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{"title"=>"Fuz regulates craniofacial development through tissue specific responses to signaling factors", "type"=>"journal", "authors"=>[{"first_name"=>"Zichao", "last_name"=>"Zhang", "scopus_author_id"=>"55597051300"}, {"first_name"=>"Bogdan J.", "last_name"=>"Wlodarczyk", "scopus_author_id"=>"35569816200"}, {"first_name"=>"Karen", "last_name"=>"Niederreither", "scopus_author_id"=>"6603956571"}, {"first_name"=>"Shankar", "last_name"=>"Venugopalan", "scopus_author_id"=>"25822722100"}, {"first_name"=>"Sergio", "last_name"=>"Florez", "scopus_author_id"=>"36247042500"}, {"first_name"=>"Richard H.", "last_name"=>"Finnell", "scopus_author_id"=>"7005924607"}, {"first_name"=>"Brad A.", "last_name"=>"Amendt", "scopus_author_id"=>"6603722981"}], "year"=>2011, "source"=>"PLoS ONE", "identifiers"=>{"scopus"=>"2-s2.0-80052836852", "sgr"=>"80052836852", "issn"=>"19326203", "doi"=>"10.1371/journal.pone.0024608", "pmid"=>"21935430", "isbn"=>"1932-6203 (Electronic)\\r1932-6203 (Linking)", "pui"=>"362566777"}, "id"=>"143cd335-2d85-3dce-bd3b-5dd089118731", "abstract"=>"The planar cell polarity effector gene Fuz regulates ciliogenesis and Fuz loss of function studies reveal an array of embryonic phenotypes. However, cilia defects can affect many signaling pathways and, in humans, cilia defects underlie several craniofacial anomalies. To address this, we analyzed the craniofacial phenotype and signaling responses of the Fuz(-/-) mice. We demonstrate a unique role for Fuz in regulating both Hedgehog (Hh) and Wnt/β-catenin signaling during craniofacial development. Fuz expression first appears in the dorsal tissues and later in ventral tissues and craniofacial regions during embryonic development coincident with cilia development. The Fuz(-/-) mice exhibit severe craniofacial deformities including anophthalmia, agenesis of the tongue and incisors, a hypoplastic mandible, cleft palate, ossification/skeletal defects and hyperplastic malformed Meckel's cartilage. Hh signaling is down-regulated in the Fuz null mice, while canonical Wnt signaling is up-regulated revealing the antagonistic relationship of these two pathways. Meckel's cartilage is expanded in the Fuz(-/-) mice due to increased cell proliferation associated with the up-regulation of Wnt canonical target genes and decreased non-canonical pathway genes. Interestingly, cilia development was decreased in the mandible mesenchyme of Fuz null mice, suggesting that cilia may antagonize Wnt signaling in this tissue. Furthermore, expression of Fuz decreased expression of Wnt pathway genes as well as a Wnt-dependent reporter. Finally, chromatin IP experiments demonstrate that β-catenin/TCF-binding directly regulates Fuz expression. These data demonstrate a new model for coordination of Hh and Wnt signaling and reveal a Fuz-dependent negative feedback loop controlling Wnt/β-catenin signaling.", "link"=>"http://www.mendeley.com/research/fuz-regulates-craniofacial-development-through-tissue-specific-responses-signaling-factors", "reader_count"=>38, "reader_count_by_academic_status"=>{"Unspecified"=>1, "Professor > Associate Professor"=>4, "Researcher"=>7, "Student > Doctoral Student"=>1, "Student > Ph. D. Student"=>9, "Student > Postgraduate"=>1, "Other"=>4, "Student > Master"=>4, "Student > Bachelor"=>6, "Professor"=>1}, "reader_count_by_user_role"=>{"Unspecified"=>1, "Professor > Associate Professor"=>4, "Researcher"=>7, "Student > Doctoral Student"=>1, "Student > Ph. D. Student"=>9, "Student > Postgraduate"=>1, "Other"=>4, "Student > Master"=>4, "Student > Bachelor"=>6, "Professor"=>1}, "reader_count_by_subject_area"=>{"Unspecified"=>4, "Engineering"=>1, "Biochemistry, Genetics and Molecular Biology"=>4, "Medicine and Dentistry"=>6, "Agricultural and Biological Sciences"=>19, "Neuroscience"=>1, "Sports and Recreations"=>1, "Pharmacology, Toxicology and Pharmaceutical Science"=>1, "Immunology and Microbiology"=>1}, "reader_count_by_subdiscipline"=>{"Engineering"=>{"Engineering"=>1}, "Medicine and Dentistry"=>{"Medicine and Dentistry"=>6}, "Neuroscience"=>{"Neuroscience"=>1}, "Sports and Recreations"=>{"Sports and Recreations"=>1}, "Immunology and Microbiology"=>{"Immunology and Microbiology"=>1}, "Agricultural and Biological Sciences"=>{"Agricultural and Biological Sciences"=>19}, "Biochemistry, Genetics and Molecular Biology"=>{"Biochemistry, Genetics and Molecular Biology"=>4}, "Unspecified"=>{"Unspecified"=>4}, "Pharmacology, Toxicology and Pharmaceutical Science"=>{"Pharmacology, Toxicology and Pharmaceutical Science"=>1}}, "reader_count_by_country"=>{"United States"=>1, "Japan"=>1, "United Kingdom"=>1}, "group_count"=>0}

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• http://doi.org/10.1016/j.ydbio.2013.07.016
• http://doi.org/10.4331/wjbc.v6.i3.121
• http://doi.org/10.1002/ajmg.a.38718
• http://doi.org/10.1016/j.ydbio.2014.07.013
• http://doi.org/10.1038/onc.2017.117
• http://doi.org/10.1016/j.yexcr.2014.01.019
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• http://doi.org/10.1016/j.tcb.2016.12.001
• http://doi.org/10.1074/jbc.M114.575654
• http://doi.org/10.1371/journal.pone.0054868
• http://doi.org/10.1083/jcb.201604048
• http://doi.org/10.1177/0022034517713688
• http://doi.org/10.1597/14-238
• http://doi.org/10.15252/embr.201745409
• http://doi.org/10.1371/journal.pgen.1007675
• http://doi.org/10.1111/joa.13096
• http://doi.org/10.1371/journal.pone.0174206
• http://doi.org/10.1111/brv.12187
• http://doi.org/10.1002/dvdy.8
• http://doi.org/10.1681/ASN.2012050526
• http://doi.org/10.1016/j.devcel.2013.05.021
• http://doi.org/10.1038/s41437-017-0033-2
• http://doi.org/10.1177/0022034517732538

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Figshare

• {"files"=>["https://ndownloader.figshare.com/files/736447"], "description"=>"<p><b>A</b>) Immunofluorescence of Patched1 in sagittal sections of E14.5 <i>Fuz^+/−</i> heterozygous embryos. Sections in the bottom panels are higher magnification of those in the top panels. Ptch1 is weakly expressed in Meckel's cartilage. <b>B</b>) In the <i>Fuz^−/−</i> embryos, Ptch1 expression is decreased overall as well as in Meckel's cartilage. <b>C</b>) Immunofluorescence of Gli2 in sagittal sections of E14.5 <i>Fuz^+/−</i> heterozygous embryos. Sections in the bottom panels are higher magnification of those in the top panels. Gli2 is highly expressed in the oral and dental epithelium and mesenchyme, but weakly expressed in the Meckel's cartilage. The expression pattern of Gli2 is similar to Ptch1, but Gli2 has increased expression in the oral mesenchyme compared to Ptch1. <b>D</b>) In the <i>Fuz^−/−</i> embryos, Gli2 expression was decreased overall as well as in Meckel's cartilage. <b>E</b>) The wild type and <i>Fuz^−/−</i> Meckel's cartilage and surrounding mesenchyme were dissected from E14.5 embryos and the mRNA was extracted, followed by reverse transcription. The real-time PCR was performed with indicated probes. Results are shown as normalized relative expression. βactin served as the reference gene. Experiments were repeated three to five times each from multiple samples. Error bars indicate S.E. *: <i>p</i>-values<0.05; **: <i>p</i>-values<0.01.</p>", "links"=>[], "tags"=>["hh", "signaling", "pathway", "effectors"], "article_id"=>406797, "categories"=>["Molecular Biology", "Cell Biology", "Genetics", "Developmental Biology"], "users"=>["Zichao Zhang", "Bogdan J. Wlodarczyk", "Karen Niederreither", "Shankar Venugopalan", "Sergio Florez", "Richard H. Finnell", "Brad A. Amendt"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0024608.g008", "stats"=>{"downloads"=>2, "page_views"=>10, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_The_Hh_signaling_pathway_effectors_are_decreased_in_E14_5_Fuz_8722_8722_mouse_embryos_/406797", "title"=>"The Hh signaling pathway effectors are decreased in E14.5 <i>Fuz^−/−</i> mouse embryos.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2013-02-20 14:51:32"}
• {"files"=>["https://ndownloader.figshare.com/files/736047"], "description"=>"<p><b>A, B</b>) Upper panels are Alcian Blue/Alizarin Red staining of cartilage and bone skeletal preparations of E16.0 <i>Fuz</i> heterozygous embryos (A) and <i>Fuz</i> null littermates (B). Ossification is reduced in the <i>Fuz</i> null embryos. Lower panels are higher magnification of the head region. The anterior region of Meckel's cartilage (MC) is deformed with an ascending branch. <b>E–H</b>) E18.5 head preparations revealing delayed bone formation and defective craniofacial structures in the <i>Fuz</i> mutant embryos (arrows denote the malformed and ossified Meckel's cartilage). Frontal (fnt), parietal (par), premaxilla (pmx), maxilla (mx), sphenoid (sb) and basioccipital (bb) bones and other facial bones are missing. Background red staining was due to soft tissues, which were left intact.</p>", "links"=>[], "tags"=>["defects", "null", "mutant"], "article_id"=>406395, "categories"=>["Molecular Biology", "Cell Biology", "Genetics", "Developmental Biology"], "users"=>["Zichao Zhang", "Bogdan J. Wlodarczyk", "Karen Niederreither", "Shankar Venugopalan", "Sergio Florez", "Richard H. Finnell", "Brad A. Amendt"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0024608.g004", "stats"=>{"downloads"=>1, "page_views"=>8, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Skeletal_defects_of_Fuz_null_mutant_embryos_/406395", "title"=>"Skeletal defects of <i>Fuz</i> null mutant embryos.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2013-02-20 14:49:15"}
• {"files"=>["https://ndownloader.figshare.com/files/736986"], "description"=>"<p><b>A</b>) Fuz acts downstream of Frizzled and Dishevelled to regulate PCP signaling. Non-canonical Wnt signaling represses Wnt/β-catenin signaling and Fuz is involved in a negative feedback loop of Wnt/β-catenin signal regulation. Fuz also regulates assembly of the apical actin cytoskeleton, which is critical for ciliogenesis. Cilia formation can be directly linked to Hedgehog signaling and Gli transcription factor activation. Activated Gli factors then regulate Hedgehog target genes. <b>B</b>) Loss of <i>Fuz</i> leads to impaired PCP signaling and up-regulation of Wnt/β-catenin signaling. In addition, it results in impaired actin cap and cilia, which inhibits the activation of Gli transcription factors and weakens Hedgehog signaling. Loss of <i>Fuz</i> also results in the up-regulation of Sox9.</p>", "links"=>[], "tags"=>["tentative", "linking", "wnt", "pcp"], "article_id"=>407335, "categories"=>["Molecular Biology", "Cell Biology", "Genetics", "Developmental Biology"], "users"=>["Zichao Zhang", "Bogdan J. Wlodarczyk", "Karen Niederreither", "Shankar Venugopalan", "Sergio Florez", "Richard H. Finnell", "Brad A. Amendt"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0024608.g012", "stats"=>{"downloads"=>10, "page_views"=>461, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_A_tentative_model_linking_Fuz_to_Shh_Wnt_and_PCP_signal_pathways_/407335", "title"=>"A tentative model linking <i>Fuz</i> to Shh, Wnt and PCP signal pathways.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2013-02-20 14:54:41"}
• {"files"=>["https://ndownloader.figshare.com/files/736756"], "description"=>"<p><b>A</b>) A schematic of the <i>Fuz</i> 2.4 kb promoter with eleven Wnt response elements (<i>Lef/Tcf</i> binding sites). Chromatin immunoprecipitation assay reveals endogenous β-catenin associated with the <i>Fuz</i> promoter chromatin in LS-8 cells. The location of the PCR primers are shown in A. <b>B</b>) A gel with specific PCR products from the immunoprecipitated chromatin and controls are shown. <b>C</b>) The <i>Fuz</i> 2.4 kb promoter was transfected into LS-8 and CHO cells and LiCl (10 mM) was added to the cell culture medium. The activities are shown as mean fold activation compared to reporter activation without LiCl and normalized to SV-40 β-galactosidase activity. Error bars indicate S.E.</p>", "links"=>[], "tags"=>["activates"], "article_id"=>407112, "categories"=>["Molecular Biology", "Cell Biology", "Genetics", "Developmental Biology"], "users"=>["Zichao Zhang", "Bogdan J. Wlodarczyk", "Karen Niederreither", "Shankar Venugopalan", "Sergio Florez", "Richard H. Finnell", "Brad A. Amendt"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0024608.g010", "stats"=>{"downloads"=>1, "page_views"=>5, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_catenin_activates_the_Fuz_promoter_/407112", "title"=>"β-catenin activates the <i>Fuz</i> promoter.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2013-02-20 14:53:14"}
• {"files"=>["https://ndownloader.figshare.com/files/736307"], "description"=>"<p>Whole-mount <i>in situ</i> hybridization assays with indicated probes were performed with E9.5 embryos. The overall decrease of <i>Ptch1</i>, and <i>Gli1</i> transcript levels are shown.</p>", "links"=>[], "tags"=>["sonic", "hedgehog"], "article_id"=>406659, "categories"=>["Molecular Biology", "Cell Biology", "Genetics", "Developmental Biology"], "users"=>["Zichao Zhang", "Bogdan J. Wlodarczyk", "Karen Niederreither", "Shankar Venugopalan", "Sergio Florez", "Richard H. Finnell", "Brad A. Amendt"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0024608.g007", "stats"=>{"downloads"=>0, "page_views"=>2, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Defective_Sonic_Hedgehog_signaling_/406659", "title"=>"Defective Sonic Hedgehog signaling.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2013-02-20 14:50:46"}
• {"files"=>["https://ndownloader.figshare.com/files/736137"], "description"=>"<p><b>A</b>) The proliferation of E14.5 Meckel's cartilage was assessed by immunofluorescence with a Ki67 antibody. <b>B</b>) The proliferation ratio is calculated by dividing the Ki67 positive cell number with DAPI cell number within Meckel's cartilage. The proliferation of mutant Meckel's cartilage (88%) is significantly increased compared with wild type (75%). Experiments were repeated three times and <i>p</i>-value is shown.</p>", "links"=>[], "tags"=>["proliferation", "cartilage"], "article_id"=>406484, "categories"=>["Molecular Biology", "Cell Biology", "Genetics", "Developmental Biology"], "users"=>["Zichao Zhang", "Bogdan J. Wlodarczyk", "Karen Niederreither", "Shankar Venugopalan", "Sergio Florez", "Richard H. Finnell", "Brad A. Amendt"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0024608.g005", "stats"=>{"downloads"=>1, "page_views"=>13, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Enhanced_cell_proliferation_in_Meckel_s_cartilage_of_the_Fuz_8722_8722_mandible_/406484", "title"=>"Enhanced cell proliferation in Meckel's cartilage of the <i>Fuz^−/−</i> mandible.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2013-02-20 14:49:47"}
• {"files"=>["https://ndownloader.figshare.com/files/735618"], "description"=>"<p><i>Fuz^LacZ</i> allele expression is shown by X-Gal staining of heterozygous <i>Fuz^LacZ/+</i> embryos. <b>A</b>) <i>Fuz^LacZ</i> expression is predominantly in the dorsal tissue at E9.5. <b>B</b>) At E11.5, <i>Fuz^LacZ</i> expression is concentrated in the brain, spinal cord and eyes. <b>C</b>) At E12.5, <i>Fuz^LacZ</i> expression begins to expand from dorsal to ventral region. Fuz expression in the oral epithelium (arrow), mesenchyme and Meckel's Cartilage is shown in a sagittal section (dotted circle) (<b>D</b>). At E14.5 embryos, the ventral expression of <i>Fuz^LacZ</i> is increased while the dorsal expression is relatively decreased (<b>C</b>). <i>Fuz^LacZ</i> expression in the oral epithelium (arrow, <b>E</b>), Meckel's Cartilage (MC) and the perichondrium (PC) is shown in a sagittal section (<b>E, F</b>). <b>G</b>) RT-PCR reveals that <i>Fuz</i> is highly expressed in LS-8 (oral epithelium), C3H10T1/2 (embryonic fibroblast), HEK 293 FT (embryonic kidney fibroblast) and SW1353 (chondrocyte) cell lines. It has relatively weak expression in MDPC-23 cells (dental mesenchyme), and no expression in CHO cells (ovary). PL, palate; TE, tongue.</p>", "links"=>[], "tags"=>["allele", "craniofacial"], "article_id"=>405966, "categories"=>["Molecular Biology", "Cell Biology", "Genetics", "Developmental Biology"], "users"=>["Zichao Zhang", "Bogdan J. Wlodarczyk", "Karen Niederreither", "Shankar Venugopalan", "Sergio Florez", "Richard H. Finnell", "Brad A. Amendt"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0024608.g001", "stats"=>{"downloads"=>0, "page_views"=>5, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Expression_of_the_Fuz_LacZ_allele_during_mouse_craniofacial_development_/405966", "title"=>"Expression of the <i>Fuz^LacZ</i> allele during mouse craniofacial development.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2013-02-20 14:46:48"}
• {"files"=>["https://ndownloader.figshare.com/files/735909"], "description"=>"<p><b>A</b>) E12.5 embryos of heterozygous (<i>Fuz^+/−</i>) and homozygous (<i>Fuz^−/−</i>) mice. The overall structure of the ventral craniofacial region is not severely affected at this stage in the <i>Fuz</i> null embryos, due to the low expression of Fuz. However, the dorsal structures including the choroid plexus (CP) differentiating from the roof of fourth ventricle, the choroid plexus extending into the lateral ventricle (CPL), and the optic recess of the diencephalon (OR) are missing in the <i>Fuz</i> null mice. The corpus striatum mediale (STM), and the cochlea (CO) are displaced in the <i>Fuz</i> null mice. Higher magnification of the mandible is shown in the bottom panels and reveals normal Meckel's cartilage formation at this stage. <b>B</b>) At E14.5 the craniofacial defects of the <i>Fuz</i> null mice are severe. The tongue muscles are fused with the mandible, the pituitary (PI) is missing and the trigeminal nerve (TG) is seen in its place and the OR is displaced, corresponding to anophthalmia in the mutant. The higher magnification sections showed a lack of upper (UI) and lower incisors (LI), no tongue (TE) and expanded Meckel's cartilage (MC) in the dorsal-ventral axis instead of anterior-posterior axis. The palate is now a piece of displaced palatal tissue (PLT). <b>C</b>) E16.5 coronal sections reveal a cleft palate in the <i>Fuz</i> null mice. The palate tissue is displaced to the lateral portions of the oral cavity and the secondary palate is not fused, due to the dorsal-ventral and medial-lateral expansion of Meckel's cartilage. The molars (ML) are shown and appear to be grossly normal in the mutant mice. The plane of section is depicted by the dotted line through the mouse drawing.</p>", "links"=>[], "tags"=>["stages", "craniofacial", "defects"], "article_id"=>406258, "categories"=>["Molecular Biology", "Cell Biology", "Genetics", "Developmental Biology"], "users"=>["Zichao Zhang", "Bogdan J. Wlodarczyk", "Karen Niederreither", "Shankar Venugopalan", "Sergio Florez", "Richard H. Finnell", "Brad A. Amendt"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0024608.g003", "stats"=>{"downloads"=>0, "page_views"=>35, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Early_stages_of_craniofacial_defects_in_the_Fuz_8722_8722_mice_/406258", "title"=>"Early stages of craniofacial defects in the <i>Fuz^−/−</i> mice.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2013-02-20 14:48:28"}
• {"files"=>["https://ndownloader.figshare.com/files/736860"], "description"=>"<p><b>A</b>) Sox9 expression was expanded in E14.5 <i>Fuz^−/−</i> Meckel's cartilage shown by immunofluorescence (bottom panel) compared to heterozygotes (<i>Fuz^+/−</i>, top panel). <b>B</b>) Real-Time PCR revealed increased <i>Sox9</i> expression as well as <i>Type II Collagen</i> (<i>Col2a1</i>) in <i>Fuz</i> null Meckel's cartilage at E14.5. <b>C</b>) Transfection of <i>Fuz</i> results in reduced <i>SOX9</i> and <i>COL2A1</i> expression in chondrocyte (SW1353) cells compared to those transfected with control vectors. Error bars indicate S.E.M.</p>", "links"=>[], "tags"=>["was"], "article_id"=>407210, "categories"=>["Molecular Biology", "Cell Biology", "Genetics", "Developmental Biology"], "users"=>["Zichao Zhang", "Bogdan J. Wlodarczyk", "Karen Niederreither", "Shankar Venugopalan", "Sergio Florez", "Richard H. Finnell", "Brad A. Amendt"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0024608.g011", "stats"=>{"downloads"=>0, "page_views"=>1, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Sox9_expression_was_increased_in_Fuz_8722_8722_Meckel_s_cartilage_/407210", "title"=>"Sox9 expression was increased in <i>Fuz^−/−</i> Meckel's cartilage.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2013-02-20 14:53:53"}
• {"files"=>["https://ndownloader.figshare.com/files/735762"], "description"=>"<p><b>A</b>) E18.5 embryos of heterozygous (<i>Fuz^+/−</i>) and homozygous (<i>Fuz^−/−</i>) mice. The null embryo (<i>Fuz^−/−</i>) has a hypoplastic maxilla and mandible, missing eyes and displaced ears. The white arrow denotes an abnormal bulge in the null mandible. <b>B</b>) The cleft palate is shown by the black arrow in E18.5 null embryos (<i>Fuz^−/−</i>). (<b>C, D</b>) H&E staining of heterozygous (<i>Fuz^+/−</i>, left) and homozygous (<i>Fuz^−/−</i>, right) head sagittal sections. The bottom panels are higher magnification of the top panels. <b>C</b>) At E18.5, the <i>Fuz</i> homozygous mandibles are shorter than heterozygotes. Meckel's cartilage expends in the dorsal-ventral axis in addition to anterior-posterior axis and the ventral end of the mutant Meckel's cartilage points down and forms the mandibular bulge. The plane of section is depicted by the dotted line through the mouse drawing. TE, tongue; MC, Meckel's cartilage; LI, lower incisor.</p>", "links"=>[], "tags"=>["defects", "deletion"], "article_id"=>406116, "categories"=>["Molecular Biology", "Cell Biology", "Genetics", "Developmental Biology"], "users"=>["Zichao Zhang", "Bogdan J. Wlodarczyk", "Karen Niederreither", "Shankar Venugopalan", "Sergio Florez", "Richard H. Finnell", "Brad A. Amendt"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0024608.g002", "stats"=>{"downloads"=>0, "page_views"=>2, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Craniofacial_defects_associated_with_a_deletion_of_Fuz_at_E18_5_/406116", "title"=>"Craniofacial defects associated with a deletion of <i>Fuz</i> at E18.5.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2013-02-20 14:47:43"}
• {"files"=>["https://ndownloader.figshare.com/files/736607"], "description"=>"<p>Immunofluorescence on sagittal sections of E14.5 embryos. <b>A</b>) β-catenin expression was increased in the oral epithelium and mesenchyme in mutant (<i>Fuz</i>^−/−) embryos. The bottom panels are the <i>Fuz^−/−</i> embryos. <b>B</b>) β-catenin expression was also increased in the <i>Fuz</i> null Meckel's cartilage (bottom panel), compared to the heterozygote (<i>Fuz</i>^+/−, top panel) samples. <b>C</b>) Lef-1 expression in the dental epithelium, oral and dental mesenchyme at E14.5. Lef-1 expression increased in the <i>Fuz</i> null oral mesenchyme (bottom panel). <b>D</b>) These are higher magnification of the boxed areas in C. Lef-1 expression was expanded in the <i>Fuz^−/−</i> mice oral mesenchyme. <b>E</b>) The expression of <i>Tcf4</i> (<i>Tcf7l2</i>) was increased in <i>Fuz</i> mutant Meckel's cartilage (bottom panels) at E14.5 compared with wild type samples (top panels). <b>F</b>) Real-time PCR with mRNA from dissected E14.5 Meckel's cartilage and surrounding mesenchyme. Canonical Wnt target gene expression was increased whereas non-canonical Wnt pathway gene expression was decreased. β-actin served as the reference gene. Experiments were repeated three to five times each from multiple samples. <b>G</b>) Topflash reporter activity was repressed by co-transfection of <i>Fuz</i> in HEK 293FT and CHO cells. The activities are shown as mean fold activation compared to reporter activation co-transfected with pcDNA3.1 empty vector and normalized to SV-40 β-galactosidase activity. Error bars indicate S.E. *: <i>p</i>-values<0.05; **: <i>p</i>-values<0.01.</p>", "links"=>[], "tags"=>["signaling", "null"], "article_id"=>406962, "categories"=>["Molecular Biology", "Cell Biology", "Genetics", "Developmental Biology"], "users"=>["Zichao Zhang", "Bogdan J. Wlodarczyk", "Karen Niederreither", "Shankar Venugopalan", "Sergio Florez", "Richard H. Finnell", "Brad A. Amendt"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0024608.g009", "stats"=>{"downloads"=>0, "page_views"=>1, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Wnt_catenin_signaling_is_increased_in_the_Fuz_null_mice_/406962", "title"=>"Wnt/β-catenin signaling is increased in the <i>Fuz</i> null mice.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2013-02-20 14:52:27"}
• {"files"=>["https://ndownloader.figshare.com/files/736240"], "description"=>"<p><b>A</b>) The primary cilia are shown by immunofluorescence with an Arl13b antibody in mandible mesenchyme at E14.5. <b>B</b>) The amount of cilia in the sagittal sections of <i>Fuz^−/−</i> mandible mesenchyme was quantitated and compared to wild type mandible mesenchyme. Error bars indicate S.E., n = 8, <i>p</i><0.01.</p>", "links"=>[], "tags"=>["cilium", "defect", "null"], "article_id"=>406591, "categories"=>["Molecular Biology", "Cell Biology", "Genetics", "Developmental Biology"], "users"=>["Zichao Zhang", "Bogdan J. Wlodarczyk", "Karen Niederreither", "Shankar Venugopalan", "Sergio Florez", "Richard H. Finnell", "Brad A. Amendt"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0024608.g006", "stats"=>{"downloads"=>0, "page_views"=>0, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_The_cilium_defect_in_the_Fuz_null_mouse_/406591", "title"=>"The cilium defect in the <i>Fuz</i> null mouse.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2013-02-20 14:50:21"}

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• {"unique-ip"=>"9", "full-text"=>"11", "pdf"=>"1", "scanned-summary"=>"0", "scanned-page-browse"=>"0", "figure"=>"0", "supp-data"=>"0", "cited-by"=>"0", "year"=>"2019", "month"=>"4"}
• {"unique-ip"=>"10", "full-text"=>"8", "pdf"=>"0", "scanned-summary"=>"0", "scanned-page-browse"=>"0", "figure"=>"10", "supp-data"=>"0", "cited-by"=>"0", "year"=>"2019", "month"=>"5"}
• {"unique-ip"=>"10", "full-text"=>"11", "pdf"=>"2", "scanned-summary"=>"0", "scanned-page-browse"=>"0", "figure"=>"0", "supp-data"=>"0", "cited-by"=>"0", "year"=>"2019", "month"=>"8"}
• {"unique-ip"=>"6", "full-text"=>"4", "pdf"=>"3", "scanned-summary"=>"0", "scanned-page-browse"=>"0", "figure"=>"0", "supp-data"=>"0", "cited-by"=>"0", "year"=>"2019", "month"=>"9"}
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Relative Metric

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F1000Prime