Transcription profiling of mouse wild type and Taf7l mutant testes

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. Experiment Overall Design: Mice on C57BL/6J strain background were selected. Testes from Taf7l mutant and wild type littermates at 8-weeks old were dissected.