Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of mice wild-type and pcd3J-/- to investigate abnormal sperm development in pcd3J

ABSTRACT: Findings from gene expression studies can help identify relevant biological pathways. RNA from three pairs of testes from wild-type and pcd3J-/- mice at postnatal day 18 was subjected to a genome-scale gene expression analysis using the Affymetrix GeneChip Mouse Gene 1.0 ST Array, which includes approximately 28,000 genes. RNA from postnatal day 18 was used to minimize the changes in gene expression that might occur in response to pathological changes in the pcd3J-/- mice, because postnatal day 18 was the earliest time point at which structural differences between testes from wild-type and pcd3J-/- mice were observed via histopathology.Three pcd3J-/- mutant mice and three corresponding wild-type (pcd3J+/+) littermates at postnatal day 18 were used for the microarray analyses.

ORGANISM(S): Mus musculus

SUBMITTER: RUI XIAO

PROVIDER: E-MEXP-2570 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:MicroRNAs (miRNAs) are a class of endogenous, non-coding RNAs that mediate post-transcriptional gene silencing by inhibiting mRNA translation and promoting mRNA decay. DICER1, an RNAse III endonuclease encoded by Dicer1, is required for processing short 21-22 nucleotide miRNAs from longer double-stranded RNA precursors. Here, we investigate the loss of Dicer1 in mouse postnatal male germ cells to determine how disruptions in the miRNA biogenesis pathway may contribute to infertility. Reduced levels of Dicer1 transcripts and DICER1 were confirmed in germ cell knock-out (GCKO) testes by postnatal day 18 (P18). Compared to wild-type (WT) at 8 weeks, GCKO males had no change in body weight, yet showed significant reductions in testis mass and sperm number. Histology and fertility tests confirmed spermatogenic failure in GCKO males. Array analyses at P18 showed 96% of miRNA genes were down-regulated and 37% of protein-coding genes were differentially expressed in GCKO testes. Interestingly, we observed preferential overexpression of genes on the sex chromosomes in GCKO testes, with more than 80% of the genes overlapping those proposed to undergo meiotic sex chromosome inactivation (MSCI) in the germ cells. Compared to WT, GCKO mice showed higher percentages of cells at early meiotic stages (leptotene and zygotene) but lower percentages at later stages (pachytene, diplotene and metaphase I), providing evidence that deletion of Dicer1 leads to disruptions in meiotic progression. Furthermore, we observed fewer elongating spermatids with proper translational activation of transition protein 2 (Tnp2), protamine 1 and 2 (Prm1 and Prm2) in GCKO testes after step 12-14. Therefore, deleting Dicer1 in early postnatal germ cells causes misregulation of transcripts encoded by genes on the sex chromosomes, impairs meiotic progression and post-meiotic translational control and results in spermatogenic failure and infertility. Total RNA, including miRNAs, were purified from a total of six individual mouse samples. The tissue collected was obtained from wild-type (control; n=3) and Dicer1 germ cell knockout (mutant; n=3) testes on P18.

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Transcription profiling of mice wild-type and pcd3J-/- to investigate abnormal sperm development in pcd3J

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