Embryonic hair follicle fate change by augmented β-catenin through Shh and Bmp signaling

Suzuki, Kentaro; Yamaguchi, Yuji; Villacorte, Mylah; Mihara, Kenichiro; Akiyama, Masashi; Shimizu, Hiroshi; Taketo, Makoto Mark; Nakagata, Naomi; Tsukiyama, Tadasuke; Yamaguchi, Terry P.; Birchmeier, Walter; Kato, Shigeaki; Yamada, Gen

doi:10.1242/dev.021295

Cited by 45 publications

(37 citation statements)

References 44 publications

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“…Treatment of vdr Ϫ/Ϫ mice with a Shh agonist transiently restores hair cycling, suggesting that defective Hedgehog signaling contributes to the hair follicle defects in these mice (17). Cross-talk between the Hedgehog and canonical Wnt signaling pathways has been observed in many organ systems, including the epidermis, where activation of the canonical Wnt pathway induces Hedgehog signaling (10,18,19), whereas the absence or inhibition of Wnt signals impairs Hedgehog expression (20,21). Because the unliganded VDR modulates the canonical Wnt signaling pathway in primary keratinocytes and co-immunoprecipitates with LEF1 and ␤-catenin (9), studies were undertaken to examine the molecular interactions of the VDR with effectors of this pathway and to determine the consequences of VDR ablation on the expression of shh and its downstream effector gli1 (22).…”

Section: Thus This Study Demonstrates a Novel Interaction Between Thmentioning

confidence: 99%

Lymphoid Enhancer-binding Factor-1 (LEF1) Interacts with the DNA-binding Domain of the Vitamin D Receptor

Luderer

Gori

Demay

2011

Journal of Biological Chemistry

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Section: Thus This Study Demonstrates a Novel Interaction Between Thmentioning

confidence: 99%

Lymphoid Enhancer-binding Factor-1 (LEF1) Interacts with the DNA-binding Domain of the Vitamin D Receptor

Luderer

Gori

Demay

2011

Journal of Biological Chemistry

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“…In recent years, much has been learned about the signals passed between epithelium and mesenchyme in hair follicle formation and regeneration (Alonso and Fuchs, 2006;Bitgood and McMahon, 1995;Chiang et al, 1999;Lyons et al, 1989;Plikus et al, 2008;Reddy et al, 2001;Suzuki et al, 2009;Wall et al, 1993), but in sensory systems such as the tongue, our understanding is much less complete. Within the lingual epithelium, Wnts, BMPs and SHH are all expressed and participate in taste papilla/bud development (Barlow, 1999;Barlow, 2003;Hall et al, 2003;Hall et al, 1999;Iwatsuki et al, 2007;Jung et al, 1999;Liu et al, 2007;Liu et al, 2004;Okubo et al, 2006;Zhou et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

Follistatin modulates a BMP autoregulatory loop to control the size and patterning of sensory domains in the developing tongue

et al. 2009

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The regenerative capacity of many placode-derived epithelial structures makes them of interest for understanding the molecular control of epithelial stem cells and their niches. Here, we investigate the interaction between the developing epithelium and its surrounding mesenchyme in one such system, the taste papillae and sensory taste buds of the mouse tongue. We identify follistatin (FST) as a mesenchymal factor that controls size, patterning and gustatory cell differentiation in developing taste papillae. FST limits expansion and differentiation of Sox2-expressing taste progenitor cells and negatively regulates the development of taste papillae in the lingual epithelium: in Fst -/-tongue, there is both ectopic development of Sox2-expressing taste progenitors and accelerated differentiation of gustatory cells. Loss of Fst leads to elevated activity and increased expression of epithelial Bmp7; the latter effect is consistent with BMP7 positive autoregulation, a phenomenon we demonstrate directly. We show that FST and BMP7 influence the activity and expression of other signaling systems that play important roles in the development of taste papillae and taste buds. In addition, using computational modeling, we show how aberrations in taste papillae patterning in Fst -/-mice could result from disruption of an FST-BMP7 regulatory circuit that normally suppresses noise in a process based on diffusion-driven instability. Because inactivation of Bmp7 rescues many of the defects observed in Fst -/-tongue, we conclude that interactions between mesenchyme-derived FST and epithelial BMP7 play a central role in the morphogenesis, innervation and maintenance of taste buds and their stem/progenitor cells.

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“…Wnt/β-catenin signaling relayed through Shh and Bmp signals is the principal regulatory mechanism of hair follicle development. 34 Studies in mice showed that follicle morphogenesis and hair growth is altered when Shh is either downregulated [10][11][12] or overexpressed. 35 This pathway is deregulated by knock-out of Gata3 in mice, the animals showing abnormal hair formation.…”

Section: Discussionmentioning

confidence: 99%

The disruption of a novel limb cis-regulatory element of SHH is associated with autosomal dominant preaxial polydactyly-hypertrichosis

et al. 2015

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The expression gradient of the morphogen Sonic Hedgehog (SHH) is crucial in establishing the number and the identity of the digits during anteroposterior patterning of the limb. Its anterior ectopic expression is responsible for preaxial polydactyly (PPD). Most of these malformations are due to the gain-of-function of the Zone of Polarizing Activity Regulatory Sequence, the only limb-specific enhancer of SHH known to date. We report a family affected with a novel condition associating PPD and hypertrichosis of the upper back, following an autosomal dominant mode of inheritance. This phenotype is consistent with deregulation of SHH expression during limb and follicle development. In affected members, we identified a 2 kb deletion located~240 kb upstream from the SHH promoter. The deleted sequence is capable of repressing the transcriptional activity of the SHH promoter in vitro, consistent with a silencer activity. We hypothesize that the deletion of this silencer could be responsible for SHH deregulation during development, leading to a PPD-hypertrichosis phenotype.

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Embryonic hair follicle fate change by augmented β-catenin through Shh and Bmp signaling

Abstract: (ex3)fl/+ BmprIA fl/fl mice. These results indicate the presence of growth factor signal cross-talk involving β-catenin signaling, which regulates the HF fate.

Cited by 45 publications

References 44 publications

Lymphoid Enhancer-binding Factor-1 (LEF1) Interacts with the DNA-binding Domain of the Vitamin D Receptor

Lymphoid Enhancer-binding Factor-1 (LEF1) Interacts with the DNA-binding Domain of the Vitamin D Receptor

Follistatin modulates a BMP autoregulatory loop to control the size and patterning of sensory domains in the developing tongue

The disruption of a novel limb cis-regulatory element of SHH is associated with autosomal dominant preaxial polydactyly-hypertrichosis

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