, the lab uncovers conserved pathways that prevent tumorigenesis through fitness-based cell elimination and microenvironmental crosstalk. Their work reveals how stress responses and apoptotic pathways are co-opted to maintain tissue integrity and suppress malignant progression.
Figures are computed from collected data and may differ slightly.
The Bcl-2/CED-9 family of proteins, which includes both antiapoptotic and proapoptotic members, plays key regulating roles in programmed cell death. We report here the identification and characterization of Drob-1, the first Drosophila member of the Bcl-2/CED-9 family to be isolated. Drob-1 contains four conserved Bcl-2 homology domains (BH1, BH2, BH3, and BH4) and a C-terminal hydrophobic domain. Ectopic expression of Drob-1 in the developing Drosophila eye resulted in a rough-eye phenotype. Fu
Members of the inhibitor of apoptosis protein (IAP) family can inhibit caspases and cell death in a variety of insect and vertebrate systems. Drosophila IAP1 (DIAP1) inhibits cell death to facilitate normal embryonic development. Here, using RNA interference, we showed that down-regulation of DIAP1 is sufficient to induce cell death in Drosophila S2 cells. Although this cell death process was accompanied by elevated caspase activity, this activation was not essential for cell death. We found tha
Cell competition is a context-dependent cell elimination through short-range cell-cell interaction, in which cells with higher fitness eliminate neighboring less-fit or oncogenic cells within the growing tissue. Cell competition can be triggered by many different factors such as heterozygous mutations in the ribosomal protein genes (which are called "Minute" mutations), elevated Myc, Yorkie/YAP, Wg/Wnt, JAK-STAT, Ras, or Src activity, and loss of Mahjong/VprBP, endocytic pathway components, or a
Cell competition is a context-dependent cell elimination via cell-cell interaction whereby unfit cells ('losers') are eliminated from the tissue when confronted with fitter cells ('winners'). Despite extensive studies, the mechanism that drives loser's death and its physiological triggers remained elusive. Here, through a genetic screen in Drosophila, we find that endoplasmic reticulum (ER) stress causes cell competition. Mechanistically, ER stress upregulates the bZIP transcription factor Xrp1,
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