The Zic2 gene directs the formation and function of node cilia to control cardiac situs

Kristen S. Barratt, Hannah C. Glanville-Jones, Ruth M. Arkell*

*Corresponding author for this work

    Research output: Contribution to journalArticlepeer-review

    22 Citations (Scopus)

    Abstract

    Summary: The first molecular herald of organ asymmetry during murine embryogenesis is found at the periphery of the node in early-somite stage embryos. Asymmetric gene expression and calcium accumulation at the node occurs in response to a left-ward flow of extracellular fluid across the node, generated by motile cilia within the pit of the node and likely sensed by immotile cilia in the periphery of the node. The ciliation of node cells is controlled by a cascade of node-restricted transcription factor activity during mid-late gastrulation. Mutation of the murine Zic2 transcription factor is associated with random cardiac situs and a loss of asymmetric gene expression at the early-somite node and in the lateral plate. Zic2 is not expressed in these regions but is transiently expressed in the mid-late gastrula node at the time of ciliogenesis. The cilia of the node are overtly abnormal in Zic2 mutant embryos being dysmorphic and short relative to wild-type littermates. The expression of the Noto, Rfx3, and Foxj1 transcription factors known to regulate ciliogenesis is greatly depleted in the mid-gastrula node of mutants, as is the expression of the Pkd1l1 gene required for cilia function. Zic2 appears to be a component of the gene regulatory network that drives ciliation of node cells during gastrulation. genesis 52:626-635, 2014.

    Original languageEnglish
    Pages (from-to)626-635
    Number of pages10
    JournalGenesis (United States)
    Volume52
    Issue number6
    DOIs
    Publication statusPublished - Jun 2014

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