Asset Details
Do you wish to reserve the book?
ZMYND11 functions in bimodal regulation of latent genes and brain-like splicing to safeguard corticogenesis
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
ZMYND11 functions in bimodal regulation of latent genes and brain-like splicing to safeguard corticogenesis
Do you wish to request the book?
ZMYND11 functions in bimodal regulation of latent genes and brain-like splicing to safeguard corticogenesis
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
ZMYND11 functions in bimodal regulation of latent genes and brain-like splicing to safeguard corticogenesis
2025
Overview
Despite the numerous pathogenic variants linked to neurodevelopmental disorders (NDDs) including autism (ASD) and intellectual disability, our understanding of the underlying mechanisms caused by risk genes remain unclear. Here, we show that mutations in
ZMYND11
, a newly implicated risk gene, impair human cortical progenitor and neuron production. ZMYND11, known for its tumor suppressor function, encodes a histone-reader that recognizes sites of transcriptional elongation and acts as a co-repressor. ZMYND11-deficient cortical neural stem cells upregulate inappropriate developmental pathways, leading to disrupted neurogenesis. In addition to its role on chromatin, ZMYND11 regulates a brain-specific RNA isoform switch involving the splicing regulator RBFOX2. Similar defects are observed in other chromatin-related ASD risk genes, some of which are partially rescued by enhancing ZMYND11 function. These findings uncover convergent pathways linking chromatin regulation and splicing to human brain development and advance our understanding of how genetic risk contributes to NDD.
Here authors report that mutations in the neurodevelopmental risk gene
ZMYND11
disrupt human cortical neuron development by altering chromatin regulation and RNA splicing.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ 13/106
/ 13/109
/ 13/31
/ 13/51
/ 13/89
/ 14/63
/ 45/41
/ 45/91
/ Animals
/ Autism
/ Brain
/ Cerebral Cortex - metabolism
/ Gene Expression Regulation, Developmental
/ Genes
/ Histones
/ Humanities and Social Sciences
/ Humans
/ Mice
/ Mutation
/ Neural Stem Cells - metabolism
/ Neurodevelopmental disorders
/ Neurons
/ Proteins
/ Risk
/ RNA
/ RNA Splicing Factors - genetics
/ RNA Splicing Factors - metabolism
/ Science
/ Splicing
