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First published online 5 March 2008
doi: 10.1242/dev.017624

Development 135, 1463-1470 (2008)
Published by The Company of Biologists 2008
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Six2 functions redundantly immediately downstream of Hoxa2

Eva Kutejova1, Bettina Engist1, Michelle Self2, Guillermo Oliver2, Pavel Kirilenko3 and Nicoletta Bobola1,3,*

1 Department of Developmental Biology, Max-Planck Institute of Immunobiology, Freiburg, Germany.
2 Department of Genetics and Tumor Cell Biology, St Jude Children's Research Hospital, Memphis, TN, USA.
3 Faculty of Human and Medical Sciences, Stopford Building, The University of Manchester, Manchester M13 9PT, UK.

* Author for correspondence (e-mail: Nicoletta.Bobola{at}manchester.ac.uk)

Accepted 25 February 2008

Hox transcription factors control morphogenesis along the head-tail axis of bilaterians. Because their direct functional targets are still poorly understood in vertebrates, it remains unclear how the positional information encoded by Hox genes is translated into morphogenetic changes. Here, we conclusively demonstrate that Six2 is a direct downstream target of Hoxa2 in vivo and show that the ectopic expression of Six2, observed in the absence of Hoxa2, contributes to the Hoxa2 mouse mutant phenotype. We propose that Six2 acts to mediate Hoxa2 control over the insulin-like growth factor pathway during branchial arch development.

Key words: Six2, Hoxa2, Branchial arch, Mouse






© The Company of Biologists Ltd 2008