Dosage compensation of an aneuploid genome in mouse spermatogenic cells
Language English Country United States Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
24790161
DOI
10.1095/biolreprod.114.118497
PII: biolreprod.114.118497
Knihovny.cz E-resources
- Keywords
- gene dosage, male sterility, meiotic silencing of unsynapsed chromatin, pachytene spermatocytes, segmental trisomy, synaptonemal complex, transcriptional profiling,
- MeSH
- Aneuploidy MeSH
- Chromatin genetics MeSH
- Phenotype MeSH
- Genome * MeSH
- Liver physiology MeSH
- Dosage Compensation, Genetic * MeSH
- Meiosis genetics MeSH
- Infertility, Male genetics MeSH
- Mice, Inbred C57BL MeSH
- Spermatocytes physiology MeSH
- Synaptonemal Complex genetics MeSH
- Pregnancy MeSH
- Body Weight genetics MeSH
- Transcriptome MeSH
- Translocation, Genetic genetics MeSH
- Trisomy genetics MeSH
- Animals MeSH
- Check Tag
- Male MeSH
- Pregnancy MeSH
- Female MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Chromatin MeSH
Autosomal trisomies and monosomies bring serious threats to embryonic development through transcriptional disarray caused primarily 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. Although the 1.6-fold change in expression of triplicated genes reflected the gene dosage in liver cells, the extra copy genes were compensated in early pachytene spermatocytes, showing 1.18-fold increase. Although more pronounced, the dosage compensation of trisomic genes was concordant with the incidence of HORMAD2 protein and histone gammaH2AX markers of unsynapsed chromatin. A possible explanation for this includes insufficient sensitivity to detect the meiotic silencing of unsynapsed chromatin markers in the 30-Mb region of the chromosome or an earlier silencing effect of another epigenetic factor. Taken together, our results indicate that the meiotic silencing of unsynapsed chromatin is the major, but most likely not the only, factor driving the dosage compensation of triplicated genes in primary spermatocytes.
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