Ets2 2018
This application is an extension of project 1560 and 5083.
Skeletal muscle accounts for almost half of the body mass and is responsible for the movement of the human body. Another critical role is maintaining homeostasis of metabolism throughout the body. Given its central role in human mobility and metabolic function, any decline in muscle mass, function or metabolic properties has adverse health and economic consequences. Muscle loss occurs in numerous of contexts including muscular dystrophy, cancer, obesity, diabetes, and chronic pulmonary disease and also ageing. Loss of muscle mass is associated with delayed recovery from illness, slowed wound healing, reduced resting metabolic rate, physical disability, poorer quality of life, and higher health care costs.
Skeletal muscle mass and functionality are regulated by activity. In muscle distinct patterns of electrical stimuli, used by motoneurons to depolarize fast or slow skeletal muscles, are sufficient to activate different transcriptional programs that affect muscle contraction speed, strength and endurance. 

We have previously identified Ets2 as a possible activity-dependent transcriptional regulator of the fast-twitch muscle program. In the following experiments we want to investigate the necessity of the transcription factor Ets2 on the activation of the “fast-twitch muscle program”.
The proposed research is important for the understanding of how muscles respond to changes in activity. This contribution will be significant because whereas numerous studies have identified factors regulating the slow muscle program, relatively less 
is known about activity-dependent regulators of fast-twitch muscles. 

Our proposed research therefore will be an important step in understanding which molecular aspects regulate the “fast-twitch muscle program”. Indeed, the mechanisms identified in this study will also serve to widen the knowledge concerning treatment (e.g. exercise strategies) and enhancement of muscle function by activity and also point to therapeutic strategies for maintaining muscle repair ability in diseases.
In these experiments we will use mice and rats. There will be used anesthesia, analgesia and sedatives. We have experienced that animals fast recover after this protocol and do not expected animals to be stressed out or to be sick.
Skeletal muscle accounts for almost half of the body mass and is responsible for the movement of the human body. Another critical role is maintaining homeostasis of metabolism throughout the body. Given its central role in human mobility and metabolic function, any decline in muscle mass, function or metabolic properties has adverse health and economic consequences. Muscle loss occurs in numerous of contexts including muscular dystrophy, cancer, obesity, diabetes, and chronic pulmonary disease and also ageing. Loss of muscle mass is associated with delayed recovery from illness, slowed wound healing, reduced resting metabolic rate, physical disability, poorer quality of life, and higher health care costs.
Skeletal muscle mass and functionality are regulated by activity. In muscle distinct patterns of electrical stimuli, used by motoneurons to depolarize fast or slow skeletal muscles, are sufficient to activate different transcriptional programs that affect muscle contraction speed, strength and endurance. 

We have previously identified Ets2 as a possible activity-dependent transcriptional regulator of the fast-twitch muscle program. In the following experiments we want to investigate the necessity of the transcription factor Ets2 on the activation of the “fast-twitch muscle program”.
The proposed research is important for the understanding of how muscles respond to changes in activity. This contribution will be significant because whereas numerous studies have identified factors regulating the slow muscle program, relatively less 
is known about activity-dependent regulators of fast-twitch muscles. 

Our proposed research therefore will be an important step in understanding which molecular aspects regulate the “fast-twitch muscle program”. Indeed, the mechanisms identified in this study will also serve to widen the knowledge concerning treatment (e.g. exercise strategies) and enhancement of muscle function by activity and also point to therapeutic strategies for maintaining muscle repair ability in diseases.
In these experiments we will use mice and rats. There will be used anesthesia, analgesia and sedatives. We have experienced that animals fast recover after this protocol and do not expected animals to be stressed out or to be sick.