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ORIGINAL RESEARCH article

Front. Cell Death
Sec. Apoptosis
Volume 3 - 2024 | doi: 10.3389/fceld.2024.1471050
This article is part of the Research Topic Cell Death in Drosophila View all articles

The histone demethylase Kdm5 controls Hidinduced cell death in Drosophila

Provisionally accepted
Andreas Bergmann Andreas Bergmann 1*Hans-Martin Herz Hans-Martin Herz 2
  • 1 University of Massachusetts Medical School, Worcester, United States
  • 2 St. Jude Children's Research Hospital, Memphis, Tennessee, United States

The final, formatted version of the article will be published soon.

    We conducted an EMS mutagenesis screen on chromosome arm 2L to identify recessive suppressors of GMR-hid-induced apoptosis in the Drosophila eye. Through this screen, we recovered three alleles of the lysine demethylase gene Kdm5. Kdm5, a member of the JmjCdomain-containing protein family, possesses histone demethylase activity towards H3K4me3.Our data suggest that Kdm5 specifically regulates Hid-induced cell death during development, as we did not observe control of Reaper-or Grim-induced cell death by Kdm5. Interestingly, GMR-hid-induced apoptosis is suppressed independently of Kdm5's demethylase activity. Our findings indicate that Rbf and dMyc are necessary for Kdm5 mosaics to suppress GMR-hidinduced cell death. Moreover, Kdm5 mosaics failed to suppress apoptosis induced by a mutant form of Hid that is resistant to inhibition by Erk-type MAPK activity. Additionally, Kdm5 dominantly enhances the wing phenotype of an activated MAPK mutant. These results collectively suggest that Kdm5 controls Hid-induced apoptosis by regulating the Rbf, dMyc, and MAPK pathways.

    Keywords: Drosophila, Cell Death, HID, KDM5, RB, MYC, MAPK

    Received: 16 Aug 2024; Accepted: 31 Oct 2024.

    Copyright: © 2024 Bergmann and Herz. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence: Andreas Bergmann, University of Massachusetts Medical School, Worcester, United States

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