DCTN1 and Atrophy: On the other hand, two heterozygous G59S DCTN1 knock-in strains generated by distinct research groups displayed halved DCTN1 protein levels and no sign of mutant protein aggregation in brain and spinal cord, suggesting that the G59S substitution might lead to rapid protein degradation in vivo, but at the same time, mice started manifesting muscle atrophy due to spinal MN loss at 10 months of age.