GSE68617
Trim33 binds and silences a class of young endogenous retroviruses in the mouse testis
Transposable elements (TEs) have been active in the mammalian genome for hundreds of millions of years and each TE has had a distinct period of transpositional activity, followed by inactivation. Mice carrying reporter transgenes can be used to model transcriptional silencing at TEs. A mutagenesis screen for modifiers of epigenetic gene silencing produced a line with a null mutation in Trim33. Heterozygous mutants displayed increased expression of the reporter transgene. ChIP-seq of Trim33 in testis revealed 9,109 peaks, mostly at promoters, across the mouse genome. Trim33 was enriched at many RLTR10B elements that are among the youngest retrotransposons in the mouse genome.  RNA-seq revealed that testis of mice haploinsufficient for Trim33 had altered expression of a small group of genes. The gene with the most significant increase, Nmnat3, was found to be transcribed from an upstream RLTR10B element. We show that Trim33 is involved in repressing RLTR10B elements in mouse testis. Overall design: Examination of Trim33 binding using ChIP sequencing and the result of Trim33 haploinsufficiency using RNA sequencing, in mouse testis