ArticleNucleic acids research2021
The SR-protein Npl3 is an essential component of the meiotic splicing regulatory network in Saccharomyces cerevisiae.
Article in Nucleic acids research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 39 citations in OpenAlex.
- Mechanism of alternative splicing of yeast HEH1 through competing 5' splice sites.Nature communications · 2025Article
- Single-molecule quantitation of RNA-binding protein occupancy and stoichiometry defines a role for Yra1 (Aly/REF) in nuclear mRNP organization.Cell reports · 2023Article
- RNA recognition by Npl3p reveals U2 snRNA-binding compatible with a chaperone role during splicing.Nature communications · 2023Article
- SRSF10 stabilizes CDC25A by triggering exon 6 skipping to promote hepatocarcinogenesis.Journal of experimental & clinical cancer research : CR · 2022Article
- Roles and Cellular Localization of GBP2 and NAB2 During the Blood Stage of Malaria Parasites.Frontiers in cellular and infection microbiology · 2021Article
- Mechanisms and regulation of spliceosome-mediated pre-mRNA splicing in Saccharomyces cerevisiae.Wiley interdisciplinary reviews. RNAReview
- Mixed Messages: Dynamic and Compositional Heterogeneity of Nuclear Messenger Ribonucleoprotein (mRNP) Complexes.Wiley interdisciplinary reviews. RNAReview
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3 authors at 1 institution in 1 country.
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Abstract
The meiotic gene expression program in Saccharomyces cerevisiae involves regulated splicing of meiosis-specific genes via multiple splicing activators (e.g. Mer1, Nam8, Tgs1). Here, we show that the SR protein Npl3 is required for meiotic splicing regulation and is essential for proper execution of the meiotic cell cycle. The loss of Npl3, though not required for viability in mitosis, caused intron retention in meiosis-specific transcripts, inefficient meiotic double strand break processing and an arrest of the meiotic cell cycle. The targets of Npl3 overlapped in some cases with other splicing regulators, while also having unique target transcripts that were not shared. In the absence of Npl3, splicing defects for three transcripts (MER2, HOP2 and SAE3) were rescued by conversion of non-consensus splice sites to the consensus sequence. Methylation of Npl3 was further found to be required for splicing Mer1-dependent transcripts, indicating transcript-specific mechanisms by which Npl3 supports splicing. Together these data identify an essential function for the budding yeast SR protein Npl3 in meiosis as part of the meiotic splicing regulatory network.
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