Endoplasmic reticulum stress signaling transmitted by ATF6 mediates apoptosis during muscle development

Nakanishi, Kazuyoshi; Sudo, Tatsuhiko; Morishima, Nobuhiro

doi:10.1083/jcb.200412024

Cited by 195 publications

(231 citation statements)

References 23 publications

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“…130,131 The functional importance of JNK activation in the ER stress pathway has not been fully explored, but ASK1 À/À cells are partially resistant to ER stress-induced apoptosis, 132 suggesting that JNK may promote apoptosis in this context. A recent report also indicates that ATF6 might mediate a proapoptotic signal during normal myoblast development, 133 implicating this upstream UPR sentinel in apoptotic pathways as well.…”

Section: Esr and Apoptosismentioning

confidence: 96%

Cellular response to endoplasmic reticulum stress: a matter of life or death

2006

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The proper functioning of the endoplasmic reticulum (ER) is critical for numerous aspects of cell physiology. Accordingly, all eukaryotes react rapidly to ER dysfunction through a set of adaptive pathways known collectively as the ER stress response (ESR). Normally, this suite of responses succeeds in restoring ER homeostasis. However, in metazoans, persistent or intense ER stress can also trigger programmed cell death, or apoptosis. ER stress and the apoptotic program coupled to it have been implicated in many important pathologies but the regulation and execution of ER stressinduced apoptosis in mammals remain incompletely understood. Here, we review what is known about the ESR in both yeast and mammals, and highlight recent findings on the mechanism and pathophysiological importance of ER stressinduced apoptosis.

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Section: Esr and Apoptosismentioning

confidence: 96%

Cellular response to endoplasmic reticulum stress: a matter of life or death

2006

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“…11,12,24,25 During myogenesis in vitro, as many as 50% of myoblasts reportedly undergo apoptosis, 9,10,15 although the extent of cell death likely depends on origin of the myoblasts and the culture conditions used for each study. Myoblasts may undergo apoptosis during myogenesis as a means of regulating muscle size.…”

Section: Discussionmentioning

confidence: 99%

“…14 Caspase-12 is also activated during muscle differentiation, and has been implicated in the initiation of apoptosis that occurs during myogenesis. 15 Activated caspases are inhibited by the IAP family of proteins, thus the IAPs serve as a shield to the final execution of apoptosis. 17 Expression levels of IAPs are dynamic, and can be regulated at the transcriptional, post-transcriptional, and post-translational levels.…”

Section: Discussionmentioning

confidence: 99%

“…[9][10][11][12][13] Interestingly, signaling pathways required for the initiation and execution of programmed cell death, or apoptosis, are activated during myogenesis. 10,[14][15][16] For example, the cysteine protease caspase 3 is not only activated during myogenesis, but also its activity is required for the initiation of myogenic differentiation. 14 The mechanism by which the majority of muscle cells undergoes caspasedependent differentiation but escapes caspase-induced apoptosis is not clear.…”

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confidence: 99%

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Prostaglandin F2α promotes muscle cell survival and growth through upregulation of the inhibitor of apoptosis protein BRUCE

Jansen

Pavlath

2008

Cell Death Differ

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During skeletal muscle growth and regeneration, the majority of differentiating myoblasts undergoes cell-cell fusion to form multinucleated myofibers, whereas a proportion of myoblasts undergoes apoptosis. The treatment of myoblasts with prostaglandin F2a (PGF2a) during myogenesis in vitro leads to the formation of large myotubes, but the mechanism by which PGF2a promotes myotube growth has not been investigated. Here, we demonstrate that PGF2a reduces cell death during myogenesis in vitro and in vivo. In addition, we show that PGF2a increases expression of the inhibitor of apoptosis protein (IAP) BRUCE through a pathway dependent on the nuclear factor of activated T cell 2 transcription factor. Importantly, PGF2a-mediated reduction in muscle cell death is dependent on BRUCE, and overexpression of BRUCE is sufficient to promote muscle cell survival and growth. These results establish a previously unrecognized link between NFAT signaling and regulation of IAP expression and are the first to identify a signaling pathway that increases BRUCE expression. In addition, our results provide evidence that increasing the pool of muscle cells available for fusion by inhibiting cell death enhances myotube growth.

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“…[18][19][20] ER stress activates IRE1 that splices the Xbp1 mRNA generating an isoform encoding the XBP1 transcription factor. 21,22 Quantification of the mRNA-seq reads that cover the splice junctions in exon 4 of the Xbp1 mRNA in the ShSC, ShA and ShB cells showed that around half the Xbp1 mRNA was spliced in the ShSC cells, but not in TEAD4 knockdown cells (Supplementary Figure 5A).…”

mentioning

confidence: 99%

Transcription factor TEAD4 regulates expression of Myogenin and the unfolded protein response genes during C2C12 cell differentiation

Benhaddou

Keime

et al. 2011

Cell Death Differ

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The TEAD (1-4) transcription factors comprise the conserved TEA/ATTS DNA-binding domain recognising the MCAT element in the promoters of muscle-specific genes. Despite extensive genetic analysis, the function of TEAD factors in muscle differentiation has proved elusive due to redundancy among the family members. Expression of the TEA/ATTS DNA-binding domain that acts as a dominant negative repressor of TEAD factors in C2C12 myoblasts inhibits their differentiation, whereas selective shRNA knockdown of TEAD4 results in abnormal differentiation characterised by the formation of shortened myotubes. Chromatin immunoprecipitation coupled to array hybridisation shows that TEAD4 occupies 867 promoters including those of myogenic miRNAs. We show that TEAD factors directly induce Myogenin, CDKN1A and Caveolin 3 expression to promote myoblast differentiation. RNA-seq identifies a set of genes whose expression is strongly reduced upon TEAD4 knockdown among which are structural and regulatory proteins and those required for the unfolded protein response. In contrast, TEAD4 represses expression of the growth factor CTGF (connective tissue growth factor) to promote differentiation. Together these results show that TEAD factor activity is essential for normal C2C12 cell differentiation and suggest a role for TEAD4 in regulating expression of the unfolded protein response genes. The TEAD transcription factors make a highly conserved family of 4 DNA-binding proteins 1,2 containing the TEA (Yeast (TEC-1), Aspergillus nidulans (AbaA) and Drosophilla (scalloped))/ATTS (Aspergillus nidulans (AbaA), Yeast (TEC-1), human TEF1, and Drosophilla (scalloped)) DNA-binding domain (DBD). 3,4 The TEA domain comprises a three-helix bundle with a homeodomain fold and binds a consensus MCAT (5 0 -CATTCCA/ T-3 0 ) element originally defined as the GT-II motif of the simian virus 40 (SV40) enhancer. 5 Mammalian TEADs are widely expressed with prominent expression in the nervous system and muscle. In-vitro, cell-based, knockout and transgenic studies have addressed the role of TEAD factors in regulation of muscle-expressed genes. 6-8 Cardiac troponin T, myosin, heavy polypeptide 7, cardiac muscle, beta (b-MHC) and Myocardin, have functional MCAT motifs in their regulatory regions. 2 Stimulation of a1-adrenergic signalling has been shown to induce cardiac hypertrophy and activate transcription of the b-MHC and skeletal a-actin genes in an MCAT-and TEAD-dependent manner in cultured neonatal rat cardiomyocytes. 9 Cardiac muscle-specific overexpression of TEAD4 in transgenic mice has been shown to induce arhythmias in vivo. 8 TEAD4 is specifically expressed in developing skeletal muscle in mouse embryos. 1 Chromatin immunoprecipitation-array hybridization (ChIP-chip) showed that TEAD4 is a direct target of the MYOD1 and MYOG transcription factors in C2C12 cells. 10 Although TEAD4 upregulation by MYOD1 and MYOG during differentiation is thought to activate transcription of muscle structural genes, mouse knockouts do not show any evident role for TEAD4 i...

show abstract

Endoplasmic reticulum stress signaling transmitted by ATF6 mediates apoptosis during muscle development

Cited by 195 publications

References 23 publications

Cellular response to endoplasmic reticulum stress: a matter of life or death

Cellular response to endoplasmic reticulum stress: a matter of life or death

Prostaglandin F2α promotes muscle cell survival and growth through upregulation of the inhibitor of apoptosis protein BRUCE

Transcription factor TEAD4 regulates expression of Myogenin and the unfolded protein response genes during C2C12 cell differentiation

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