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Published online 1 May 2006. doi:10.1083/jcb.200509084
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 173, Number 3, 333-339
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 Notch signaling via Hes1 transcription factor maintains survival of melanoblasts and melanocyte stem cells

Mariko Moriyama1, Masatake Osawa1, Siu-Shan Mak1, Toshiyuki Ohtsuka2, Norio Yamamoto3, Hua Han4, Véronique Delmas5, Ryoichiro Kageyama2, Friedrich Beermann6, Lionel Larue5, and Shin-Ichi Nishikawa1

1 Laboratory for Stem Cell Biology, RIKEN Center for Developmental Biology, Hyogo 650-0047, Japan
2 Institute for Virus Research, Kyoto University, Kyoto 606-8507, Japan
3 National Institute on Deafness and Other Communication Disorders, National Institutes of Health, Porter Neuroscience Research Center, Bethesda, MD 20892
4 Department of Medical Genetics and Developmental Biology, Fourth Military Medical University, Xian 710032, China
5 Developmental Genetics of Melanocytes, Centre National de la Recherche Scientifique UMR146, Institut Curie, 91405 Orsay, France
6 Swiss Institute for Experimental Cancer Research, CH-1066 Epalinges, Switzerland

Correspondence to Masatake Osawa: mosawa{at}cdb.riken.jp

Melanoblasts (Mbs) are thought to be strictly regulated by cell–cell interactions with epidermal keratinocytes, although the precise molecular mechanism of the regulation has been elusive. Notch signaling, whose activation is mediated by cell–cell interactions, is implicated in a broad range of developmental processes. We demonstrate the vital role of Notch signaling in the maintenance of Mbs, as well as melanocyte stem cells (MSCs). Conditional ablation of Notch signaling in the melanocyte lineage leads to a severe defect in hair pigmentation, followed by intensive hair graying. The defect is caused by a dramatic elimination of Mbs and MSCs. Furthermore, targeted overexpression of Hes1 is sufficient to protect Mbs from the elimination by apoptosis. Thus, these data provide evidence that Notch signaling, acting through Hes1, plays a crucial role in the survival of immature Mbs by preventing initiation of apoptosis.

Abbreviations used in this paper: d2EGFP, destabilized EGFP; DAPT, (3,5-difluorophenylacetyl)-L-alanyl-L-2-phenylglycine t-butyl ester; Dct, dopachrome tautomerase; E, embryonic day; HF, hair follicle; HM, hair matrix; LPP, lower permanent portion; Mb, melanoblast; MC, melanocyte; MSC, melanocyte stem cell; NICD, Notch intracellular domain; P, postnatal day; Q-PCR, quantitative PCR; Tg, transgenic; Tyr, tyrosinase.


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