ArticleBMC biology2006
CBFbeta is a facultative Runx partner in the sea urchin embryo.
Article in BMC biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Exploring the crosstalk of immune cells: The impact of dysregulated RUNX family genes in kidney renal clear cell carcinoma.Heliyon · 2024Article
- Muscle Regeneration in Holothurians without the Upregulation of Muscle Genes.International journal of molecular sciences · 2022Article
- Identification of the Transcriptional Regulatory Role of RUNX2 by Network Analysis in Lung Cancer Cells.Biomedicines · 2022Article
- RUNX family: Oncogenes or tumor suppressors (Review).Oncology reports · 2019Review
- The Runx transcriptional co-activator, CBFbeta, is essential for invasion of breast cancer cells.Molecular cancer · 2010Article
- Preliminary study on polymorphism analysis of SpRunt-1 gene by PCR-SSCP in Strongylocentrotus intermedius and its association with growth traits.Molecular biology reports · 2010Article
- Is Runx a linchpin for developmental signaling in metazoans?Journal of cellular biochemistry · 2009Article
- The evolutionary origin of the Runx/CBFbeta transcription factors--studies of the most basal metazoans.BMC evolutionary biology · 2008Article
- Runx expression is mitogenic and mutually linked to Wnt activity in blastula-stage sea urchin embryos.PloS one · 2008Article
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Authors and funding
6 authors.
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Abstract
backgroundRunx 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.
resultsSpCBFbeta 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.
conclusionSpCBFbeta is a facultative Runx partner that appears to be required specifically for cell differentiation.
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