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Next Generation Sequencing Facilitates Quantitative Analysis of germ cell RA signaling mutant and control THY1+ spermatogonia Transcriptomes


ABSTRACT: Purpose: The goal of this sequencing is to investigate alterations in gene expression that result from impaired retinoid signaling compared with control, and how the RA signaling controls spermatogonia differentiation Methods: THY1+ spermatogonia mRNA profiles of 4-day-old control and germ cell specific impaired retinoid signaling mice were generated by High-throughput sequencing Results: Gene ontology (GO) analysis of the genes at the top of the ranked genes indicated enrichment in genes associated with roles in reproduction, transcription and spermatogenesis. In total, we identified 1633 and 742 transcripts (Reads Per Kilobase of transcript per Million mapped reads (RPKM) > 1) that were significantly (p-value < 0.05, > 1.5-fold difference) down- and up-regulated, respectively, in the germ cell mutants compared with the controls. Most importantly, we found that the majority of transcripts of replication-dependent core histone genes, histone cluster 1 (Hist1) were downregulated in germ cell mutants. THY1+ spermatogonia mRNA profiles of 4-day old germ cell specific impaired retinoid signaling and control mice were generated by deep sequencing, twice, using Illumina HiSeq 2000

ORGANISM(S): Mus musculus

SUBMITTER: Yao Chen 

PROVIDER: E-GEOD-79863 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Retinoid signaling controls spermatogonial differentiation by regulating expression of replication-dependent core histone genes.

Chen Yao Y   Ma Li L   Hogarth Cathryn C   Wei Gang G   Griswold Michael D MD   Tong Ming-Han MH  

Development (Cambridge, England) 20160310 9


Retinoic acid (RA) signaling is crucial for spermatogonial differentiation, which is a key step for spermatogenesis. We explored the mechanisms underlying spermatogonial differentiation by targeting expression of a dominant-negative mutant of retinoic acid receptor α (RARα) specifically to the germ cells of transgenic mice to subvert the activity of endogenous receptors. Here we show that: (1) inhibition of retinoid signaling in germ cells completely blocked spermatogonial differentiation identi  ...[more]

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