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• W2017167688 abstract "In mice, melanocytes survive throughout life only in the hair follicles, disappearing from the interfollicular skin after birth. This situation could be changed simply by the forced expression of melanocyte growth/differentiation /survival factor such as Kitl, HGF or ET3 in the basal layer of the skin (Barsh and Cotsarelis, 2007). Surprisingly, Foxn1, a gene mutated in nude mice and encoding a transcription factor, was found to be important to direct keratinocytes to receive pigmented melanosomes from melanocytes (Weiner et al., 2007). Macroscopic nudity of the nude mouse stems from malformation of the hair shaft, presumably caused by a lack of certain hair keratins; and these coiled, fragile hair shafts fail to pass through the epidermal skin. In this sense, the ‘nude’ mutation is literally misleading, as it gives the impression of a hairless condition. Weiner et al. used the human keratin 5 promoter to direct Foxn1 expression in basal keratinocytes and observed that transgenic mice exhibited ectopic pigmentation of their skin, similar to mice transgenic for Kitl mentioned above. They also observed that the ‘nude’ melanocytes migrated normally to the hair bulb, formed clusters of melanocytes, produced pigment, and transferred the pigment to medullary keratinocytes all as normal, but found that the adjacent cortical keratinocytes were unpigmented. Therefore, during the second hair cycle, nude follicles developed little cortical pigmentation of the hair. Considering the fact that Foxn1 is expressed in differentiating precursors of the hair cortex, the cortical defect is primarily the cause of nude non-melanized hair, suggesting the role of pigment recipient cells to be instructing melanocytes where to place the pigment. In humans, rudimental hair follicles in most parts of the skin are apparently enough to be ‘nude’; but instead, Foxn1 is expressed in normal adult skin including basal and supra-basal keratinocytes to attract melanocytes throughout life. In this sense, Foxn1 might be a key to pigment otherwise colourless epidermal keratinocytes in humans. It should be noted that the human nude phenotype clinically examined did not show any pigment abnormalities (Claudio Pignata, personal communication), implying that some part of the molecular mechanisms is different between human and mouse. An instructive role of keratinocytes in melanocyte development is evident in other reports (Hearing, 2007). Weiner et al. showed that Foxn1 expression-induced FGF2 expression through specific interaction with the FGF2 gene promoter and FGF2 is a possible Fox1 downstream soluble attractant, as supported by the administration of FGF2 function-blocking antibodies to reduce the number of melanocytes in Foxn1 transgenic mice. The process of the transfer of pigment granules from melanocytes to keratinocytes remains mostly a ‘black box’ (Hearing, 2007), and elucidating the machinery for this transportation system must finally be linked with Foxn1 function. Therefore, a search for direct downstream genes of Foxn1 might help to elucidate the components of the transportation system. A recent report described another nude phenotype lacking phospholipase C-δ1 (Nakamura et al., 2008) and this enzyme surely functions downstream of Foxn1. This finding is quite valuable for understanding the molecular mechanisms responsible for the nude phenotype, especially in light of the fact that phospholipase C-δ1 KO mice showed no macroscopic abnormalities of their thymus and whiskers, indicating the possibility that the nude phenotype could selectively be more focused on its hair and pigmentation aspects." @default.
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• W2017167688 date "2008-06-01" @default.
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• W2017167688 title "Colourless side of the nude mutation: Foxn1 and hair pigmentation" @default.
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• W2017167688 doi "https://doi.org/10.1111/j.1755-148x.2008.00464.x" @default.
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