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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, RESULTS. Meshes: Aging, Amino Acid Sequence, Animals, Anterior Horn Cells, Base Sequence, Cell Line, Gene Expression, Gene Targeting, Humans, Mice, Mice, Inbred C57BL, Mice, Knockout, Molecular Sequence Data, Motor Activity, Motor Neurons, Muscle Fibers, Fast-Twitch, Muscle Fibers, Skeletal, Muscle Fibers, Slow-Twitch, Mutant Proteins, Nerve Tissue Proteins, Neuromuscular Junction, Presynaptic Terminals, Protein Transport.
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Does gas7-deficient mouse reveal roles in motor function and muscle fiber composition during aging? Context: Growth arrest-specific gene 7 (Gas7) has previously been shown to be involved in neurite outgrowth in vitro; however, its actual role has yet to be determined. To investigate the physiological function of Gas7 in vivo, here we generated a Gas7-deficient mouse strain with a labile Gas7 mutant protein whose functions are similar to wild-type Gas7. Our data show that aged Gas7-deficient mice have motor activity defects due to decreases in the number of spinal motor neurons and in muscle strength, of which the latter may be caused by changes in muscle fiber composition as shown in the soleus. In cross sections of the soleus of Gas7-deficient mice, gross morphological features and levels of myosin heavy chain I (MHC I) and MHC II markers revealed significantly fewer fast fibers. In addition, we found that nerve terminal sprouting, which may be associated with slow and fast muscle fiber composition, was considerably reduced at neuromuscular junctions (NMJ) during aging.
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These findings indicate that Gas7 is involved in motor neuron function associated with muscle strength maintenance. Final Decision: yes