{"id":{"repo_id":"vt","oai_identifier":"oai:vtechworks.lib.vt.edu:10919/76784"},"canonical_url":"https://search.dev.ndltd.org/etd/vt/oai:vtechworks.lib.vt.edu:10919/76784","repository":{"repo_id":"vt","name":"Virginia Tech","base_url":"https://vtechworks.lib.vt.edu/oai/request"},"display":{"title":"Inactivation of Stac3 causes skeletal muscle defects and perinatal death in mice","abstract":"The Src homology 3 domain (SH3) and cysteine rich domain (C1) 3 (Stac3) gene is a novel gene copiously expressed in skeletal muscle. The objective of this research was to determine the role of Stac3 in development, specifically in skeletal muscle. We achieved this objective by evaluating the phenotypic effects of Stac3 gene inactivation on development in mice. At birth homozygous Stac3 null (Stac3-/-) mice died perinatally and remained in fetal position with limp limbs, but possessed otherwise normal organs based on gross and histological evaluations. The primary phenotypes displayed at term in Stac3-/- mice were reduced late gestational body weights, increased prevalence of myotubes with centrally located nuclei and severe deformities throughout all skeletal muscles. At embryonic day 18.5 (E18.5) Stac3-/- mice displayed a 12.7% reduction (P < 0.001) in weight compared to wild type (Stac3+/+) or heterozygous (Stac3+/-) littermates while at E15.5 body weights and morphology were similar. At birth (P0) and at E17.5, Stac3-/- mice had 59% and 24% (P < 0.001) more myotubes with centrally located nuclei, respectively, than Stac3+/- or Stac3+/+ littermates. Stac3-/- mice also displayed increased myotube and myofiber cross sectional area at P0 (P < 0.001) and E17.5 (P < 0.05) with disorganized fiber bundling. Overall, these data show Stac3 is necessary for development of viable offspring and suggest Stac3 plays a critical role in fetal development where its primary phenotype is exhibited in skeletal muscle.","abstract_html":"The Src homology 3 domain (SH3) and cysteine rich domain (C1) 3 (Stac3) gene is a novel gene copiously expressed in skeletal muscle. The objective of this research was to determine the role of Stac3 in development, specifically in skeletal muscle. We achieved this objective by evaluating the phenotypic effects of Stac3 gene inactivation on development in mice. At birth homozygous Stac3 null (Stac3-/-) mice died perinatally and remained in fetal position with limp limbs, but possessed otherwise normal organs based on gross and histological evaluations. The primary phenotypes displayed at term in Stac3-/- mice were reduced late gestational body weights, increased prevalence of myotubes with centrally located nuclei and severe deformities throughout all skeletal muscles. At embryonic day 18.5 (E18.5) Stac3-/- mice displayed a 12.7% reduction (P &lt; 0.001) in weight compared to wild type (Stac3+/+) or heterozygous (Stac3+/-) littermates while at E15.5 body weights and morphology were similar. At birth (P0) and at E17.5, Stac3-/- mice had 59% and 24% (P &lt; 0.001) more myotubes with centrally located nuclei, respectively, than Stac3+/- or Stac3+/+ littermates. Stac3-/- mice also displayed increased myotube and myofiber cross sectional area at P0 (P &lt; 0.001) and E17.5 (P &lt; 0.05) with disorganized fiber bundling. Overall, these data show Stac3 is necessary for development of viable offspring and suggest Stac3 plays a critical role in fetal development where its primary phenotype is exhibited in skeletal muscle.","abstract_has_math":false,"creators":["Reinholt, Brad Michael"],"institution":"Virginia Tech","degree_name":"Master of Science in Life Sciences","degree_level":"masters","degree_discipline":"Animal and Poultry Sciences","degree_department":"Animal and Poultry Sciences","school":null,"contributors":[],"advisors":[],"committee_chairs":["Jiang, Honglin","Gerrard, David E."],"committee_members":["Grant, Alan L."],"year":2012,"date_issued":"2012-01-27","date_published":"2012-01-27","updated_at":"2026-07-22T22:20:17Z","subjects":["SH3 domain","C1 domain","myogenesis","SH3 and cysteine rich domain 3 (Stac3)"],"languages":["en_US"],"rights":["In Copyright"],"rights_urls":["http://rightsstatements.org/vocab/InC/1.0/"],"identifier_entries":[{"key":"dc:identifier.other","label":"Dc Identifier Other","values":["etd-02102012-112645"],"render_values":[{"text":"etd-02102012-112645","href":null,"code":true}]}]},"links":{"outbound_url":"http://hdl.handle.net/10919/76784","outbound_label":"Handle","outbound_source":"dc:identifier.uri"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor.committeechair","label":"Committee Chair","values":["Jiang, Honglin","Gerrard, David E."]},{"key":"dc:contributor.committeemember","label":"Committee Member","values":["Grant, Alan L."]},{"key":"dc:contributor.department","label":"Department","values":["Animal and Poultry Sciences"]},{"key":"dc:creator","label":"Author","values":["Reinholt, Brad Michael"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.accessioned","label":"Dc Date Accessioned","values":["2017-04-04T19:49:14Z"]},{"key":"dc:date.available","label":"Dc Date Available","values":["2017-04-04T19:49:14Z","2016-10-17"]},{"key":"dc:date.issued","label":"Date","values":["2012-01-27"]},{"key":"dc:publisher","label":"Institution","values":["Virginia Tech"]},{"key":"dc:type","label":"Dc Type","values":["Thesis"]},{"key":"dc:type.dcmitype","label":"Dc Type Dcmitype","values":["Text"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Animal and Poultry Sciences"]},{"key":"thesis:degree_level","label":"Degree Level","values":["masters"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Master of Science in Life Sciences"]},{"key":"thesis:institution_name","label":"Thesis Institution Name","values":["Virginia Polytechnic Institute and State University"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["SH3 domain","C1 domain","myogenesis","SH3 and cysteine rich domain 3 (Stac3)"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language.iso","label":"Language (ISO)","values":["en_US"]},{"key":"dc:rights","label":"Dc Rights","values":["In Copyright"]},{"key":"dc:rights.uri","label":"Rights URI","values":["http://rightsstatements.org/vocab/InC/1.0/"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier.other","label":"Dc Identifier Other","values":["etd-02102012-112645"]},{"key":"dc:identifier.uri","label":"Identifier URI","values":["http://hdl.handle.net/10919/76784"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["The Src homology 3 domain (SH3) and cysteine rich domain (C1) 3 (Stac3) gene is a novel gene copiously expressed in skeletal muscle. The objective of this research was to determine the role of Stac3 in development, specifically in skeletal muscle. We achieved this objective by evaluating the phenotypic effects of Stac3 gene inactivation on development in mice. At birth homozygous Stac3 null (Stac3-/-) mice died perinatally and remained in fetal position with limp limbs, but possessed otherwise normal organs based on gross and histological evaluations. The primary phenotypes displayed at term in Stac3-/- mice were reduced late gestational body weights, increased prevalence of myotubes with centrally located nuclei and severe deformities throughout all skeletal muscles. At embryonic day 18.5 (E18.5) Stac3-/- mice displayed a 12.7% reduction (P < 0.001) in weight compared to wild type (Stac3+/+) or heterozygous (Stac3+/-) littermates while at E15.5 body weights and morphology were similar. At birth (P0) and at E17.5, Stac3-/- mice had 59% and 24% (P < 0.001) more myotubes with centrally located nuclei, respectively, than Stac3+/- or Stac3+/+ littermates. Stac3-/- mice also displayed increased myotube and myofiber cross sectional area at P0 (P < 0.001) and E17.5 (P < 0.05) with disorganized fiber bundling. Overall, these data show Stac3 is necessary for development of viable offspring and suggest Stac3 plays a critical role in fetal development where its primary phenotype is exhibited in skeletal muscle."]},{"key":"dc:description.degree","label":"Dc Description Degree","values":["Master of Science"]},{"key":"dc:title","label":"Title","values":["Inactivation of Stac3 causes skeletal muscle defects and perinatal death in mice"]}]}],"canonical_facts":{"dc:contributor.committeechair":["Jiang, Honglin","Gerrard, David E."],"dc:contributor.committeemember":["Grant, Alan L."],"dc:contributor.department":["Animal and Poultry Sciences"],"dc:creator":["Reinholt, Brad Michael"],"dc:date.accessioned":["2017-04-04T19:49:14Z"],"dc:date.available":["2017-04-04T19:49:14Z","2016-10-17"],"dc:date.issued":["2012-01-27"],"dc:description.abstract":["The Src homology 3 domain (SH3) and cysteine rich domain (C1) 3 (Stac3) gene is a novel gene copiously expressed in skeletal muscle. The objective of this research was to determine the role of Stac3 in development, specifically in skeletal muscle. We achieved this objective by evaluating the phenotypic effects of Stac3 gene inactivation on development in mice. At birth homozygous Stac3 null (Stac3-/-) mice died perinatally and remained in fetal position with limp limbs, but possessed otherwise normal organs based on gross and histological evaluations. The primary phenotypes displayed at term in Stac3-/- mice were reduced late gestational body weights, increased prevalence of myotubes with centrally located nuclei and severe deformities throughout all skeletal muscles. At embryonic day 18.5 (E18.5) Stac3-/- mice displayed a 12.7% reduction (P < 0.001) in weight compared to wild type (Stac3+/+) or heterozygous (Stac3+/-) littermates while at E15.5 body weights and morphology were similar. At birth (P0) and at E17.5, Stac3-/- mice had 59% and 24% (P < 0.001) more myotubes with centrally located nuclei, respectively, than Stac3+/- or Stac3+/+ littermates. Stac3-/- mice also displayed increased myotube and myofiber cross sectional area at P0 (P < 0.001) and E17.5 (P < 0.05) with disorganized fiber bundling. Overall, these data show Stac3 is necessary for development of viable offspring and suggest Stac3 plays a critical role in fetal development where its primary phenotype is exhibited in skeletal muscle."],"dc:description.degree":["Master of Science"],"dc:identifier.other":["etd-02102012-112645"],"dc:identifier.uri":["http://hdl.handle.net/10919/76784"],"dc:language.iso":["en_US"],"dc:publisher":["Virginia Tech"],"dc:rights":["In Copyright"],"dc:rights.uri":["http://rightsstatements.org/vocab/InC/1.0/"],"dc:subject":["SH3 domain","C1 domain","myogenesis","SH3 and cysteine rich domain 3 (Stac3)"],"dc:title":["Inactivation of Stac3 causes skeletal muscle defects and perinatal death in mice"],"dc:type":["Thesis"],"dc:type.dcmitype":["Text"],"thesis:degree_discipline":["Animal and Poultry Sciences"],"thesis:degree_level":["masters"],"thesis:degree_name":["Master of Science in Life Sciences"],"thesis:institution_name":["Virginia Polytechnic Institute and State University"]},"updated_at":"2026-07-22T22:20:17Z"}