{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Takesono A"],"funding":["Intramural NIH HHS","Wellcome Trust","Biotechnology and Biological Sciences Research Council"],"pagination":["3371-6"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3295254"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["109(9)"],"pubmed_abstract":["The yolk syncytial layer (YSL) in the zebrafish embryo is a multinucleated syncytium essential for embryo development, but the molecular mechanisms underlying YSL formation remain largely unknown. Here we show that zebrafish solute carrier family 3 member 2 (Slc3a2) is expressed specifically in the YSL and that slc3a2 knockdown causes severe YSL defects including clustering of the yolk syncytial nuclei and enhanced cell fusion, accompanied by disruption of microtubule networks. Expression of a constitutively active RhoA mimics the YSL phenotypes caused by slc3a2 knockdown, whereas attenuation of RhoA or ROCK activity rescues the slc3a2-knockdown phenotypes. Furthermore, slc3a2 knockdown significantly reduces tyrosine phosphorylation of c-Src, and overexpression of a constitutively active S"],"journal":["Proceedings of the National Academy of Sciences of the United States of America"],"pubmed_title":["Solute carrier family 3 member 2 (Slc3a2) controls yolk syncytial layer (YSL) formation by regulating microtubule networks in the zebrafish embryo."],"pmcid":["PMC3295254"],"funding_grant_id":["BB/C51454X/1","BB/F010222/1"],"pubmed_authors":["Takesono A","Cartwright E","Dawid IB","Wilson SW","Moger J","Faroq S","Kudoh T","Farooq S"],"additional_accession":[]},"is_claimable":false,"name":"Solute carrier family 3 member 2 (Slc3a2) controls yolk syncytial layer (YSL) formation by regulating microtubule networks in the zebrafish embryo.","description":"The yolk syncytial layer (YSL) in the zebrafish embryo is a multinucleated syncytium essential for embryo development, but the molecular mechanisms underlying YSL formation remain largely unknown. Here we show that zebrafish solute carrier family 3 member 2 (Slc3a2) is expressed specifically in the YSL and that slc3a2 knockdown causes severe YSL defects including clustering of the yolk syncytial nuclei and enhanced cell fusion, accompanied by disruption of microtubule networks. Expression of a constitutively active RhoA mimics the YSL phenotypes caused by slc3a2 knockdown, whereas attenuation of RhoA or ROCK activity rescues the slc3a2-knockdown phenotypes. Furthermore, slc3a2 knockdown significantly reduces tyrosine phosphorylation of c-Src, and overexpression of a constitutively active S","dates":{"release":"2012-01-01T00:00:00Z","publication":"2012 Feb","modification":"2026-07-15T08:16:39.092Z","creation":"2019-03-27T00:50:54Z"},"accession":"S-EPMC3295254","cross_references":{"pubmed":["22331904"],"doi":["10.1073/pnas.1200642109"]}}