The WNT signalling modulator, Wise, is expressed in an interaction-dependent manner during hair-follicle cycling.

We used microarray hybridization to identify genes induced in the dermal papilla (DP) during anagen as a result of the interaction with epithelial matrix cells. We identified inhibitors of the bone morphogenetic protein (BMP) and transforming growth factor beta (TGFbeta)-signalling pathway, as well as the rat homologue of the Xenopus-secreted WNT modulator Wise. A large number of genes previously determined to be expressed in the DP were shown to be expressed in both the DP and dermal sheath (DS). Genes induced in the DP during anagen included modulators of genes expressed additionally in the DS as well as specialized extracellular matrix components. Expression of some of these genes were lost when the DP cells were cultured, suggesting that their expression was interaction dependent. One such gene, the WNT-signalling modulator Wise, was expressed in the DP and not in the non-inductive DS and was additionally expressed at high levels in the precortex and in the putative bulge region. In addition to the reported WNT-signalling modulation role, we show that Wise reduced both BMP and TGFbeta signalling in transformed fibroblasts. We speculate that loss of gene expression in cultured cells is a model for the loss of gene expression observed at catagen.

[1]  B. Morgan,et al.  Wnt signaling through the beta-catenin pathway is sufficient to maintain, but not restore, anagen-phase characteristics of dermal papilla cells. , 2004, The Journal of investigative dermatology.

[2]  Alison Rowe,et al.  Wise, a context-dependent activator and inhibitor of Wnt signalling , 2003, Development.

[3]  I. Weissman,et al.  Wnt proteins are lipid-modified and can act as stem cell growth factors , 2003, Nature.

[4]  E. Fuchs,et al.  Links between signal transduction, transcription and adhesion in epithelial bud development , 2003, Nature.

[5]  S. Dupont,et al.  Mapping Wnt/β-catenin signaling during mouse development and in colorectal tumors , 2003, Proceedings of the National Academy of Sciences of the United States of America.

[6]  D. Fishman,et al.  Periostin secreted by epithelial ovarian carcinoma is a ligand for alpha(V)beta(3) and alpha(V)beta(5) integrins and promotes cell motility. , 2002, Cancer research.

[7]  H. Lodish,et al.  Context-specific Effects of Fibulin-5 (DANCE/EVEC) on Cell Proliferation, Motility, and Invasion , 2002, The Journal of Biological Chemistry.

[8]  W. Birchmeier,et al.  Expression of DeltaNLef1 in mouse epidermis results in differentiation of hair follicles into squamous epidermal cysts and formation of skin tumours. , 2002, Development.

[9]  M. Ridanpää,et al.  Dynamic expression and nuclear accumulation of β-catenin during the development of hair follicle-derived structures , 2001, Mechanisms of Development.

[10]  C. Jahoda,et al.  Hair follicle dermal sheath cells: unsung participants in wound healing , 2001, The Lancet.

[11]  Sarah E. Millar,et al.  Characterization of Wnt gene expression in developing and postnatal hair follicles and identification of Wnt5a as a target of Sonic hedgehog in hair follicle morphogenesis , 2001, Mechanisms of Development.

[12]  W. Birchmeier,et al.  β-Catenin Controls Hair Follicle Morphogenesis and Stem Cell Differentiation in the Skin , 2001, Cell.

[13]  B. Hogan,et al.  Inhibition of Bmp signaling affects growth and differentiation in the anagen hair follicle , 2000, The EMBO journal.

[14]  J. Watson,et al.  Gene expression in rat dermal papilla cells: analysis of 2529 ESTs. , 2000, Genomics.

[15]  R. Burgeson,et al.  Wnt signaling maintains the hair-inducing activity of the dermal papilla. , 2000, Genes & development.

[16]  G. Dotto,et al.  Control of murine hair follicle regression (catagen) by TGF‐β1 in vivo , 2000, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[17]  S. Germain,et al.  Homeodomain and winged-helix transcription factors recruit activated Smads to distinct promoter elements via a common Smad interaction motif. , 2000, Genes & development.

[18]  R. Beddington,et al.  Wnt signaling in Xenopus embryos inhibits bmp4 expression and activates neural development. , 1999, Genes & development.

[19]  E. Fuchs,et al.  Multiple roles for activated LEF/TCF transcription complexes during hair follicle development and differentiation. , 1999, Development.

[20]  Christoph Peters,et al.  Noggin is a mesenchymally derived stimulator of hair-follicle induction , 1999, Nature Cell Biology.

[21]  R. Paus Principles of Hair Cycle Control , 1998, The Journal of dermatology.

[22]  K. Oritani,et al.  Lymphopoiesis and matrix glycoprotein SC1/ECM2. , 1998, Leukemia & lymphoma.

[23]  K. Yoshizato,et al.  Role of hair papilla cells on induction and regeneration processes of hair follicles , 1998, Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society.

[24]  J. Smith,et al.  Establishment of a BMP-4 morphogen gradient by long-range inhibition. , 1998, Developmental biology.

[25]  T. Kealey,et al.  The role of IGF-I in human skin and its appendages: morphogen as well as mitogen? , 1997, The Journal of investigative dermatology.

[26]  A. Mould,et al.  The CUB domains of procollagen C-proteinase enhancer control collagen assembly solely by their effect on procollagen C-proteinase/bone morphogenetic protein-1. , 1997, Matrix biology : journal of the International Society for Matrix Biology.

[27]  B. Hogan,et al.  Failure of ventral body wall closure in mouse embryos lacking a procollagen C-proteinase encoded by Bmp1, a mammalian gene related to Drosophila tolloid. , 1996, Development.

[28]  C. Jahoda,et al.  Hair matrix germinative epidermal cells confer follicle-inducing capabilities on dermal sheath and high passage papilla cells. , 1996, Development.

[29]  T. Sun,et al.  Message of nexin 1, a serine protease inhibitor, is accumulated in the follicular papilla during anagen of the hair cycle. , 1995, Journal of cell science.

[30]  J. Couchman,et al.  Association of versican with dermal matrices and its potential role in hair follicle development and cycling. , 1995, The Journal of investigative dermatology.

[31]  I. Blitz,et al.  Anterior neurectoderm is progressively induced during gastrulation: the role of the Xenopus homeobox gene orthodenticle. , 1995, Development.

[32]  T. Springer,et al.  Cloning from purified high endothelial venule cells of hevin, a close relative of the antiadhesive extracellular matrix protein SPARC. , 1995, Immunity.

[33]  Y. Sasai,et al.  Regulation of neural induction by the Chd and Bmp-4 antagonistic patterning signals in Xenopus , 1995, Nature.

[34]  Y. Sasai,et al.  Xenopus chordin: A novel dorsalizing factor activated by organizer-specific homeobox genes , 1994, Cell.

[35]  K. Miyazono,et al.  Latent transforming growth factor-beta 1 associates to fibroblast extracellular matrix via latent TGF-beta binding protein , 1994, The Journal of cell biology.

[36]  C. Bondy,et al.  Insulin-like growth factor-II and its binding proteins in placental development. , 1992, Endocrinology.

[37]  J. Smith,et al.  Bone morphogenetic protein 4: a ventralizing factor in early Xenopus development. , 1992, Development.

[38]  B. Blumberg,et al.  Organizer-specific homeobox genes in Xenopus laevis embryos. , 1991, Science.

[39]  Josephine C. Adams,et al.  Changes in keratinocyte adhesion during terminal differentiation: Reduction in fibronectin binding precedes α 5 β 1 integrin loss from the cell surface , 1990, Cell.

[40]  T. Sun,et al.  Label-retaining cells reside in the bulge area of pilosebaceous unit: Implications for follicular stem cells, hair cycle, and skin carcinogenesis , 1990, Cell.

[41]  R. Oliver,et al.  Changes in hair growth characteristics following the wounding of vibrissa follicles in the hooded rat. , 1984, Journal of embryology and experimental morphology.

[42]  R. Oliver,et al.  Vibrissa dermal papilla cell aggregative behaviour in vivo and in vitro. , 1984, Journal of embryology and experimental morphology.