ArticlePLoS biology2022
The microprotein Nrs1 rewires the G1/S transcriptional machinery during nitrogen limitation in budding yeast.
Article in PLoS biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 7 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 16 citations in OpenAlex.
- Article
- Discovering the hidden function in fungal genomes.Nature communications · 2024Review
- Biochemistry and Protein Interactions of the CYREN Microprotein.Biochemistry · 2023Article
- Review
- The G1/S repressor WHI5 is expressed at similar levels throughout the cell cycle.BMC research notes · 2022Article
- Correction: The microprotein Nrs1 rewires the G1/S transcriptional machinery during nitrogen limitation in budding yeast.PLoS biology · 2022Article
- What programs the size of animal cells?Frontiers in cell and developmental biology · 2022Review
Corrections and comments
- Erratum issued
Authors and funding
13 authors at 4 institutions in 3 countries.
Funding
Abstract
Commitment to cell division at the end of G1 phase, termed Start in the budding yeast Saccharomyces cerevisiae, is strongly influenced by nutrient availability. To identify new dominant activators of Start that might operate under different nutrient conditions, we screened a genome-wide ORF overexpression library for genes that bypass a Start arrest caused by absence of the G1 cyclin Cln3 and the transcriptional activator Bck2. We recovered a hypothetical gene YLR053c, renamed NRS1 for Nitrogen-Responsive Start regulator 1, which encodes a poorly characterized 108 amino acid microprotein. Endogenous Nrs1 was nuclear-localized, restricted to poor nitrogen conditions, induced upon TORC1 inhibition, and cell cycle-regulated with a peak at Start. NRS1 interacted genetically with SWI4 and SWI6, which encode subunits of the main G1/S transcription factor complex SBF. Correspondingly, Nrs1 physically interacted with Swi4 and Swi6 and was localized to G1/S promoter DNA. Nrs1 exhibited inherent transactivation activity, and fusion of Nrs1 to the SBF inhibitor Whi5 was sufficient to suppress other Start defects. Nrs1 appears to be a recently evolved microprotein that rewires the G1/S transcriptional machinery under poor nitrogen conditions.
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Registered trials
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