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- W2802953888 endingPage "1621.e15" @default.
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- W2802953888 abstract "Diverse biological systems utilize fluctuations (“noise”) in gene expression to drive lineage-commitment decisions. However, once a commitment is made, noise becomes detrimental to reliable function, and the mechanisms enabling post-commitment noise suppression are unclear. Here, we find that architectural constraints on noise suppression are overcome to stabilize fate commitment. Using single-molecule and time-lapse imaging, we find that—after a noise-driven event—human immunodeficiency virus (HIV) strongly attenuates expression noise through a non-transcriptional negative-feedback circuit. Feedback is established through a serial cascade of post-transcriptional splicing, whereby proteins generated from spliced mRNAs auto-deplete their own precursor unspliced mRNAs. Strikingly, this auto-depletion circuitry minimizes noise to stabilize HIV’s commitment decision, and a noise-suppression molecule promotes stabilization. This feedback mechanism for noise suppression suggests a functional role for delayed splicing in other systems and may represent a generalizable architecture of diverse homeostatic signaling circuits." @default.
- W2802953888 created "2018-05-17" @default.
- W2802953888 creator A5007620652 @default.
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- W2802953888 date "2018-06-01" @default.
- W2802953888 modified "2023-10-15" @default.
- W2802953888 title "A Post-Transcriptional Feedback Mechanism for Noise Suppression and Fate Stabilization" @default.
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- W2802953888 doi "https://doi.org/10.1016/j.cell.2018.04.005" @default.
- W2802953888 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6044448" @default.