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Human Molecular Genetics Advance Access originally published online on August 1, 2007
Human Molecular Genetics 2007 16(21):2583-2590; doi:10.1093/hmg/ddm210
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© 2007 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Lymphotoxin-ß regulates periderm differentiation during embryonic skin development

Chang-Yi Cui1, Makoto Kunisada1, Diana Esibizione1,2, Sergei I. Grivennikov3, Yulan Piao1, Sergei A. Nedospasov4 and David Schlessinger1,*

1 Laboratory of Genetics, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA, 2 Department of Histology, Embryology and Applied Biology, University of Bologna, Bologna 40126, Italy, 3 Basic Research Laboratory, National Cancer Institute, PO Box B, Frederick, MD 21702, USA and 4 Engelhardt Institute of Molecular Biology, Russian Academy of Sciences, Moscow 119991, Russia

* To whom correspondence should be addressed at: Laboratory of Genetics, National Institute on Aging/NIH 333 Cassell Dr.,Suite 3000, Baltimore, MD 21224, USA. Tel: +1 4105588337; Fax: +1 4105588331; E-mail: schlessingerd{at}grc.nia.nih.gov

Received May 3, 2007; Accepted July 24, 2007

Lymphotoxin-ß (LTß) is a key regulator of immune system development, but also affects late stages in hair development. In addition, high expression of LTß at an early stage in epidermis hinted at a further function in hair follicle induction or epithelial development. We report that hair follicles were normally induced in LTß–/– skin, but the periderm detached from the epidermis earlier, accompanied by premature appearance of keratohyalin granules. Expression profiling revealed dramatic down-regulation of a gene cluster encoding periderm-specific keratin-associated protein 13 and four novel paralogs in LTß–/– skin prior to periderm detachment. Epidermal differentiation markers, including small proline-rich proteins, filaggrins and several keratins, were also affected, but transiently in LTß–/– skin at the time of abnormal periderm detachment. As expected, Tabby mice, which lack the EDA gene, the putative upstream regulator of LTß in skin, showed similar though milder periderm histopathology and alterations in gene expression. Overall, LTß shows a primary early function in periderm differentiation, with later transient effects on epidermal and hair follicle differentiation.


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