ArticleGenes & development2009
SMD and NMD are competitive pathways that contribute to myogenesis: effects on PAX3 and myogenin mRNAs.
Article in Genes & development, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 127 papers.
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Who cites it
127 citing papers in PubMed, 191 citations in OpenAlex.
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- FMRP drives mRNP targets into translationally silenced complexes.Molecular cell · 2025Article
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- Role of UPF1-LIN28A interaction during early differentiation of pluripotent stem cells.Nature communications · 2024Article
- Nonsense-mediated mRNA decay, a simplified view of a complex mechanism.BMB reports · 2023Review
- Staufen1 controls mitochondrial metabolism via HIF2α in embryonal rhabdomyosarcoma and promotes tumorigenesis.Cellular and molecular life sciences : CMLS · 2023Article
- Compromised nonsense-mediated RNA decay results in truncated RNA-binding protein production upon DUX4 expression.Cell reports · 2023Article
- The nexus between RNA-binding proteins and their effectors.Nature reviews. Genetics · 2023Review
- UPF1-From mRNA Degradation to Human Disorders.Cells · 2023Review
- A Patient with Corticobasal Syndrome and Progressive Non-Fluent Aphasia (CBS-PNFA), with Variants inGenes · 2022Article
- AKT constitutes a signal-promoted alternative exon-junction complex that regulates nonsense-mediated mRNA decay.Molecular cell · 2022Article
67 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
UPF1 functions in both Staufen 1 (STAU1)-mediated mRNA decay (SMD) and nonsense-mediated mRNA decay (NMD), which we show here are competitive pathways. STAU1- and UPF2-binding sites within UPF1 overlap so that STAU1 and UPF2 binding to UPF1 appear to be mutually exclusive. Furthermore, down-regulating the cellular abundance of STAU1, which inhibits SMD, increases the efficiency of NMD, whereas down-regulating the cellular abundance of UPF2, which inhibits NMD, increases the efficiency of SMD. Competition under physiological conditions is exemplified during the differentiation of C2C12 myoblasts to myotubes: The efficiency of SMD increases and the efficiency of NMD decreases, consistent with our finding that more STAU1 but less UPF2 bind UPF1 in myotubes compared with myoblasts. Moreover, an increase in the cellular level of UPF3X during myogenesis results in an increase in the efficiency of an alternative NMD pathway that, unlike classical NMD, is largely insensitive to UPF2 down-regulation. We discuss the remarkable balance between SMD and the two types of NMD in view of data indicating that PAX3 mRNA is an SMD target whose decay promotes myogenesis whereas myogenin mRNA is a classical NMD target encoding a protein required for myogenesis.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.