β-Catenin Controls Hair Follicle Morphogenesis and Stem Cell Differentiation in the Skin

Huelsken, Joerg; Vogel, Regina; Erdmann, Bettina; Cotsarelis, George; Birchmeier, Walter

doi:10.1016/s0092-8674(01)00336-1

Cited by 1,233 publications

(1,209 citation statements)

References 88 publications

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“…Likewise, keratinocyte-specific β-catenin deletion did not result in epidermal and oral fusions. 47 This suggests that in addition to Wnt/β-catenin signaling, RIPK4 has to exert additional functions.…”

Section: G H and I)mentioning

confidence: 99%

A novel RIPK4–IRF6 connection is required to prevent epithelial fusions characteristic for popliteal pterygium syndromes

et al. 2014

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Receptor-interacting protein kinase 4 (RIPK4)-deficient mice have epidermal defects and fusion of all external orifices. These are similar to Bartsocas-Papas syndrome and popliteal pterygium syndrome (PPS) in humans, for which causative mutations have been documented in the RIPK4 and IRF6 (interferon regulatory factor 6) gene, respectively. Although genetically distinct, these syndromes share the anomalies of marked pterygia, syndactyly, clefting and hypoplastic genitalia. Despite the strong resemblance of these two syndromes, no molecular connection between the transcription factor IRF6 and the kinase RIPK4 was known and the mechanism underlying the phenotype was unclear. Here we describe that RIPK4 deficiency in mice causes epithelial fusions associated with abnormal periderm development and aberrant ectopic localization of E-cadherin on the apical membrane of the outer peridermal cell layers. In Xenopus, RIPK4 depletion causes the absence of ectodermal epiboly and concomitant gastrulation defects that phenocopy ectopic expression of dominant-negative IRF6. We found that IRF6 controls RIPK4 expression and that wild-type, but not kinase-dead, RIPK4 can complement the gastrulation defect in Xenopus caused by IRF6 malfunctioning. In contrast to the mouse, we observed only minor effects on cadherin membrane expression in Xenopus RIPK4 morphants. However, gastrulation defects were associated with a virtual absence of cortical actin in the ectodermal cells that face the blastocoel cavity and this was phenocopied in embryos expressing dominant-negative IRF6. A role for RIPK4 in actin cytoskeleton organization was also revealed in mouse epidermis and in human epithelial HaCaT cells. In conclusion, we showed that in mice RIPK4 is implicated in cortical actin organization and in E-cadherin localization or function, which can explain the characteristic epithelial fusions observed in PPSs. In addition, we provide a novel molecular link between IRF6 and RIPK4 that unifies the different PPSs to a common molecular pathway.

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Section: G H and I)mentioning

confidence: 99%

A novel RIPK4–IRF6 connection is required to prevent epithelial fusions characteristic for popliteal pterygium syndromes

et al. 2014

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“…Wnts act as hematopoietic stem cell growth factors Willert et al, 2003) and promote proliferation of intestinal stem cells (Korinek et al, 1998;Pinto et al, 2003). They can also act as regulators of differentiation; in epidermal stem cells high levels of Wnt signaling generated by expression of a truncated ␤-catenin promote hair follicle formation (Gat et al, 1998), while mutation or inhibition of ␤-catenin results in epidermal differentiation (Huelsken et al, 2001;Niemann et al, 2002).…”

Section: Signaling In Adult Neural and Other Stem Cell Nichesmentioning

confidence: 99%

“…A wide range of instructive signals can, therefore, regulate stem cell behavior. Soluble factors such as BMPs (Xie and Spradling, 1998;Kobielak et al, 2003;Zhang et al, 2003;Andl et al, 2004;He et al, 2004;Yamashita et al, 2005), FGFs (Kashiwakura and Takahashi, 2005), Shh (Madison et al, 2005;Crosnier et al, 2006), and Wnts (Gat et al, 1998;Korinek et al, 1998;Huelsken et al, 2001;Niemann et al, 2002;Reya et al, 2003;Willert et al, 2003) are present within the niche and can originate from support cells, stem cells themselves, or differentiated cell. Cell-to-cell contact-mediated signaling is also present in adult niches in the form of connexins (Juneja et al, 1999;Plum et al, 2000), ephrins/eph (Batlle et al, 2002;Holmberg et al, 2006) and Notch (Harada et al, 1999;Lowell et al, 2000;Conboy and Rando, 2002;Calvi et al, 2003;Conboy et al, 2003;Kumano et al, 2003;Tummers and Thesleff, 2003;Hadland et al, 2004;Fre et al, 2005;Robert-Moreno et al, 2005;van Es et al, 2005;Spradling, 2006, 2007;Song et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

The microenvironment of the embryonic neural stem cell: Lessons from adult niches?

Lathia

Rao

Mattson

et al. 2007

Developmental Dynamics

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A better understanding of the signals regulating embryonic neural stem cells is clearly an important goal. However, many studies on neural stem cell biology are conducted on the slowly-dividing cells found in the adult CNS, where specialized microenvironments or niches maintain the stem cells throughout life. By contrast, the embryonic VZ is a transient structure that does not fulfill the criteria conventionally used to define niches. In this review we will examine whether, despite these differences, the signals found in other adult stem cell niches are present in the VZ. Using the similarities and differences we observe, we will reconsider whether the location of embryonic stem cell populations such as the VZ can be thought of as niches. Finally, we will ask how these lessons from the niche inform our understanding of neurodevelopmental diseases and cancers of the CNS. Developmental Dynamics 236:3267-3282, 2007.

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“…Wnts are divided at least into three groups according to their signal transduction pathways: the canonical pathway in which b-catenin stabilization occurs, the planar cell polarity (PCP) pathway and the Wnt/Ca 2+ pathway [62]. Canonical Wnt/b-catenin signaling plays an important role in HF induction and fate [63][64][65][66][67][68][69], and expression of several Wnts, Wnt ligands and inhibitors is specifically elevated in developing and postnatal HFs [61,[70][71][72]. On the other hand, forced activation of b-catenin signaling promotes HF fate in both embryonic and postnatal skin [67,[73][74][75].…”

Section: Molecular Control Of Hair Follicle Development and Cyclingmentioning

confidence: 99%

Biology of Human Hair: Know Your Hair to Control It

Araújo

Fernandes

Cavaco‐Paulo

et al. 2010

Biofunctionalization of Polymers and Their Applications

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Hair can be engineered at different levels-its structure and surfacethrough modification of its constituent molecules, in particular proteins, but also the hair follicle (HF) can be genetically altered, in particular with the advent of siRNA-based applications. General aspects of hair biology are reviewed, as well as the most recent contributions to understanding hair pigmentation and the regulation of hair development. Focus will also be placed on the techniques developed specifically for delivering compounds of varying chemical nature to the HF, indicating methods for genetic/biochemical modulation of HF components for the treatment of hair diseases. Finally, hair fiber structure and chemical characteristics will be discussed as targets for keratin surface functionalization.

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β-Catenin Controls Hair Follicle Morphogenesis and Stem Cell Differentiation in the Skin

Cited by 1,233 publications

References 88 publications

A novel RIPK4–IRF6 connection is required to prevent epithelial fusions characteristic for popliteal pterygium syndromes

A novel RIPK4–IRF6 connection is required to prevent epithelial fusions characteristic for popliteal pterygium syndromes

The microenvironment of the embryonic neural stem cell: Lessons from adult niches?

Biology of Human Hair: Know Your Hair to Control It

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