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CBFbeta is a facultative Runx partner in the sea urchin embryo

Robertson, Anthony J. and Dickey-Sims, Carrie and Ransick, Andrew and Rupp, Dawn E. and McCarthy, John J. and Coffman, James A. (2006) CBFbeta is a facultative Runx partner in the sea urchin embryo. BMC Biology, 4 (4). ISSN 1741-7007. doi:10.1186/1741-7007-4-4.

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Background: Runx proteins are developmentally important metazoan transcription factors that form a heterodimeric complex with the non-homologous protein Core Binding Factor beta (CBFbeta). CBFbeta allosterically enhances Runx DNA binding but does not bind DNA itself. We report the initial characterization of SpCBFbeta, the heterodimeric partner of SpRunt-1 from the sea urchin Stronylocentrotus purpuratus. Results: SpCBFbeta is remarkably similar to its mammalian homologues, and like them it enhances the DNA binding of the Runt domain. SpCBFbeta is entirely of zygotic provenance and its expression is similar that of SpRunt-1, accumulating globally at late blastula stage then later localizing to endoderm and oral ectoderm. Unlike SpRunt-1, however, SpCBFbeta is enriched in the endodermal mid- and hindgut of the pluteus larva, and is not highly expressed in the foregut and ciliated band. We showed previously that morpholino antisense-mediated knockdown of SpRunt-1 leads to differentiation defects, as well as to extensive post-blastula stage apoptosis caused by under-expression of the Runx target gene SpPKC1. In contrast, we show here that knockdown of SpCBFbeta does not negatively impact cell survival or SpPKC1 expression, although it does lead to differentiation defects similar to those associated with SpRunt-1 deficiency. Moreover, SpRunt-1 containing a single amino acid substitution that abolishes its ability to interact with SpCBFbeta retains the ability to rescue cell survival in SpRunt-1 morphant embryos. Chromatin immunoprecipitation shows that while the CyIIIa promoter engages both proteins, the SpPKC1 promoter only engages SpRunt-1. Conclusion: SpCBFbeta is a facultative Runx partner that appears to be required specifically for cell differentiation.

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Additional Information:© 2006 Robertson et al., licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. We thank Dr. Eric Davidson for reviewing this manuscript prior to submission, the four anonymous reviewers for helpful comments that further improved the manuscript, and the Molecular Biology Core of the Stowers Institute for DNA sequencing. This work was funded by the Stowers Institute for Medical Research and by a grant from the NIH (GM070840).
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ID Code:1686
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Deposited On:11 Feb 2006
Last Modified:08 Nov 2021 19:35

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