Inactivation of Stac3 causes skeletal muscle defects and perinatal death in mice

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dc.contributor.authorReinholt, Brad Michaelen
dc.contributor.committeecochairJiang, Honglinen
dc.contributor.committeecochairGerrard, David E.en
dc.contributor.committeememberGrant, Alanen
dc.contributor.departmentAnimal and Poultry Sciencesen
dc.date.accessioned2017-04-04T19:49:14Zen
dc.date.adate2012-03-13en
dc.date.available2017-04-04T19:49:14Zen
dc.date.issued2012-01-27en
dc.date.rdate2016-10-17en
dc.date.sdate2012-02-10en
dc.description.abstractThe 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.en
dc.description.degreeMaster of Scienceen
dc.identifier.otheretd-02102012-112645en
dc.identifier.sourceurlhttp://scholar.lib.vt.edu/theses/available/etd-02102012-112645/en
dc.identifier.urihttp://hdl.handle.net/10919/76784en
dc.language.isoen_USen
dc.publisherVirginia Techen
dc.rightsIn Copyrighten
dc.rights.urihttp://rightsstatements.org/vocab/InC/1.0/en
dc.subjectSH3 domainen
dc.subjectC1 domainen
dc.subjectmyogenesisen
dc.subjectSH3 and cysteine rich domain 3 (Stac3)en
dc.titleInactivation of Stac3 causes skeletal muscle defects and perinatal death in miceen
dc.typeThesisen
dc.type.dcmitypeTexten
thesis.degree.disciplineAnimal and Poultry Sciencesen
thesis.degree.grantorVirginia Polytechnic Institute and State Universityen
thesis.degree.levelmastersen
thesis.degree.nameMaster of Science in Life Sciencesen

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