Title page for ETD etd-02102012-112645

Type of Document Master's Thesis
Author Reinholt, Brad Michael
Author's Email Address bmreinholt@gmail.com
URN etd-02102012-112645
Title Inactivation of Stac3 causes skeletal muscle defects and perinatal death in mice
Degree Master of Science In the Life Sciences
Department Animal and Poultry Sciences
Advisory Committee
Advisor Name Title
Gerrard, David E. Committee Co-Chair
Jiang, Honglin Committee Co-Chair
Grant, Alan Committee Member
  • SH3 domain
  • C1 domain
  • myogenesis
  • SH3 and cysteine rich domain 3 (Stac3)
Date of Defense 2012-01-27
Availability unrestricted
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.
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