Abstract
During transcription, most eukaryotic genes generate multiple alternative cleavage and polyadenylation (APA) sites, leading to the production of transcript isoforms with variable lengths in the 3’ untranslated region (3’UTR). In contrast to somatic cells, male germ cells, especially pachytene spermatocytes and round spermatids, express a distinct reservoir of mRNAs with shorter 3’UTRs that are essential for spermatogenesis and male fertility. However, the mechanisms underlying the enrichment of shorter 3’UTR transcripts in the developing male germ cells remain unknown. Here, we report that UPF2-mediated nonsense-mediated mRNA decay (NMD) plays an essential role in male germ cells by eliminating ubiquitous genes-derived, longer 3’UTR transcripts, and that this role is independent of its canonical role in degrading “premature termination codon” (PTC)-containing transcripts in somatic cell lineages. This report provides physiological evidence supporting a noncanonical role of the NMD pathway in achieving global 3’UTR shortening in the male germ cells during spermatogenesis.
Highlights
Spermatogenesis is a complex cellular differentiation process through which male germline stem cells develop sequentially into spermatogonia, spermatocytes, spermatids, and eventually spermatozoa [1]
These mRNA transcripts are sequestered in ribonucleoprotein particles (RNPs), in which the mRNA transcripts are stabilized by RNAbinding proteins (RBPs) and small noncoding RNAs, and physically separated from the translational machinery
UPF2 is a novel component of the chromatoid body (CB)
Summary
3’UTR length control has been identified as a critical mechanism through which the cell establishes and maintains its functional identity. Developing male germ cells, especially spermatocytes and spermatids, display a transcriptome enriched in short 3’UTR transcripts, which has been demonstrated to be essential for spermatogenesis. It remains unknown how global 3’UTR shortening is achieved. In spermatocytes, and when spermatocytes develop into round spermatids, those long 3’UTR transcripts are selectively degraded by UPF2-dependent nonsense-mediated mRNA decay (NMD), leading to enrichment of the shorter 3’UTR transcripts. We provide physiological evidence supporting a non-canonical role of NMD in the control of 3’UTR length in male germ cells
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