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Bhadra, M.P., Horikoshi, N., Pushpavallipvalli, S.N., Sarkar, A., Bag, I., Krishnan, A., Lucchesi, J.C., Kumar, R., Yang, Q., Pandita, R.K., Singh, M., Bhadra, U., Eissenberg, J.C., Pandita, T.K. (2012). The role of MOF in the ionizing radiation response is conserved in Drosophila melanogaster.  Chromosoma 121(1): 79--90.
FlyBase ID
FBrf0217202
Publication Type
Research paper
Abstract
In Drosophila, males absent on the first (MOF) acetylates histone H4 at lysine 16 (H4K16ac). This acetylation mark is highly enriched on the male X chromosome and is required for dosage compensation in Drosophila but not utilized for such in mammals. Recently, we and others reported that mammalian MOF, through H4K16ac, has a critical role at multiple stages in the DNA damage response (DDR) and double-strand break repair pathways. The goal of this study was to test whether mof is similarly required for the response to ionizing radiation (IR) in Drosophila. We report that Drosophila mof mutations in males and females, as well as mof knockdown in SL-2 cells, reduce post-irradiation survival. MOF depletion in SL-2 cells also results in an elevated frequency of metaphases with chromosomal aberrations, suggesting that MOF is involved in DDR. Mutation in Drosophila mof also results in a defective mitotic checkpoint, enhanced apoptosis, and a defective p53 response post-irradiation. In addition, IR exposure enhanced H4K16ac levels in Drosophila as it also does in mammals. These results are the first to demonstrate a requirement for MOF in the whole animal IR response and suggest that the role of MOF in the response to IR is conserved between Drosophila and mammals.
PubMed ID
PubMed Central ID
PMC4151556 (PMC) (EuropePMC)
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    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    Chromosoma
    Title
    Chromosoma
    Publication Year
    1939-
    ISBN/ISSN
    0009-5915
    Data From Reference
    Alleles (4)
    Genes (4)