UNC-39, the C. elegans homolog of the human myotonic dystrophy-associated 
homeodomain protein Six5, regulates cell motility and differentiation

Yanowitz, Judith L.; Shakir, M. Afaq; Hedgecock, Edward M.; Hutter, Harald; Fire, Andrew Z.; Lundquist, Erik A.

doi:10.1016/j.ydbio.2004.05.010

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UNC-39, the C. elegans homolog of the human myotonic dystrophy-associated homeodomain protein Six5, regulates cell motility and differentiation

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Hutter, Harald
Max Planck Research Group Developmental Genetics of the nervous system (Harald Hutter), Max Planck Institute for Medical Research, Max Planck Society;

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http://www.sciencedirect.com/science/article/pii/S0012160604003537/pdfft?md5=79262db587b75922c5308b9b744f7da0&pid=1-s2.0-S0012160604003537-main.pdf
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Citation

Yanowitz, J. L., Shakir, M. A., Hedgecock, E. M., Hutter, H., Fire, A. Z., & Lundquist, E. A. (2004). UNC-39, the C. elegans homolog of the human myotonic dystrophy-associated homeodomain protein Six5, regulates cell motility and differentiation. Developmental Biology, 272(2), 389-402. doi:10.1016/j.ydbio.2004.05.010.

Cite as: https://hdl.handle.net/11858/00-001M-0000-002A-627D-B

Abstract

Mutations in the unc-39 gene of C. elegans lead to migration and differentiation defects in a subset of mesodermal and ectodermal cells, including muscles and neurons. Defects include mesodermal specification and differentiation as well a neuronal migration and axon pathfinding defects. Molecular analysis revealed that unc-39 corresponds to the previously named gene ceh-35 and that the UNC-39 protein belongs to the Six4/5 family of homeodomain transcription factors and is similar to human Six5, a protein implicated in the pathogenesis of type I myotonic dystrophy (DM1). We show that human Six5 and UNC-39 are functional homologs, suggesting that further characterization of the C. elegans unc-39 gene might provide insight into the etiology of DM1.