A GREATER UNDERSTANDING OF MECHANISMS REGULATING MUSCLE GROWTH AND DEVELOPMENT IS ESSENTIAL TO IMPROVE MEAT PRODUCTION IN DOMESTIC ANIMALS. MUSCLE GROWTH RESULTS FROM INCREASES IN NUMBERS AND/OR SIZE OF MUSCLE FIBERS. MYOSTATIN (MSTN) INHIBITS MUSCLE GROWTH AND NATURAL OR INDUCED MUTATIONS OF THE MSTN GENE INCREASES MUSCLE GROWTH IN MAMMALS AND FISH. HOWEVER, MECHANISMS (FIBER NUMBER/SIZE) OF ENHANCING MUSCLE GROWTH BY INACTIVATION OF THE MSTN GENE ARE DIFFERENT AND DEGREES OF THE DIFFERENCES VARY AMONG DIFFERENT SPECIES. SO FAR, ANY AVIAN MODEL WITH AN INACTIVE MSTN GENE HAS NOT BEEN DEVELOPED. WE RECENTLY DEVELOPED A QUAIL LINE WITH AN INACTIVE MSTN GENE. THE PROPOSED RESEARCH IS FOCUSED ON CHARACTERIZATION OF PRO-MYOGENIC ACTIVITY OF MSTN INACTIVATION IN THE QUAIL MODEL. IN MAMMALS, INCREASED TOTAL MYOFIBER NUMBERS (HYPERPLASIA) ARE DETERMINED DURING FETAL DEVELOPMENT WITH A CONTINUOUS MATERNAL SUPPLY OF NUTRIENTS AND ENERGY. HOWEVER, AVIAN EMBRYOGENESIS OCCURS INDEPENDENT OF THE HENS IN AN EGG CONSISTING OF A FIXED SIZE AND CONTAINING A LIMITED SUPPLY OF NUTRIENTS. THEREFORE, WE WILL ALSO INVESTIGATE THE INTERACTION OF THESE EGG ENVIRONMENTAL FACTORS AND GENETICS ON THE RESULTING PHENOTYPE OF MSTN INACTIVATION IN THE AVIAN MODEL. THIS EXPLORATORY GRANT WILL GENERATE VALUABLE INFORMATION THAT WILL BE A FOUNDATION FOR A FUTURE STUDY FOCUSING ON 1) DETERMINING THE CRITICAL TIME WINDOW OF MSTN FUNCTION SO AS TO DEVELOP APPROACHES TO INACTIVATE MSTN AT SPECIFIC PERMISSIVE STAGES OF MUSCLE DEVELOPMENT OR AGES, 2) STUDYING COMPARATIVE ASPECTS IN MOLECULAR AND CELLULAR MECHANISMS, AND 3) EXTENDING THIS PROOF-OF CONCEPT IN OTHER MAJOR POULTRY SPECIES.