The bHLH protein MyoR inhibits the differentiation of early embryonic endoderm

Yu, Liming; Sangster, Niquiche; Perez, Ana V.; McCormick, Paulette J.

doi:10.1111/j.1432-0436.2004.07207005.x

Cited by 11 publications

(6 citation statements)

References 28 publications

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“…Expression of the analysed endoderm markers followed trends extensively described in literature, but they are not exclusively expressed by definitive endoderm that still lacks a specific marker not expressed elsewhere (Abe et al, 1996;Hamazaki et al, 2001;Kubo et al, 2004). Nevertheless, the patterns of Sox17 and MyoR point to a limited population of definitive endoderm cells contributing to EBs (Kubo et al, 2004;Yu et al, 2004). In the first part of this study, we confirmed EBs expression of pancreatic markers by quantitative RT-PCR and immunocytochemistry.…”

Section: Discussionsupporting

confidence: 81%

Expression of regulatory genes for pancreas development during murine embryonic stem cell differentiation

Mfopou¹,

Willems²,

Leyns³

et al. 2005

Int. J. Dev. Biol.

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Insulin-producing cells derived from embryonic stem cells could be surrogates for beta cells in diabetes therapy. However, their derivation remains hard to achieve with current protocols which rely on initial embryoid body formation. We assume that factors known to inhibit pancreas development contribute to this limitation in vitro. To evaluate this hypothesis, embryoid bodies were examined after different culture periods by real time RT-PCR to profile the expression of genes known to regulate embryonic pancreas development. Our data indicate that transcripts for pancreas markers (insulin, glucagon and amylase ) were expressed during differentiation, but the highest levels achieved were at least 10 5 times lower than in the adult mouse pancreas. Notch signalling was activated as suggested by Delta, Jagged, Ngn3 and NeuroD1 profiles. However, Sonic hedgehog, a known inhibitor of pancreas induction in vivo drastically increased in day 6 embryoid bodies, while Inhibin βA and βB were down-regulated and follistatin up-regulated. Members of the Fibroblast-and Transforming Growth Factor families which pattern the endoderm were expressed at low levels, while those that inhibit pancreas development were highly transcribed. The profile of pancreas regulators expressed in embryoid bodies is therefore not compatible with differentiation of pancreatic and insulin-producing cells. These findings provide an explanation for the limited derivation of such cells to date, in addition to basic information for establishing novel differentiation protocols.

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Section: Discussionsupporting

confidence: 81%

Expression of regulatory genes for pancreas development during murine embryonic stem cell differentiation

Mfopou¹,

Willems²,

Leyns³

et al. 2005

Int. J. Dev. Biol.

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“…Notably, the two phases of Musculin expressions are functionally different. Moreover, twophase expressions of musculin are also reported in mice model [32,35]. Taken together, our results revealed that the expression patterns of Musculin between mice and Head muscle develops in two distinct populations: branchiomeric and nonbranchiomeric [30,36].…”

Section: Discussionsupporting

confidence: 72%

Essential roles of basic helix-loop-helix transcription factors, Capsulin and Musculin, during craniofacial myogenesis of zebrafish

Lee

Chang

Hsu

et al. 2011

Cell. Mol. Life Sci.

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Capsulin and Musculin are basic helix-loop-helix transcription factors, but their biophysiological roles in zebrafish cranial myogenesis are unclear. Expressions of endogenous capsulin transcripts are detected at the central- (~24-hpf) and at dorsal- and ventral-mesoderm cores (~30-72 hpf) of branchial arches. In contrast, musculin transcripts are expressed as a two-phase manner: early phase (20-22 hpf) expressions of musculin are detected at the head mesoderm, whereas late-phase (36-72 hpf) are detected at all presumptive head-muscle precursors. Knockdown of either capsulin or musculin leads to loss of all cranial muscles without affecting trunk muscle development. The defective phenotypes of Capsulin- and Musculin-morphant can be rescued by co-injection of mRNA of each other. Both myf5 and myod transcripts are down-regulated in the Capsulin-morphant while myod transcripts are up-regulated in the Musculin-morphant. Therefore, we propose a putative regulatory network to understand how capsulin/musculin regulate distinctly either myf5 or myod during zebrafish craniofacial myogenesis.

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“…Transcriptional regulation might occur through the formation of MSC and/or TCF21 homodimers (Eben-Massari et al, 1998) or heterodimers, either with each other or with other factors such as E-proteins, which have been shown to interact with MSC (EbenMassari et al, 1998;Lu et al, 1999) and TCF21 (Lu et al, 1998). MSC has been shown to act as a repressor of the skeletal muscle program in non-myogenic lineages (Yu et al, 2003;Yu et al, 2004). Indeed, MSC strongly represses MYOD-E12 (TCF3 -Mouse Genome Informatics)-mediated activation of an MCKpromoter reporter construct in vitro but fails to activate transcription of the same construct in isolation or in the presence of E12 protein (Lu et al, 1999), suggesting that MSC-E12 competes with MYOD-E12 for the same binding sites or that MSC sequesters the E12 co-activator.…”

Section: Msc and Tcf21 Are Direct Upstream Activators Of Myf5 And Myomentioning

confidence: 99%

Musculin and TCF21 coordinate the maintenance of myogenic regulatory factor expression levels during mouse craniofacial development

et al. 2012

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SUMMARYThe specification of the skeletal muscle lineage during craniofacial development is dependent on the activity of MYF5 and MYOD, two members of the myogenic regulatory factor family. In the absence of MYF5 or MYOD there is not an overt muscle phenotype, whereas in the double Myf5;MyoD knockout branchiomeric myogenic precursors fail to be specified and skeletal muscle is not formed. The transcriptional regulation of Myf5 is controlled by a multitude of regulatory elements acting at different times and anatomical locations, with at least five operating in the branchial arches. By contrast, only two enhancers have been implicated in the regulation of MyoD. In this work, we characterize an enhancer element that drives Myf5 expression in the branchial arches from 9.5 days post-coitum and show that its activity in the context of the entire locus is dependent on two highly conserved E-boxes. These binding sites are required in a subset of Myf5-expressing cells including both progenitors and those which have entered the myogenic pathway. The correct levels of expression of Myf5 and MyoD result from activation by musculin and TCF21 through direct binding to specific enhancers. Consistent with this, we show that in the absence of musculin the timing of activation of Myf5 and MyoD is not affected but the expression levels are significantly reduced. Importantly, normal levels of Myf5 expression are restored at later stages, which might explain the absence of particular muscles in the Msc;Tcf21 double-knockout mice.

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The bHLH protein MyoR inhibits the differentiation of early embryonic endoderm

Cited by 11 publications

References 28 publications

Expression of regulatory genes for pancreas development during murine embryonic stem cell differentiation

Expression of regulatory genes for pancreas development during murine embryonic stem cell differentiation

Essential roles of basic helix-loop-helix transcription factors, Capsulin and Musculin, during craniofacial myogenesis of zebrafish

Musculin and TCF21 coordinate the maintenance of myogenic regulatory factor expression levels during mouse craniofacial development

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