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First published online August 10, 2007

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Network deployments for developmental plasticity

Cell fates in sea urchin embryos are remarkably labile. For example, mesodermal lineages can activate the transcriptional gene regulatory network (GRN) that drives skeletogenesis if the micromere precursors of the primary mesenchyme cells (PMCs, the cells that form the embryonic skeleton) are removed. To determine the molecular basis of this plasticity, Ettensohn and colleagues have examined the conversion of non-skeletogenic mesoderm (NSM) to a PMC fate during gastrulation and reveal that most, but not all, of the upstream transcription factors in the skeletogenic GRN are recapitulated by transfating cells (see p. 3077). They show that the transcription factor alx1, a key component of the skeletogenic GRN, is expressed in transfating NSMs, that alx1 expression in transfating NSMs and in PMCs requires MAPK signalling, and that alx1 expression in micromeres normally suppresses NSMs from transfating. However, the transcription factor pmar1 (which activates the skeletogenic GRN in PMCs) is not needed in transfating NSMs. Thus, the skeletogenic GRN is activated by distinct mechanisms during normal and regulative development.

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Related articles in Development:

Gene regulatory networks and developmental plasticity in the early sea urchin embryo: alternative deployment of the skeletogenic gene regulatory network

Charles A. Ettensohn, Chisato Kitazawa, Melani S. Cheers, Jennifer D. Leonard, and Tara Sharma
Development 2007 134: 3077-3087. [Abstract] [Full Text]  

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in Development Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content Social Bookmarking                         What's this?