Deficiency in the multicopy Sycp3-like X-linked genes Slx and Slxl1 causes major defects in spermatid differentiation
Source: NCBI BioProject (ID PRJNA140039)

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Project name: Mus musculus
Description: The gene Sly is present in multiple copies on the mouse Y chromosome and encodes a protein that is required for the epigenetic regulation of postmeiotic sex chromosome expression. The X chromosome carries two multicopy genes related to Sly: Slx and Slxl1. Here we investigate the role of Slx/Slxl1 using transgenically-delivered small interfering RNAs to disrupt their function. We show that Slx and Slxl1 are important for normal sperm differentiation and male fertility. Slx/Slxl1 deficiency leads to delay in spermatid elongation and sperm release. A high proportion of delayed spermatids are eliminated via apoptosis, with a consequent reduced sperm count. The remaining spermatozoa are abnormal with impaired motility and fertilizing abilities. Microarray analyses reveal that Slx/Slxl1 deficiency affects the metabolic processes occurring in the spermatid cytoplasm but does not lead to a global perturbation of sex chromosome expression; this is in contrast with the effect of Sly deficiency which leads to an up-regulation of X and Y chromosome genes.Overall design: Total RNA isolated from separated round spermatids of young adult males (8 weeks postpartum) with shSLX or shSLY targeted knockdown, compared to age- and strain-matched controls.
Data type: Transcriptome or Gene expression
Sample scope: Multiisolate
Relevance: ModelOrganism
Organization: School of Biosciences, University of Kent
Literatures
  1. PMID: 20739462
Release date: 2011-05-11
Last updated: 2011-05-10