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dc.contributor.authorBei, Yanxia
dc.contributor.authorHogan, Jennifer
dc.contributor.authorBerkowitz, Laura A.
dc.contributor.authorSoto, Martha C.
dc.contributor.authorRocheleau, Christian Ernest
dc.contributor.authorPang, Ka Ming
dc.contributor.authorCollins, John J.
dc.contributor.authorMello, Craig C.
dc.date2022-08-11T08:09:02.000
dc.date.accessioned2022-08-23T16:16:12Z
dc.date.available2022-08-23T16:16:12Z
dc.date.issued2002-07-12
dc.date.submitted2008-07-16
dc.identifier.citation<p>Dev Cell. 2002 Jul;3(1):113-25.</p>
dc.identifier.issn1534-5807 (Print)
dc.identifier.doi10.1016/S1534-5807(02)00185-5
dc.identifier.pmid12110172
dc.identifier.urihttp://hdl.handle.net/20.500.14038/34276
dc.description.abstractIn early C. elegans embryos, signaling between a posterior blastomere, P2, and a ventral blastomere, EMS, specifies endoderm and orients the division axis of the EMS cell. Although Wnt signaling contributes to this polarizing interaction, no mutants identified to date abolish P2/EMS signaling. Here, we show that two tyrosine kinase-related genes, src-1 and mes-1, are required for the accumulation of phosphotyrosine between P2 and EMS. Moreover, src-1 and mes-1 mutants strongly enhance endoderm and EMS spindle rotation defects associated with Wnt pathway mutants. SRC-1 and MES-1 signal bidirectionally to control cell fate and division orientation in both EMS and P2. Our findings suggest that Wnt and Src signaling function in parallel to control developmental outcomes within a single responding cell.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12110172&dopt=Abstract ">Link to article in PubMed</a></p>
dc.relation.urlhttps://doi.org/10.1016/S1534-5807(02)00185-5
dc.subjectAnimals; Body Patterning; Caenorhabditis elegans; *Caenorhabditis elegans Proteins; Cell Division; Cell Lineage; Cell Polarity; DNA-Binding Proteins; Embryo, Nonmammalian; Endoderm; Gene Expression Regulation, Developmental; Helminth Proteins; High Mobility Group Proteins; Molecular Sequence Data; Phosphotyrosine; Proto-Oncogene Proteins; Sequence Homology, Amino Acid; Sequence Homology, Nucleic Acid; Signal Transduction; Wnt Proteins; *Zebrafish Proteins; src-Family Kinases
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleSRC-1 and Wnt signaling act together to specify endoderm and to control cleavage orientation in early C. elegans embryos
dc.typeJournal Article
dc.source.journaltitleDevelopmental cell
dc.source.volume3
dc.source.issue1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/gsbs_sp/93
dc.identifier.contextkey549655
html.description.abstract<p>In early C. elegans embryos, signaling between a posterior blastomere, P2, and a ventral blastomere, EMS, specifies endoderm and orients the division axis of the EMS cell. Although Wnt signaling contributes to this polarizing interaction, no mutants identified to date abolish P2/EMS signaling. Here, we show that two tyrosine kinase-related genes, src-1 and mes-1, are required for the accumulation of phosphotyrosine between P2 and EMS. Moreover, src-1 and mes-1 mutants strongly enhance endoderm and EMS spindle rotation defects associated with Wnt pathway mutants. SRC-1 and MES-1 signal bidirectionally to control cell fate and division orientation in both EMS and P2. Our findings suggest that Wnt and Src signaling function in parallel to control developmental outcomes within a single responding cell.</p>
dc.identifier.submissionpathgsbs_sp/93
dc.contributor.departmentProgram in Molecular Medicine
dc.contributor.departmentGraduate School of Biomedical Sciences
dc.source.pages113-25


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