1: Dev Biol. 2001 Nov 15;239(2):270-80. 

Hypaxial muscle migration during primary myogenesis in Xenopus laevis.

Martin BL, Harland RM.

Department of Molecular and Cell Biology, University of California, Berkeley,
California 94720-3202, USA.

In contrast to many vertebrates, the ventral body wall muscles and limb muscles
of Xenopus develop at different times. The ventral body wall forms in the
tadpole, while limb (appendicular) muscles form during metamorphosis to the
adult frog. In organisms that have been examined thus far, a conserved mechanism
has been shown to control migratory muscle precursor specification, migration,
and differentiation. Here, we show that the process of ventral body wall
formation in Xenopus laevis is similar to hypaxial muscle development in
chickens and mice. Cells specified for the migratory lineage display an
upregulation of pax3 in the ventro-lateral region of the somite. These
pax3-positive cells migrate ventrally, away from the somite, and undergo
terminal differentiation with the expression of myf-5, followed by myoD. Several
other genes are selectively expressed in the migrating muscle precursor
population, including neural cell adhesion molecule (NCAM), Xenopus kit related
kinase (Xkrk1), and Xenopus SRY box 5 (sox5). We have also found that muscle
precursor migration is highly coordinated with the migration of neural
crest-derived melanophores. However, by extirpating neural crest at an early
stage and allowing embryos to develop, we determined that muscle precursor
migration is not dependent on physical or genetic interaction with melanophores.
Copyright 2001 Academic Press.

PMID: 11784034 [PubMed - indexed for MEDLINE]


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2: J Biol Chem. 2000 Oct 6;275(40):30757-60. 

Regulation of the microphthalmia-associated transcription factor gene by the
Waardenburg syndrome type 4 gene, SOX10.

Verastegui C, Bille K, Ortonne JP, Ballotti R.

INSERM U385, Biologie et Physiopathologie de la Peau, Faculte de Medecine,
Avenue de Valombrose, Nice, 06107 Cedex, France.

The absence of melanocytes from the cochlea and epidermis is responsible of
deafness and hypopigmentation, two symptoms shared by the four Waardenburg
syndrome (WS) subtypes. Microphthalmia-associated transcription factor (MITF)
controls melanocyte survival and differentiation. Mutations, which impair MITF
function or expression, result in an abnormal melanocyte development leading to
the WS2. WS1 and WS3 are caused by mutation in the gene encoding the
transcription factor Pax3, which regulates MITF expression. Recently, mutations
in SOX10, a gene encoding a SRY-related transcription factor, have been reported
in patients with WS4. However, the molecular basis of the defective melanocyte
development in these patients remained to be elucidated. In the present report,
we demonstrate that Sox10 is a strong activator of the MITF promoter, and we
identify a Sox10 binding site between -264 and -266 of the MITF promoter.
Finally, we show that three SOX10 mutations found in WS4 abolish the
transcriptional activity of the resulting Sox10 proteins toward the MITF
promoter. Taken together, our observations bring new and meaningful information
concerning the molecular process that leads to a defective melanocyte
development in WS4 patients with SOX10 mutations.

PMID: 10938265 [PubMed - indexed for MEDLINE]


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3: J Neurosci. 1998 Jan 1;18(1):237-50. 

Sox10, a novel transcriptional modulator in glial cells.

Kuhlbrodt K, Herbarth B, Sock E, Hermans-Borgmeyer I, Wegner M.

Zentrum fur Molekulare Neurobiologie, Universitat Hamburg, D-20246 Hamburg,
Germany.

Sox proteins are characterized by possession of a DNA-binding domain with
similarity to the high-mobility group domain of the sex determining factor SRY.
Here, we report on Sox10, a novel protein with predominant expression in glial
cells of the nervous system. During development Sox10 first appeared in the
forming neural crest and continued to be expressed as these cells contributed to
the forming PNS and finally differentiated into Schwann cells. In the CNS, Sox10
transcripts were originally confined to glial precursors and later detected in
oligodendrocytes of the adult brain. Functional studies failed to reveal
autonomous transcriptional activity for Sox10. Instead, Sox10 functioned
synergistically with the POU domain protein Tst-1/Oct6/SCIP with which it is
coexpressed during certain stages of Schwann cell development. Synergy depended
on binding to adjacent sites in target promoters, was mediated by the N-terminal
regions of both proteins, and could not be observed between Sox10 and several
other POU domain proteins. Interestingly, Sox10 also modulated the function of
Pax3 and Krox-20, two other transcription factors involved in Schwann cell
development. We propose a role for Sox10 in conferring cell specificity to the
function of other transcription factors in developing and mature glia.

PMID: 9412504 [PubMed - indexed for MEDLINE]


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