Deletion in the Y chromosome of B10.BR-Y mice alters transcription from MSYq genes and has moderate effect on DNA methylation.

B10.BR-Y male mice with large deletion in the male-specific region of the Y chromosome long arm (MSYq) are very useful experimental model which requires, however, more detailed characterization. In the present study, the influence of the deletion on transcript levels of MSYq genes (Ssty1, Ssty2, Sly, Srsy, Asty, Orly) and homologous to them X-linked genes (Sstx, Slx, Slxl1, Srsx) was assessed. Quantitative PCR analysis showed that in testes of B10.BR-Y males activity of Ssty1 is unchanged, but transcription from all other MSYq genes is highly reduced and reaches from 59 % to only 5 % of the control levels. The decrease in expression of MSYq genes is accompanied by the two-fold increase in expression of Slx and Slxl1 genes. This is the first functional characterization of the deletion in B10.BR-Y strain. Another aim of the study was to reveal the mechanism through which deleted Y chromosome of B10.BR-Y males could alter phenotype of their female progeny, what was documented in our previous works. Epigenetic inheritance hypothesis was tested by microarray analysis of DNA methylation in B10.BR-Y and control B10.BR sperm. The assessment revealed moderate differences and allowed concluding that the mutated Y chromosome can influence traits of females from the next generation partially through altering sperm DNA methylation, but probably some additional mechanisms are engaged here. Breeding data indicate that feminization of pre- and neonatal environment in which next generation females develop is one of such additional mechanisms.