Cachexia is a systemic metabolic syndrome characterized by progressive muscle wasting. Cachectic muscle wasting presents as a comorbidity with pathological illnesses like cancer, chronic inflammation, and type 2 diabetes. The development of cachexia complicates treatment of these diseases and worsens clinical outcomes. Thus, it has become the focus of intense investigation. While many of the upstream mechanisms that propagate cachectic muscle wasting have been brought to light, little is known of the downstream mechanisms which would be more clinically relevant. Here, we have adopted a Drosophila model of cachectic muscle wasting to elucidate a novel role of the transcriptional regulator, cabut (cbt), in selective degeneration of flight muscles over jump muscles. We report that cbt impairs mitochondrial function and expends vital glycogen stores from the flight muscles. Our results contend that the resilience of the jump muscles to degeneration resides in their low oxidative output and sporadic energetic requirements. Furthermore, we have implicated cbt as a positive regulator of jump muscle fiber number during muscle development
