TAF7L REGULATES EARLY STAGES OF MALE GERM CELL DEVELOPMENT
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ABSTRACT:
PROVIDER: PRJNA1010219 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR25779154_1.fastq.gz | Fastqsanger.gz | |||
| SRR25779154_2.fastq.gz | Fastqsanger.gz | |||
| SRR25779155_1.fastq.gz | Fastqsanger.gz | |||
| SRR25779155_2.fastq.gz | Fastqsanger.gz | |||
| SRR25779156_1.fastq.gz | Fastqsanger.gz |
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Project description:Male germ cell development is dependent on the orchestrated regulation of gene networks. TATA-box binding protein associated factors (TAFs) facilitate interactions of TATA-binding protein with the TATA element, which is known to coordinate gene transcription during organogenesis. TAF7 like (Taf7l) is situated on the X chromosome and has been implicated in testis development. We examined the biology of TAF7L in testis development using the rat. Taf7l was prominently expressed in preleptotene to leptotene spermatocytes. To study the impact of TAF7L on the testis we generated a global loss-of-function rat model using CRISPR/Cas9 genome editing. Exon 3 of the Taf7l gene was targeted. A founder was generated possessing a 110 bp deletion within the Taf7l locus, which resulted in a frameshift and the premature appearance of a stop codon. The mutation was effectively transmitted through the germline. Deficits in TAF7L did not adversely affect pregnancy or postnatal survival. However, the Taf7l disruption resulted in male infertility due to compromised testis development and failed sperm production. Mutant germ cells suffer meiotic arrest at late zygotene/early pachynema stages, with defects in sex body formation. This testis phenotype was more pronounced than previously described for the subfertile Taf7l null mouse. We conclude that TAF7L is essential for male germ cell development in the rat.
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Project description:TFIID is a general transcription factor required for transcription of most protein-coding genes by RNA polymerase II. TAF7L is an X-linked germ cell-specific paralogue of TAF7, which is a generally expressed component of TFIID. Here we report the generation of Taf7l mutant mice by homologous recombination in embryonic stem cells using the Cre-loxP strategy. While spermatogenesis is completed in Taf7l mutant mice, the weight of Taf7l mutant testis is decreased and the amount of sperm in the epididymis is sharply reduced. Mutant epididymal sperm exhibit abnormal morphology including folded tails. Sperm motility is significantly reduced, and Taf7l mutant males are fertile with reduced litter size. Microarray profiling reveals that the abundance of six gene transcripts (including Fscn1) in Taf7l mutant testis decreases by > 2-fold. In particular, FSCN1 is an F-action-bundling protein and thus may be critical for normal sperm morphology and sperm motility. Although deficiency of Taf7l may be compensated in part by Taf7, Taf7l has apparently evolved new specialized functions in the gene-selective transcription in male germ-cell differentiation. Our mouse studies suggest that mutations in human TAF7L gene might be implicated in X-linked oligozoospermia in men. Keywords: genetic modification
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