This study shows that mouse eyelashes offer an excellent in vivo model for the quantitative and qualitative analysis of eyelash morphology, development, growth cycle, exogen and pharmacological modulation. This model will help to elucidate the unknown molecular controls of eyelash growth, and to develop novel drugs to treat eyelash disorders.

inducing fast recruitment of MiTF into the nucleus, to activate transcription of enzymes and proteins related to melanogenesis and, at the same time, prevent MiTF degradation by lowering the level of P-ERK. Thus, the ability of IB-MECA to elevate DOPA oxidase activity, melanin synthesis and cell dendricity is in line with MiTF role in regulating melanin synthesis, melanosome transport and dendricity (23).In skin explants, IB-MECA induced an increase in melanization, when applied topically. Histological data show an increase in deposition of melanin in keratinocytes. A possible clinical application of IB-MECA can be envisaged in the treatment of hypopigmentation disorders. Thus, it may be suggested that the activation of melanocytes located in the peripheral zones of the depigmented areas, as in vitiligo (24), by IB-MECA could increase melanocyte dendricity and melanin deposition into keratinocytes in the hypopigmented lesions of the skin. AcknowledgementsWe thank the late Eliezer Flescher (Tel-Aviv University, Israel) for providing B16F1 melanoma cells and Leonid Mittelman and Alex Barbul (Tel-Aviv University) for their support in confocal and RIC microscopic measurements. Author contributionLea Madi designed and performed the research and wrote the study, Rafi Korenstein designed the research and wrote the study, Bianca RosenbergHaggen designed the ex vivo studies and Abraham Nyska performed the histopathology evaluation. Conflict of interestsLea Madi and Rafi Korenstein are inventors of a patent on modulation of skin pigmentation. Bianca Rosenberg and Abraham Nyska state no conflict of interest. Supporting InformationAdditional Supporting Information may be found in the online version of this article: Figure S1. The effect of IB-MECA on melanogenesis of B16 melanoma cells. Figure S2. The effect of IB-MECA on cAMP level. Figure S3. The effect of IB-MECA and wortmannin on PI3K/AKT signaling pathway. Figure S4. MiTF expression and localization, following exposure of B16 -melanoma cells to IB-MECA. Figure S5. The effect of IB-MECA on DOPA oxidase activity in B16 -melanoma cells. Figure S6. Images of B16 melanoma cells exposed to dual treatment of 10 lM MECA or/and 1 lM PD98059 or each one alone on melanin contents in the cell pellets. Figure S7. Melanosomes average density in skin exposed to IB-MECA.Appendix S1. Materials and methods. D-91054 Erlangen, Germany, Tel.: +49-9131-8534311, Fax: +49-9131-8536597, e-mail: miyuki.tauchi@uk-erlangen.de Abstract: Mammalian target of rapamycin (mTOR) is a central regulator of cell proliferation and survival. There is limited evidence that mTOR influences hair follicles (HFs), which undergo cycles of quiescence (telogen), growth (anagen) and regression (catagen). We sought to investigate whether mTOR, in particular mTOR complex 1 (mTORC1), regulates the hair growth cycle by employing biochemical, immunohistochemical and functional approaches in vivo. Here, we demonstrate that quantitative analysis of mTORC1 kinase activity shows phase-dependent changes, and phosphorylate...