MeCP2 NID interaction with RNA: implications for Rett syndrome-relevant protein regulation

Read full text
Authors: Katrina Good, Hilmar Strickfaden, Tahir Muhammad, John B. Vincent, Michael J. Hendzel, Christopher J. Nelson, Juan Ausió
Cited by: 0
References: 59

Abstract

Mutations in the X-linked MECP2 gene cause the progressive neurodevelopmental disorder Rett syndrome. Pathogenic missense mutation hotspots exist in the protein's Methyl DNA binding Domain (MBD), and the Nuclear receptor Co-Repressor (NCoR) Interaction Domain (NID), indicating these regions as critical for MeCP2 function. The NID binds to a co-repressor complex allowing transcriptional repression at target genes. A putative RNA Binding Domain (RBD) was identified that overlaps with the NID, yet the role that RNA interaction plays in MeCP2 function remains underexplored. Using cell-based and in vitro molecular assays, we validated RNA interaction at the NID/RBD of MeCP2 both to a dsRNA probe in vitro and to the lncRNA NEAT1_2 in cells. As expected, this region did not appear to affect MeCP2-chromatin interactions; however, we found that RNA-RBD interaction precludes MeCP2-NCoR binding in cells. Taken together, we find that RNA interaction at this non-canonical RNA binding domain regulates important MeCP2-protein interactions and therefore may be a key part of the pathophysiology of Rett syndrome.

Fields of Study & Subjects

Genetics and Neurodevelopmental Disorders Ubiquitin and proteasome pathways RNA modifications and cancer

Publication details

Journal / source
Human Molecular Genetics
Volume
35
Issue
7
Publication date
1 January 2026
Language
EN