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Open Access Research article

CBFβ is a facultative Runx partner in the sea urchin embryo

Anthony J Robertson12, Carrie Dickey-Sims1, Andrew Ransick3, Dawn E Rupp1, John J McCarthy14 and James A Coffman12*

Author Affiliations

1 Stowers Institute for Medical Research, 1000 E. 50th Street, Kansas City, MO 64110, USA

2 Mount Desert Island Biological Laboratory, PO Box 35, Salisbury Cove, ME 04672, USA

3 Division of Biology 156-29, California Institute of Technology, Pasadena, CA 91125, USA

4 Department of Physiology, University of Kentucky College of Medicine, Lexington, Kentucky, 40506, USA

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BMC Biology 2006, 4:4  doi:10.1186/1741-7007-4-4

Published: 9 February 2006

Abstract

Background

Runx proteins are developmentally important metazoan transcription factors that form a heterodimeric complex with the non-homologous protein Core Binding Factor β (CBFβ). CBFβ allosterically enhances Runx DNA binding but does not bind DNA itself. We report the initial characterization of SpCBFβ, the heterodimeric partner of SpRunt-1 from the sea urchin Stronylocentrotus purpuratus.

Results

SpCBFβ is remarkably similar to its mammalian homologues, and like them it enhances the DNA binding of the Runt domain. SpCBFβ 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, SpCBFβ 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 SpCBFβ 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 SpCBFβ 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

SpCBFβ is a facultative Runx partner that appears to be required specifically for cell differentiation.