5 Multiple Tissue Interactions and Signal Transduction Pathways Control Somite Myogenesis

Borycki, Anne‐Gaëlle; Emerson, Charles P.

doi:10.1016/s0070-2153(08)60757-7

Cited by 83 publications

(61 citation statements)

References 242 publications

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“…Interestingly, this has been correlated with an increased rate of apoptosis in neural tissues (Phelan et al, 1997) suggesting that inhibition of apoptosis by Pax-3 might be an important feature for the survival of cells in embryogenesis. Indeed, recent antisense experiments on explanted mesoderm cultures, using the same oligonucleotides developed for our studies (Bernasconi et al, 1996), con®rm that downregulation of Pax-3 results in increased apoptosis in vivo (Borycki et al, 1999). Embryos which are defective for Bcl-xl show embryonic lethality around day 13 of development with characterized defects in neuronal cells and lymphocytes (Motoyama et al, 1995).…”

Section: Discussionmentioning

confidence: 67%

Transcriptional modulation of the anti-apoptotic protein BCL-XL by the paired box transcription factors PAX3 and PAX3/FKHR

et al. 2000

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The aberrant expression of the transcription factors PAX3 and PAX3/FKHR associated with rhabdomyosarcoma (RMS), solid tumors displaying muscle cell features, suggests that these proteins play an important role in the pathogenesis of RMS. We could previously demonstrate that one of the oncogenic functions of PAX3 and PAX3/FKHR in RMS is protection from apoptosis. BCL-XL is a prominent anti-apoptotic protein present in normal skeletal muscle and RMS cells. In the present study, we establish that BCL-XL is transcriptionally modulated by PAX3 and PAX3/FKHR, since enhanced expression of both PAX proteins stimulates transcription of endogenous BCL-XL mRNA in a cell type speci®c manner. Further, we present evidence that both PAX3 and PAX3/FKHR can transcriptionally activate the Bcl-x gene promoter in cotransfection assays. Using electrophoretic mobility shift assays, an ATTA binding site for PAX3 and PAX3/FKHR could be localized in the upstream promoter region (position 742 to 739). Finally, ectopic overexpression of either PAX3, PAX3/FKHR or BCL-XL can rescue tumor cells from apoptosis induced by antisense treatment. These results suggest that at least part of the anti-apoptotic e ect of PAX3 and PAX3/FKHR is mediated through direct transcriptional modulation of the prominent antiapoptotic protein BCL-XL.

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Section: Discussionmentioning

confidence: 67%

Transcriptional modulation of the anti-apoptotic protein BCL-XL by the paired box transcription factors PAX3 and PAX3/FKHR

et al. 2000

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“…Some Wnts induce the expression of the intrasomitic transcriptional modulators of Shh signaling, e.g., Gli 2 and -3, in the medial somite compartment. This allows amplification/maintenance of the committed myoblasts (Borycki and Emerson, 2000).…”

Section: Overview Of Axial Muscle Differentiationmentioning

confidence: 99%

The differentiation and morphogenesis of craniofacial muscles

Noden

Francis‐West

2006

Developmental Dynamics

355

358

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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.

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“…This was unexpected, as several studies have suggested that PAX gene function is redundant to the concurrent expression of other PAX family members (Mansouri and Gruss, 1998;Bouchard et al, 2000). In contrast, crossregulation and evidence for hierarchical regulation of PAX genes during development (Pfeffer et al, 1998;Borycki et al, 1999) may explain the nonredundant effects of silencing PAX2 expression.…”

Section: Pax Genes Are Frequently Expressed In Cancermentioning

confidence: 99%

“…In affected mutant tissues, dysmorphogenesis is associated with increased apoptosis in cells that normally express the PAX gene (Borycki et al, 1999;Ostrom et al, 2000;Porteous et al, 2000;Torban et al, 2000;van Raamsdonk and Tilghman, 2000). Conversely, deregulated expression of PAX2 blocks caspase 2-induced apoptosis in HEK293 cells, suggesting a role for PAX2 in cell survival.…”

Section: Introductionmentioning

confidence: 99%

Paired-Box genes are frequently expressed in cancer and often required for cancer cell survival

et al. 2003

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The paired-box (PAX) genes encode a family of nine wellcharacterized paired-box transcription factors, with important roles in development and disease. Although PAX genes are primarily expressed in the embryo, constitutive expression promotes tissue hyperplasia. Rare tumorspecific mutations of PAX genes implicate an oncogenic role, and persistent PAX expression characterizes several tumors. Yet, a cancer-wide analysis of PAX gene expression to investigate a general role for PAX genes has not been performed. We analysed the pattern and requirement for PAX gene expression in a panel of common cancer cell lines. Very frequent PAX gene expression was identified in tumor cell lines, including lymphoma, breast, ovarian, lung, and colon cancer. In addition, the PAX2 gene was frequently expressed in a panel of 406 common primary tumor tissues. Apoptosis was rapidly induced in ovarian and bladder cancer cell lines following RNA interference to silence PAX2 expression, despite concomitant TP53 and/or HRAS mutations. These data suggest that PAX genes are frequently expressed in cancer, and that endogenous PAX gene expression is required for the growth and survival of cancer cells.

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5 Multiple Tissue Interactions and Signal Transduction Pathways Control Somite Myogenesis

Cited by 83 publications

References 242 publications

Transcriptional modulation of the anti-apoptotic protein BCL-XL by the paired box transcription factors PAX3 and PAX3/FKHR

Transcriptional modulation of the anti-apoptotic protein BCL-XL by the paired box transcription factors PAX3 and PAX3/FKHR

The differentiation and morphogenesis of craniofacial muscles

Paired-Box genes are frequently expressed in cancer and often required for cancer cell survival

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