T‐box binding site mediates the dorsal activation of myf‐5 in Xenopus gastrula embryos

T-box transcription factor tbx6 and basic-helix-loop-helix transcription factor pMesogenin1 are reported to be involved in paraxial mesodermal differentiation. To clarify the relationship between these genes in Xenopus laevis, we isolated pMesogenin2, which showed high homology with pMesogenin1. Both pMesogenin1 and 2 appeared to be transcriptional activators and were induced by a hormone-inducible version of Xtbx6 without secondary protein synthesis in animal cap assays. The pMesogenin2 promoter contained three potential T-box binding sites with which Xtbx6 protein was shown to interact, and a reporter gene construct containing these sites was activated by Xtbx6. Xtbx6 knockdown reduced pMesogenin1 and 2 expressions, but not vice versa. Xtbx6 and pMesogenin1 and 2 knockdowns caused similar phenotypic abnormalities including somite malformation and ventral body wall muscle hypoplasia, suggesting that Xtbx6 is a direct regulator of pMesogenin1 and 2, which are both involved in somitogenesis and myogenesis including that of body wall muscle in Xenopus laevis. Developmental Dynamics 237: 3749 -3761, 2008.

Section: Xtbx6 and Pmesogenin1 And 2 Involvement In Somite Formation supporting

confidence: 93%

pMesogenin1 and 2 function directly downstream of Xtbx6 in Xenopus somitogenesis and myogenesis

Tazumi

Yabe

Yokoyama

et al. 2008

“…Tbx1 could also regulate cell survival and proliferation of the myogenic precursors. Arguments to support the hypothesis that Tbx1 may regulate myogenic determination are that, in the cranial meso- derm, Tbx1 is expressed before Myf5 expression and that there are T-box binding sites in the Myf5 promoter, at least one of which has been shown to have some functional significance (Lin et al, 2003, Kelly et al, 2004. Our data showing that there is an increase in the number of myocytes after forced Tbx1 overexpression could also be taken as evidence that Tbx1 is sufficient to drive cells into the myogenic lineage.…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, T-box binding sites have been identified in the Myf5 promoter (Lin et al, 2003;Kelly et al, 2004). To analyze precisely when Tbx1 expression is activated relative to craniofacial muscle differentiation, its onset of expression was compared with that of capsulin, temporally the first marker of craniofacial muscle differentiation, by whole-mount in situ hybridization from stage 7 to 13 embryos.…”

Section: Expression Analysis Of Tbx1 During Craniofacial and Limb Devmentioning

confidence: 99%

“…Arguments for an intrinsic role include data showing that the ascidian T-box gene As-T2 is necessary and sufficient to induce myogenic differentiation and there is a functional T-box binding site in the Xenopus Myf5 promoter (Mitani et al, 2001;Lin et al, 2003). T-box genes have also been implicated in muscle development in C. elegans and sea urchins (Mitani et al, 1999(Mitani et al, , 2001.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Tbx1 regulation of myogenic differentiation in the limb and cranial mesoderm

Dastjerdi

Robson

Walker

et al. 2006

The T-box transcription factor Tbx1 has been implicated in DiGeorge syndrome, the most frequent syndrome due to a chromosomal deletion. Gene inactivation of Tbx1 in mice results in craniofacial and branchial arch defects, including myogenic defects in the first and second branchial arches. A T-box binding site has been identified in the Xenopus Myf5 promoter, and in other species, T-box genes have been implicated in myogenic fate. Here we analyze Tbx1 expression in the developing chick embryo relating its expression to the onset of myogenic differentiation and cellular fate within the craniofacial mesoderm. We show that Tbx1 is expressed before capsulin, the first known marker of branchial arch 1 and 2 muscles. We also show that, as in the mouse, Tbx1 is expressed in endothelial cells, another mesodermal derivative, and, therefore, Tbx1 alone cannot specify the myogenic lineage. In addition, Tbx1 expression was identified in both chick and mouse limb myogenic cells, initially being restricted to the dorsal muscle mass, but in contrast, to the head, here Tbx1 is expressed after the onset of myogenic commitment. Functional studies revealed that loss of Tbx1 function reduces the number of myocytes in the head and limb, whereas increasing Tbx1 activity has the converse effect. Finally, analysis of the Tbx1-mesoderm-specific knockout mouse demonstrated the cell autonomous requirement for Tbx1 during myocyte development in the cranial mesoderm. Developmental Dynamics 236:353-363, 2007.

“…Tbx1 in turn regulates expression of fgf10 and, additionally, in the secondary heart field, fgf8 (Garg et al, 2001;Yamagishi et al, 2003;Roberts et al, 2005). Functional T-box binding sites have been identified in the Xenopus myf5 promoter, suggesting a cellautonomous role (Lin et al, 2003).…”

Section: Molecular Biographies Of Developing Head Musclesmentioning

confidence: 99%

The differentiation and morphogenesis of craniofacial muscles

Noden

Francis‐West

2006

355

358

Unraveling the complex tissue interactions necessary to generate the structural and functional diversity present among craniofacial muscles is challenging. These muscles initiate their development within a mesenchymal population bounded by the brain, pharyngeal endoderm, surface ectoderm, and neural crest cells. This set of spatial relations, and in particular the segmental properties of these adjacent tissues, are unique to the head. Additionally, the lack of early epithelialization in head mesoderm necessitates strategies for generating discrete myogenic foci that may differ from those operating in the trunk. Molecular data indeed indicate dissimilar methods of regulation, yet transplantation studies suggest that some head and trunk myogenic populations are interchangeable. The first goal of this review is to present key features of these diversities, identifying and comparing tissue and molecular interactions regulating myogenesis in the head and trunk. Our second focus is on the diverse morphogenetic movements exhibited by craniofacial muscles. Precursors of tongue muscles partly mimic migrations of appendicular myoblasts, whereas myoblasts destined to form extraocular muscles condense within paraxial mesoderm, then as large cohorts they cross the mesoderm:neural crest interface en route to periocular regions. Branchial muscle precursors exhibit yet another strategy, establishing contacts with neural crest populations before branchial arch formation and maintaining these relations through subsequent stages of morphogenesis. With many of the prerequisite stepping-stones in our knowledge of craniofacial myogenesis now in place, discovering the cellular and molecular interactions necessary to initiate and sustain the differentiation and morphogenesis of these neglected craniofacial muscles is now an attainable goal.