期刊
DEVELOPMENTAL CELL
卷 14, 期 4, 页码 616-623出版社
CELL PRESS
DOI: 10.1016/j.devcel.2008.01.009
关键词
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资金
- NHLBI NIH HHS [T32HL69768, R01 HL075256, R21 HL083965, HL075256, R01 HL089641, R21 HL083965-02, R01 HL089641-01A1, T32 HL069768] Funding Source: Medline
The CASTOR (CST) transcription factor was initially identified for its role in maintaining stem cell competence in the Drosophila dorsal midline. Here we report that Xenopus CST affects cardiogenesis. In CST-depleted embryos, cardiomyocytes at the ventral midline arrest and are maintained as cardiac progenitors, while cells in more dorsal regions of the heart undergo their normal program of differentiation. Cardia bifida results from failed midline differentiation, even though cardiac cell migration and initial cell fate specification occur normally. Our fate mapping studies reveal that this ventral midline population of cardiomyocytes ultimately gives rise to the outer curvature of the heart; however, CST-depleted midline cells overproliferate and remain a coherent population of nonintegrated cells positioned on the outer wall of the ventricle. These midline-specific requirements for CST suggest the regulation of cardiomyocyte differentiation is regionalized along a dorsal-ventral axis and that this patterning occurs prior to heart tube formation.
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