Thomas and colleagues (pp. 1122-1133) demonstrate severe dysregulation of developmentally regulated alternative splicing and polyadenylation in congenital myotonic dystrophy (CDM). In doing so, they also highlight the importance of these post-transcriptional processes during normal fetal muscle development. Finally, they generate and characterize a mouse model of CDM that lacks all three Muscleblind-like proteins. © 2017 Jagannathan and Bradley; Published by Cold Spring Harbor Laboratory Press.
Sujatha Jagannathan, Robert K Bradley. Congenital myotonic dystrophy-an RNA-mediated disease across a developmental continuum. Genes & development. 2017 Jun 01;31(11):1067-1068
PMID: 28717044
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