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<PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Manual"><PMID Version="1">12810586</PMID><DateCompleted><Year>2003</Year><Month>09</Month><Day>03</Day></DateCompleted><DateRevised><Year>2022</Year><Month>03</Month><Day>09</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0950-1991</ISSN><JournalIssue CitedMedium="Print"><Volume>130</Volume><Issue>15</Issue><PubDate><Year>2003</Year><Month>Aug</Month></PubDate></JournalIssue><Title>Development (Cambridge, England)</Title><ISOAbbreviation>Development</ISOAbbreviation></Journal><ArticleTitle>Fgf3 and Fgf10 are required for mouse otic placode induction.</ArticleTitle><Pagination><StartPage>3379</StartPage><EndPage>3390</EndPage><MedlinePgn>3379-90</MedlinePgn></Pagination><Abstract><AbstractText>The inner ear, which contains the sensory organs specialised for audition and balance, develops from an ectodermal placode adjacent to the developing hindbrain. Tissue grafting and recombination experiments suggest that placodal development is directed by signals arising from the underlying mesoderm and adjacent neurectoderm. In mice, Fgf3 is expressed in the neurectoderm prior to and concomitant with placode induction and otic vesicle formation, but its absence affects only the later stages of otic vesicle morphogenesis. We show here that mouse Fgf10 is expressed in the mesenchyme underlying the prospective otic placode. Embryos lacking both Fgf3 and Fgf10 fail to form otic vesicles and have aberrant patterns of otic marker gene expression, suggesting that FGF signals are required for otic placode induction and that these signals emanate from both the hindbrain and mesenchyme. These signals are likely to act directly on the ectoderm, as double mutant embryos showed normal patterns of gene expression in the hindbrain. Cell proliferation and survival were not markedly affected in double mutant embryos, suggesting that the major role of FGF signals in otic induction is to establish normal patterns of gene expression in the prospective placode. Finally, examination of embryos carrying three out of the four mutant Fgf alleles revealed intermediate phenotypes, suggesting a quantitative requirement for FGF signalling in otic vesicle formation.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Wright</LastName><ForeName>Tracy J</ForeName><Initials>TJ</Initials><AffiliationInfo><Affiliation>Department of Human Genetics, University of Utah, Salt Lake City, UT 84112-5330, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mansour</LastName><ForeName>Suzanne L</ForeName><Initials>SL</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 DC004185</GrantID><Acronym>DC</Acronym><Agency>NIDCD NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 DC005608</GrantID><Acronym>DC</Acronym><Agency>NIDCD NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>DC00473</GrantID><Acronym>DC</Acronym><Agency>NIDCD NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>DC04185</GrantID><Acronym>DC</Acronym><Agency>NIDCD NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D013487">Research Support, U.S. Gov't, P.H.S.</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Development</MedlineTA><NlmUniqueID>8701744</NlmUniqueID><ISSNLinking>0950-1991</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C496464">Fgf10 protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C489197">Fgf3 protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051526">Fibroblast Growth Factor 10</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051518">Fibroblast Growth Factor 3</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011518">Proto-Oncogene Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017468">Receptors, Fibroblast Growth Factor</NameOfSubstance></Chemical><Chemical><RegistryNumber>62031-54-3</RegistryNumber><NameOfSubstance UI="D005346">Fibroblast Growth Factors</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.10.1</RegistryNumber><NameOfSubstance UI="C496349">Fgfr1 protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.10.1</RegistryNumber><NameOfSubstance UI="D020794">Receptor Protein-Tyrosine Kinases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.10.1</RegistryNumber><NameOfSubstance UI="D051496">Receptor, Fibroblast Growth Factor, Type 1</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004423" MajorTopicYN="N">Ear</DescriptorName><QualifierName UI="Q000196" MajorTopicYN="Y">embryology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004627" MajorTopicYN="N">Embryonic Induction</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051526" MajorTopicYN="N">Fibroblast Growth Factor 10</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051518" MajorTopicYN="N">Fibroblast Growth Factor 3</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005346" MajorTopicYN="N">Fibroblast Growth Factors</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008648" MajorTopicYN="N">Mesoderm</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009154" MajorTopicYN="N">Mutation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011518" MajorTopicYN="N">Proto-Oncogene Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020794" MajorTopicYN="N">Receptor Protein-Tyrosine Kinases</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051496" MajorTopicYN="N">Receptor, Fibroblast Growth Factor, Type 1</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017468" MajorTopicYN="N">Receptors, Fibroblast Growth Factor</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2003</Year><Month>6</Month><Day>18</Day><Hour>5</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2003</Year><Month>9</Month><Day>4</Day><Hour>5</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2003</Year><Month>6</Month><Day>18</Day><Hour>5</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">12810586</ArticleId><ArticleId IdType="doi">10.1242/dev.00555</ArticleId></ArticleIdList></PubmedData></PubmedArticle></PubmedArticleSet>