BACKGROUND: Autophagy is a ubiquitous cellular process responsible for the bulk 
degradation of cytoplasmic components through the autophagosomal-lysosomal 
pathway. In skeletal muscle, autophagy has been regarded as a key regulator for 
muscle mass maintenance, and its imbalance leads to sarcopenia. However, the 
underlying mechanism is poorly understood.
RESULTS: In this study, we demonstrate that ceMTM3, a FYVE-domain containing 
myotubalarin family phosphatase, is required for the maintenance of muscle 
fibers by preventing excessive autophagy in Caenorhabditis elegans. Knockdown of 
ceMTM3 by using feeding-based RNA interference caused loss of muscle fibers 
accompanied by shortening of muscle cell and body size in aged C. elegans worms. 
This was preceded by the occurrence of excessive autophagy in the muscle and 
other tissues, which subsequently resulted in increased lysosomal activity and 
necrotic cell death. However, knockdown of ceMTM3 did not aggravate the 
abnormalities of muscle wasting in autophagy-deficient atg-18 mutant worms.
CONCLUSIONS: Our data suggest an important role of ceMTM3 in regulating 
autophagy and maintaining muscle fibers. This study may have clinical 
implications for prevention and treatment of sarcopenia.