Loss of function of male‐specific lethal 3 (Msl3) does not affect spermatogenesis in rodents

Abstract

AbstractBackgroundMale‐specific lethal 3 (Msl3) is a member of the chromatin‐associated male‐specific lethal MSL complex, which is responsible for the transcriptional upregulation of genes on the X chromosome in males of Drosophila. Although the dosage complex operates differently in mammals, the Msl3 gene is conserved from flies to humans. Msl3 is required for meiotic entry during Drosophila oogenesis. Recent reports indicate that also in primates, Msl3 is expressed in undifferentiated germline cells before meiotic entry. However, if Msl3 plays a role in the meiotic entry of mammals has yet to be explored.ResultsTo understand, if Msl3a plays a role in the meiotic entry of mammals, we used mouse spermatogenesis as a study model. Analyses of single‐cell RNA‐seq data revealed that, in mice, Msl3 is mostly expressed in meiotic cells. To test the role of Msl3 in meiosis, we used a male germline‐specific Stra8‐iCre driver and a newly generated Msl3flox conditional knock‐out mouse line. Msl3 conditional loss‐of‐function in spermatogonia did not cause spermatogenesis defects or changes in the expression of genes related to meiosis.ConclusionsOur data suggest that, in mice, Msl3 exhibits delayed expression compared to Drosophila and primates, and loss‐of‐function mutations disrupting the chromodomain of Msl3 alone do not impede meiotic entry in rodents.