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Par6 regulates skeletogenesis and gut differentiation in sea urchin larvae

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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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Acknowledgments

We thank Hideki Katow, Rudolf A. Raff, and Takashi Yamamoto for providing the P4, B2C2 monoclonal antibodies, and sm30 cDNA, respectively. We also thank staff of the Research Center for Marine Biology, Tohoku University, for supplying adult sea urchins. We thank the reviewers whose thoughtful suggestions helped us to improve the manuscript. This study was supported by JSPS KAKENHI nos. 06J00270 and 21570222 to AY and MY, respectively.

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Correspondence to Masaaki Yamaguchi.

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Communicated by H Nishida

Kosuke Shiomi and Atsuko Yamazaki contributed equally to this study.

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Shiomi, K., Yamazaki, A., Kagawa, M. et al. Par6 regulates skeletogenesis and gut differentiation in sea urchin larvae. Dev Genes Evol 222, 269–278 (2012). https://doi.org/10.1007/s00427-012-0409-5

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  • DOI: https://doi.org/10.1007/s00427-012-0409-5

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