Investigating the Homologue of the Mammalian Gene Myocyte Stress 1 in Drosophila Melanogaster

The stress responsive gene myocyte stress 1 (ms1) has been implicated in the initiation of cardiac and skeletal muscle hypertrophy. Upregulation of ms1 is observed shortly after stress induction in rat hearts before the development of left ventricular hypertrophy. The protein sequence of MS1 is highly conserved across many species including the fruit fly model organism Drosophila melanogaster, with high levels of homology found in the actin binding domain. Here, the potential Drosophila homologue of ms1 (dms1, designated CG3630) has been investigated to determine the function and the level of functional homology to mammalian ms1. The role of this gene in the Drosophila heart and somatic muscle has been examined by manipulating the expression of dms1. Knockdown of dms1 affects somatic muscle function, reducing the ability of flies to climb and decreasing their daily activity levels. Overexpression of dms1 appears to increase climbing ability, but does not affect daily activity, suggesting that muscle strength is increased but energy is not. Expression of mouse MS1 in Drosophila muscle appears to have a similar effect to dms1 on muscle function, but under starvation conditions may increase longevity, whereas dms1 does not. This suggests a fundamental difference in function between mammalian and Drosophila ms1 in metabolism. The results of this project revealed an important role for dms1 in the function of Drosophila muscle, and have contributed to the development of a fruit fly model for research into this gene