Dosage Compensation of an Aneuploid Genome in Mouse Spermatogenic Cells
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ABSTRACT: Autosomal trisomies and monosomies bring serious threats to embryonic development through transcriptional disarray primarily caused by the dosage effect of the aneuploid part of the genome. The present study compared the effect of a mouse viable 30 Mb segmental trisomy on the genome-wide transcriptional profile of somatic (liver) cells and male germ cells. While the 1.6-fold change in expression of triplicated genes reflected the gene dosage in liver cells, the extra copy was almost fully compensated in early pachytene spermatocytes, showing 1.18-fold increase. Allele-specific semi-quantitative evaluation of steady-state mRNA levels of the triplicated Amdhd2 gene revealed silencing evenly distributed among all three copies in these meiotic cells. Although more pronounced, the dosage compensation of trisomic genes was concordant with the incidence of HORMAD2 and γH2AX markers of unsynapsed chromatin. The possible explanations include insufficient sensitivity to detect both MSUC markers in the 30 Mb region of the chromosome, or an early silencing effect of another epigenetic factor. Taken together, our results indicate that the meiotic silencing of unsynapsed chromatin is the major but not the only factor driving the dosage compensation of triplicated genes in primary spermatocytes. We compared the global expression profiles in isolated popoulations of meiotic cells and liver cells of Ts43H trisomic males and their t121/D17 euploid siblings.
ORGANISM(S): Mus musculus
SUBMITTER: David Homolka
PROVIDER: E-GEOD-54683 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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