ArticleGenome biology2015
Loss of function of myosin chaperones triggers Hsf1-mediated transcriptional response in skeletal muscle cells.
Article in Genome biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 33 citations in OpenAlex.
- A Nanos3-containing protein complex can activate RNA translation in primordial germ cells in vivo.EMBO reports · 2026Article
- Hsf1 is essential for proteotoxic stress response in smyd1b-deficient embryos and fish survival under heat shock.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Article
- Expression of Smyd1b_tv1 by Alternative Splicing in Cardiac Muscle is Critical for Sarcomere Organization in Cardiomyocytes and Heart Function.Molecular and cellular biology · 2024Article
- Morphological and Molecular Responses ofInternational journal of molecular sciences · 2022Article
- Multiomic atlas with functional stratification and developmental dynamics of zebrafish cis-regulatory elements.Nature genetics · 2022Article
- Smyd1 is essential for myosin expression and sarcomere organization in craniofacial, extraocular, and cardiac muscles.Journal of genetics and genomics = Yi chuan xue bao · 2021Article
- A systems biology approach reveals neuronal and muscle developmental defects after chronic exposure to ionising radiation in zebrafish.Scientific reports · 2019Article
- Single-Cell RNA Sequencing of Human Embryonic Stem Cell Differentiation Delineates Adverse Effects of Nicotine on Embryonic Development.Stem cell reports · 2019Article
- Myomesin is part of an integrity pathway that responds to sarcomere damage and disease.PloS one · 2019Article
- Semantic Multi-Classifier Systems Identify Predictive Processes in Heart Failure Models across Species.Biomolecules · 2018Article
- Chaperones and the Proteasome System: Regulating the Construction and Demolition of Striated Muscle.International journal of molecular sciences · 2017Review
- Microtome-integrated microscope system for high sensitivity tracking of in-resin fluorescence in blocks and ultrathin sections for correlative microscopy.Scientific reports · 2017Article
- Article
- Dysferlin-mediated phosphatidylserine sorting engages macrophages in sarcolemma repair.Nature communications · 2016Article
- Whole transcriptome data analysis of zebrafish mutants affecting muscle development.Data in brief · 2016Article
- A compact unc45b-promoter drives muscle-specific expression in zebrafish and mouse.Genesis (New York, N.Y. : 2000) · 2016Article
- Gene expression and functional analysis of Aha1a and Aha1b in stress response in zebrafish.Comparative biochemistry and physiology. Part B, Biochemistry & molecular biologyArticle
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMutations in myosin chaperones Unc45b and Hsp90aa1.1 as well as in the Unc45b-binding protein Smyd1b impair formation of myofibrils in skeletal muscle and lead to the accumulation of misfolded myosin. The concomitant transcriptional response involves up-regulation of the three genes encoding these proteins, as well as genes involved in muscle development. The transcriptional up-regulation of unc45b, hsp90aa1.1 and smyd1b is specific to zebrafish mutants with myosin folding defects, and is not triggered in other zebrafish myopathy models.
resultsBy dissecting the promoter of unc45b, we identify a Heat shock factor 1 (Hsf1) binding element as a mediator of unc45b up-regulation in myofibers lacking myosin folding proteins. Loss-of-function of Hsf1 abolishes unc45b up-regulation in mutants with defects in myosin folding.
conclusionsTaken together, our data show that skeletal muscle cells respond to defective myosin chaperones with a complex gene program and suggest that this response is mediated by Hsf1 activation.
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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.