ArticleDevelopment genes and evolution2012
Par6 regulates skeletogenesis and gut differentiation in sea urchin larvae.
Article in Development genes and evolution, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 4 citations in OpenAlex.
- Micromere formation and its evolutionary implications in the sea urchin.Current topics in developmental biology · 2022Article
- Influence of cell polarity on early development of the sea urchin embryo.Developmental dynamics : an official publication of the American Association of Anatomists · 2015Article
- Systems genetic analysis of osteoblast-lineage cells.PLoS genetics · 2012Article
- The small GTPase Arf6 regulates sea urchin morphogenesis.Differentiation; research in biological diversityArticle
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Partitioning-defective (par) genes were originally identified as genes that are essential for the asymmetric division of the Caenorhabditis elegans zygote. Studies have since revealed that the gene products are part of an evolutionarily conserved PAR-atypical protein kinase C system involved in cell polarity in various biological contexts. In this study, we analyzed the function of par6 during sea urchin morphogenesis by morpholino-mediated knockdown and by manipulation swapping of the primary mesenchyme cells (PMCs). Loss of Par6 resulted in defects in skeletogenesis and gut differentiation in larvae. Phenotypic analyses of chimeras constructed by PMC swapping showed that Par6 in non-PMCs is required for differentiation of archenteron into functional gut. In contrast, Par6 in both PMCs and ectodermal cells cooperatively regulates skeletogenesis. We suggest that Par6 in PMCs plays an immediate role in the deposition of biomineral in the syncytial cable, whereas Par6 in ectoderm may stabilize skeletal rods via an unknown signal(s).
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