Shh maintains dermal papilla identity and hair morphogenesis via a Noggin–Shh regulatory loop
Identifieur interne : 002705 ( Pmc/Checkpoint ); précédent : 002704; suivant : 002706Shh maintains dermal papilla identity and hair morphogenesis via a Noggin–Shh regulatory loop
Auteurs : Wei-Meng Woo [États-Unis] ; Hanson H. Zhen [États-Unis] ; Anthony E. Oro [États-Unis]Source :
- Genes & Development [ 0890-9369 ] ; 2012.
Abstract
Recently, studies have shown that many lethal epithelial cancers depend on the tumor-derived Shh ligand acting on the tumor stroma for growth. In this study by Oro and colleagues, the authors investigate the role of dermal-specific Shh signaling in dermal papillae formation and hair growth. During hair follicle morphogenesis, dermal papillae function as signaling centers that regulate morphogenesis; however, the molecular basis of dermal papillae formation is unclear. By using both a conventional Cre-lox genetic model and a new RNAi/hair reconstitution technique, the authors demonstrate that Shh acts on the dermal compartment to maintain its own expression through inducing Noggin. Thus, these findings provide novel insight into the actions of Shh in different cell populations within the same tissue during morphogenesis.
Url:
DOI: 10.1101/gad.187401.112
PubMed: 22661232
PubMed Central: 3371411
Affiliations:
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Zhen</name><affiliation wicri:level="2"><nlm:aff id="aff1">Program in Epithelial Biology, Stanford University School of Medicine, Stanford, California 94305</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Californie</region></placeName><wicri:cityArea>Program in Epithelial Biology, Stanford University School of Medicine, Stanford</wicri:cityArea></affiliation></author><author><name sortKey="Oro, Anthony E" sort="Oro, Anthony E" uniqKey="Oro A" first="Anthony E." last="Oro">Anthony E. Oro</name><affiliation wicri:level="2"><nlm:aff id="aff1">Program in Epithelial Biology, Stanford University School of Medicine, Stanford, California 94305</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Californie</region></placeName><wicri:cityArea>Program in Epithelial Biology, Stanford University School of Medicine, Stanford</wicri:cityArea></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">22661232</idno><idno type="pmc">3371411</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3371411</idno><idno type="RBID">PMC:3371411</idno><idno type="doi">10.1101/gad.187401.112</idno><date when="2012">2012</date><idno type="wicri:Area/Pmc/Corpus">002E10</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">002E10</idno><idno type="wicri:Area/Pmc/Curation">002E09</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">002E09</idno><idno type="wicri:Area/Pmc/Checkpoint">002705</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Checkpoint">002705</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Shh maintains dermal papilla identity and hair morphogenesis via a Noggin–Shh regulatory loop</title><author><name sortKey="Woo, Wei Meng" sort="Woo, Wei Meng" uniqKey="Woo W" first="Wei-Meng" last="Woo">Wei-Meng Woo</name><affiliation wicri:level="2"><nlm:aff id="aff1">Program in Epithelial Biology, Stanford University School of Medicine, Stanford, California 94305</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Californie</region></placeName><wicri:cityArea>Program in Epithelial Biology, Stanford University School of Medicine, Stanford</wicri:cityArea></affiliation></author><author><name sortKey="Zhen, Hanson H" sort="Zhen, Hanson H" uniqKey="Zhen H" first="Hanson H." last="Zhen">Hanson H. Zhen</name><affiliation wicri:level="2"><nlm:aff id="aff1">Program in Epithelial Biology, Stanford University School of Medicine, Stanford, California 94305</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Californie</region></placeName><wicri:cityArea>Program in Epithelial Biology, Stanford University School of Medicine, Stanford</wicri:cityArea></affiliation></author><author><name sortKey="Oro, Anthony E" sort="Oro, Anthony E" uniqKey="Oro A" first="Anthony E." last="Oro">Anthony E. Oro</name><affiliation wicri:level="2"><nlm:aff id="aff1">Program in Epithelial Biology, Stanford University School of Medicine, Stanford, California 94305</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Californie</region></placeName><wicri:cityArea>Program in Epithelial Biology, Stanford University School of Medicine, Stanford</wicri:cityArea></affiliation></author></analytic><series><title level="j">Genes & Development</title><idno type="ISSN">0890-9369</idno><idno type="eISSN">1549-5477</idno><imprint><date when="2012">2012</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Recently, studies have shown that many lethal epithelial cancers depend on the tumor-derived Shh ligand acting on the tumor stroma for growth. In this study by Oro and colleagues, the authors investigate the role of dermal-specific Shh signaling in dermal papillae formation and hair growth. During hair follicle morphogenesis, dermal papillae function as signaling centers that regulate morphogenesis; however, the molecular basis of dermal papillae formation is unclear. By using both a conventional Cre-lox genetic model and a new RNAi/hair reconstitution technique, the authors demonstrate that Shh acts on the dermal compartment to maintain its own expression through inducing Noggin. Thus, these findings provide novel insight into the actions of Shh in different cell populations within the same tissue during morphogenesis.</p></div></front></TEI><pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Genes Dev</journal-id><journal-id journal-id-type="iso-abbrev">Genes Dev</journal-id><journal-id journal-id-type="publisher-id">GAD</journal-id><journal-title-group><journal-title>Genes & Development</journal-title></journal-title-group><issn pub-type="ppub">0890-9369</issn><issn pub-type="epub">1549-5477</issn><publisher><publisher-name>Cold Spring Harbor Laboratory Press</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">22661232</article-id><article-id pub-id-type="pmc">3371411</article-id><article-id pub-id-type="medline">8711660</article-id><article-id pub-id-type="doi">10.1101/gad.187401.112</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Paper</subject></subj-group></article-categories><title-group><article-title>Shh maintains dermal papilla identity and hair morphogenesis via a Noggin–Shh regulatory loop</article-title><alt-title alt-title-type="left-running">Woo et al.</alt-title><alt-title alt-title-type="right-running">A Noggin–Shh loop controls hair growth</alt-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Woo</surname><given-names>Wei-Meng</given-names></name><xref ref-type="aff" rid="aff1"></xref></contrib><contrib contrib-type="author"><name><surname>Zhen</surname><given-names>Hanson H.</given-names></name><xref ref-type="aff" rid="aff1"></xref></contrib><contrib contrib-type="author"><name><surname>Oro</surname><given-names>Anthony E.</given-names></name><xref ref-type="aff" rid="aff1"></xref><xref ref-type="corresp" rid="cor1">1</xref></contrib></contrib-group><aff id="aff1">Program in Epithelial Biology, Stanford University School of Medicine, Stanford, California 94305</aff><author-notes><corresp id="cor1"><label>1</label>Corresponding author.E-mail <email>Oro@stanford.edu</email>.</corresp></author-notes><pub-date pub-type="ppub"><day>1</day><month>6</month><year>2012</year></pub-date><volume>26</volume><issue>11</issue><fpage>1235</fpage><lpage>1246</lpage><history><date date-type="received"><day>13</day><month>1</month><year>2012</year></date><date date-type="accepted"><day>25</day><month>4</month><year>2012</year></date></history><permissions><copyright-statement>Copyright © 2012 by Cold Spring Harbor Laboratory Press</copyright-statement><copyright-year>2012</copyright-year></permissions><self-uri xlink:title="pdf" xlink:type="simple" xlink:href="1235.pdf"></self-uri><abstract abstract-type="precis"><p>Recently, studies have shown that many lethal epithelial cancers depend on the tumor-derived Shh ligand acting on the tumor stroma for growth. In this study by Oro and colleagues, the authors investigate the role of dermal-specific Shh signaling in dermal papillae formation and hair growth. During hair follicle morphogenesis, dermal papillae function as signaling centers that regulate morphogenesis; however, the molecular basis of dermal papillae formation is unclear. By using both a conventional Cre-lox genetic model and a new RNAi/hair reconstitution technique, the authors demonstrate that Shh acts on the dermal compartment to maintain its own expression through inducing Noggin. Thus, these findings provide novel insight into the actions of Shh in different cell populations within the same tissue during morphogenesis.</p></abstract><abstract><p>During hair follicle morphogenesis, dermal papillae (DPs) function as mesenchymal signaling centers that cross-talk with overlying epithelium to regulate morphogenesis. While the DP regulates hair follicle formation, relatively little is known about the molecular basis of DP formation. The morphogen Sonic hedgehog (Shh) is known for regulating hair follicle epithelial growth, with excessive signaling resulting in basal cell carcinomas. Here, we investigate how dermal-specific Shh signaling contributes to DP formation and hair growth. Using a Cre-lox genetic model and RNAi in hair follicle reconstitution assays, we demonstrate that dermal <italic>Smoothened</italic> (<italic>Smo</italic>) loss of function results in the loss of the DP precursor, the dermal condensate, and a stage 2 hair follicle arrest phenotype reminiscent of <italic>Shh<sup>−/−</sup></italic> skin. Surprisingly, dermal Smo does not regulate cell survival or epithelial proliferation. Rather, molecular screening and immunostaining studies reveal that dermal Shh signaling controls the expression of a subset of DP-specific signature genes. Using a hairpin/cDNA lentiviral system, we show that overexpression of the Shh-dependent gene Noggin, but not Sox2 or Sox18, can partially rescue the dermal Smo knockdown hair follicle phenotype by increasing the expression of epithelial Shh. Our findings suggest that dermal Shh signaling regulates specific DP signatures to maintain DP maturation while maintaining a reciprocal Shh–Noggin signaling loop to drive hair follicle morphogenesis.</p></abstract><kwd-group><kwd>Hedgehog pathway</kwd><kwd>dermal papilla</kwd><kwd>hair follicle</kwd><kwd>Noggin</kwd></kwd-group></article-meta></front></pmc><affiliations><list><country><li>États-Unis</li></country><region><li>Californie</li></region></list><tree><country name="États-Unis"><region name="Californie"><name sortKey="Woo, Wei Meng" sort="Woo, Wei Meng" uniqKey="Woo W" first="Wei-Meng" last="Woo">Wei-Meng Woo</name></region><name sortKey="Oro, Anthony E" sort="Oro, Anthony E" uniqKey="Oro A" first="Anthony E." last="Oro">Anthony E. Oro</name><name sortKey="Zhen, Hanson H" sort="Zhen, Hanson H" uniqKey="Zhen H" first="Hanson H." last="Zhen">Hanson H. Zhen</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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