Tsushima, Robert G.Virdi, Amanvir2022-08-082022-08-082022-04-052022-08-08http://hdl.handle.net/10315/39629The SNARE protein, syntaxin-1A (STX1A) is expressed in the adult rodent heart, yet its role is not fully established. This thesis explored STX1As role in cardiac excitation-contraction (EC) coupling in male and female mouse hearts. Heart-specific homozygous and heterozygous STX1A knockouts were achieved via a tamoxifen-inducible Cre-Lox system. Echocardiography revealed significant systolic dysfunction post-STX1A knockout (week 0), with recovery beginning at week 1 and an absence of sex differences in cardiac function. Transient thickening of the posterior wall (week 1) and delayed contractions (week 0-3) were seen. No genetic compensation of STX2, 3, or 4 was seen, however, EC coupling genes, Cav1.2, RyR2, and SERCA2a, declined at week 0 and recovered at week 3, aligning with the phenotype recovery. Control Cre+ mice remained unchanged, suggesting the transient systolic dysfunction stems from compromised transcription of Ca2+ handling genes. Therefore, STX1A may facilitate normal EC coupling gene expression in adult mouse hearts.Author owns copyright, except where explicitly noted. Please contact the author directly with licensing requests.Cellular biologyElectronic Thesis or Dissertation2022-08-08SNARESyntaxin-1AExcitation-contraction couplingMammalian heartLeft ventricleHeart-specific STX1A KOTransient systolic dysfunctionCalcium handling gene expressionEchocardiographyRT-qPCRCardiac functionMouse heartCardiac sex differencesTamoxifen-inducible Cre-Lox systemContractile function of heartEndocrine function of heart