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Mef2ca is required in cranial neural crest to effect Endothelin1 signaling in zebrafish.

ABSTRACT: Mef2 genes encode highly conserved transcription factors involved in somitic and cardiac mesoderm development in diverse bilaterians. Vertebrates have multiple mef2 genes. In mice, mef2c is required for heart and vascular development. We show that a zebrafish mef2c gene (mef2ca) is required in cranial neural crest (CNC) for proper head skeletal patterning. mef2ca mutants have head skeletal phenotypes resembling those seen upon partial loss-of-function of endothelin1 (edn1). Furthermore, mef2ca interacts genetically with edn1, arguing that mef2ca functions within the edn1 pathway. mef2ca is expressed in CNC and this expression does not require edn1 signaling. Mosaic analyses reveal that mef2ca is required in CNC for pharyngeal skeletal morphogenesis. Proper expression of many edn1-dependent target genes including hand2, bapx1, and gsc, depends upon mef2ca function. mef2ca plays a critical role in establishing the proper nested expression patterns of dlx genes. dlx5a and dlx6a, known Edn1 targets, are downregulated in mef2ca mutant pharyngeal arch CNC. Surprisingly, dlx4b and dlx3b are oppositely affected in mef2ca mutants. dlx4b expression is abolished while the edn1-dependent dlx3b is ectopically expressed in more dorsal CNC. Together our results support a model in which CNC cells require mef2ca downstream of edn1 signaling for proper craniofacial development.

SUBMITTER: Miller CT

PROVIDER: S-EPMC2148033 | biostudies-literature | 2007 Aug

REPOSITORIES: biostudies-literature

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mef2ca is required in cranial neural crest to effect Endothelin1 signaling in zebrafish.

Miller Craig T CT Swartz Mary E ME Khuu Patricia A PA Walker Macie B MB Eberhart Johann K JK Kimmel Charles B CB

Developmental biology 20070524 1

Mef2 genes encode highly conserved transcription factors involved in somitic and cardiac mesoderm development in diverse bilaterians. Vertebrates have multiple mef2 genes. In mice, mef2c is required for heart and vascular development. We show that a zebrafish mef2c gene (mef2ca) is required in cranial neural crest (CNC) for proper head skeletal patterning. mef2ca mutants have head skeletal phenotypes resembling those seen upon partial loss-of-function of endothelin1 (edn1). Furthermore, mef2ca i ...[more]

PMID: 17574232

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Project description:The neural crest-a key innovation of the vertebrates-gives rise to diverse cell types including melanocytes, neurons and glia of the peripheral nervous system, and chondrocytes of the jaw and skull. Proper development of the cephalic region is dependent on the tightly-regulated specification and migration of cranial neural crest cells (NCCs). The core PCP proteins Frizzled and Disheveled have previously been implicated in NCC migration. Here we investigate the functions of the core PCP proteins Prickle1a and Prickle1b in zebrafish cranial NCC development. Using analysis of pk1a and pk1b mutant embryos, we uncover similar roles for both genes in facilitating cranial NCC migration. Disruption of either gene causes pre-migratory NCCs to cluster together at the dorsal aspect of the neural tube, where they adopt aberrant polarity and movement. Critically, in investigating Pk1-deficient cells that fail to migrate ventrolaterally, we have also uncovered roles for pk1a and pk1b in the epithelial-to-mesenchymal transition (EMT) of pre-migratory NCCs that precedes their collective migration to the periphery. Normally, during EMT, pre-migratory NCCs transition from a neuroepithelial to a bleb-based and subsequently, mesenchymal morphology capable of directed migration. When either Pk1a or Pk1b is disrupted, NCCs continue to perform blebbing behaviors characteristic of pre-migratory cells over extended time periods, indicating a block in a key transition during EMT. Although some Pk1-deficient NCCs transition successfully to mesenchymal, migratory morphologies, they fail to separate from neighboring NCCs. Additionally, Pk1b-deficient NCCs show elevated levels of E-Cadherin and reduced levels of N-Cadherin, suggesting that Prickle1 molecules regulate Cadherin levels to ensure the completion of EMT and the commencement of cranial NCC migration. We conclude that Pk1 plays crucial roles in cranial NCCs both during EMT and migration. These roles are dependent on the regulation of E-Cad and N-Cad.

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Mef2ca is required in cranial neural crest to effect Endothelin1 signaling in zebrafish.

Publications

mef2ca is required in cranial neural crest to effect Endothelin1 signaling in zebrafish.

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