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Human Molecular Genetics Advance Access published online on March 6, 2009
Human Molecular Genetics, doi:10.1093/hmg/ddp089
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Published by Oxford University Press 2009

Requirement for Shh and Fox family genes at different stages in sweat gland development

Makoto Kunisada, Chang-Yi Cui*, Yulan Piao, Minoru S.H. Ko and David Schlessinger

Laboratory of Genetics, National Institute on Aging, National Institutes of Health, NIH Biomedical Research Center, Baltimore MD 21224, USA

* Corresponding author: Chang-Yi Cui, MD/PhD, Laboratory of Genetics, National Institute on Aging, 251 Bayview Boulevard, Suite 100, Baltimore, Maryland 21224, USA Tel: +1 4105588129; Fax: +1 4105588331; Email: CuiC{at}grc.nia.nih.gov

Received December 12, 2008; Revised February 20, 2009; Accepted February 20, 2009

Sweat glands play a fundamental role in thermal regulation in man, but the molecular mechanism of their development remains unknown. To initiate analyses, we compared the model of Eda mutant Tabby mice, in which sweat glands were not formed, to wild-type mice. We inferred developmental stages and critical genes based on observations at 7 time points spanning embryonic, postnatal and adult life. In wild-type footpads, sweat gland germs were detected at E17.5. The coiling of secretory portions started at postnatal day 1 (P1), and sweat gland formation was essentially complete by P5. Consistent with a controlled morphological progression, expression profiling revealed stage-specific gene expression changes. Similar to the development of hair follicles – the other major skin appendage controlled by EDA – sweat gland induction and initial progression was accompanied by Eda-dependent up-regulation of the Shh pathway. During the further development of sweat gland secretory portions, Foxa1 and Foxi1, not at all expressed in hair follicles, were progressively up-regulated in wild-type but not in Tabby footpads. Upon completion of wild-type development, Shh declined to Tabby levels, but Fox family genes remained at elevated levels in mature sweat glands. The results provide a framework for the further analysis of phased downstream regulation of gene action, possibly by a signaling cascade, in response to Eda.


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