Dosage compensation of an aneuploid genome in mouse spermatogenic cells
Jazyk angličtina Země Spojené státy americké Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
24790161
DOI
10.1095/biolreprod.114.118497
PII: biolreprod.114.118497
Knihovny.cz E-zdroje
- Klíčová slova
- gene dosage, male sterility, meiotic silencing of unsynapsed chromatin, pachytene spermatocytes, segmental trisomy, synaptonemal complex, transcriptional profiling,
- MeSH
- aneuploidie MeSH
- chromatin genetika MeSH
- fenotyp MeSH
- genom * MeSH
- játra fyziologie MeSH
- kompenzace dávky (genetika) * MeSH
- meióza genetika MeSH
- mužská infertilita genetika MeSH
- myši inbrední C57BL MeSH
- spermatocyty fyziologie MeSH
- synaptonemální komplex genetika MeSH
- těhotenství MeSH
- tělesná hmotnost genetika MeSH
- transkriptom MeSH
- translokace genetická genetika MeSH
- trizomie genetika MeSH
- zvířata MeSH
- Check Tag
- mužské pohlaví MeSH
- těhotenství MeSH
- ženské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- 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.
Citace poskytuje Crossref.org
