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Background  DNA damage generally results in the activation of ATM/ATR kinases and the downstream checkpoint kinases Chk1/Chk2. In  Drosophila melanogaster,  the ATR homologue  meiotic 41  ( mei-41)  is pivotal to DNA damage repair and cell cycle checkpoint signalling. Although various  mei-41  mutant alleles have been analyzed in the past, no gain-of-function allele is yet available. To fill this gap, we have generated transgenic flies allowing temporal and tissue-specific induction of  mei-41.Results  Overexpression of  mei-41  in wing and eye anlagen affects proliferation and a G2/M checkpoint even in the absence of genomic stress. Similar consequences were observed following the overexpression of the downstream kinase Grapes (Grp) but not of Loki (Lok), encoding the respective  Drosophila  Chk1 and Chk2 homologues, in agreement with their previously reported activities. Moreover, we show that irradiation induced cell cycle arrest was prolonged in the presence of ectopic  mei-41  expression. Similar to irradiation stress,  mei-41  triggered the occurrence of a slower migrating form of Grp, implying specific phosphorylation of Grp in response to either signal. Using a p53R-GFP biosensor, we further show that overexpression of  mei-41  was sufficient to elicit a robust p53 activation in vivo.    Conclusion  We conclude that overexpression of the  Drosophila  ATR homologue  mei-41  elicits an effectual DNA damage response irrespective of irradiation.    Electronic supplementary material  The online version of this article (10.1186/s41065-018-0066-4) contains supplementary material, which is available to authorized users.

Overexpression of the Drosophila ATR homologous checkpoint kinase Mei-41 induces a G2/M checkpoint in Drosophila imaginal tissue