Loss of mouse Stmn2 function causes motor neuropathy.

(Neuron 110, 1671–1688; May 18, 2022) It was brought to our attention that there is a clerical mistake in one of the panels of Figure 1 (Figure 1E) in our recent publication. The representative blots for the CNS Stmn2 protein levels in the F2 generation of Stmn2 mutants included an incorrect duplicated blot for the GAPDH loading control in the brain samples. We have corrected this error and replaced the figure online with one that includes the correct blot for the GAPDH loading control for those samples. We would like to profoundly apologize to the readers for the oversight and honest mistake.Figure 1E. CRISPR/Cas9 editing of Stmn2 (original)View Large Image Figure ViewerDownload Hi-res image Download (PPT) Loss of mouse Stmn2 function causes motor neuropathyGuerra San Juan et al.NeuronMarch 15, 2022In BriefThe TDP43-regulated gene STMN2 provides a potential connection between TDP43 dysfunction and motor neuropathy as observed in ALS. Guerra San Juan, Nash, et al. demonstrate that mouse Stmn2 is essential for maintaining normal motor function in vivo; its deficiency results in neuromuscular junction denervation, muscle atrophy, and impaired motor behavior. Full-Text PDF Open Archive