Thanks to @xiaoliwu.bsky.social, @lisatraunmueller.bsky.social, and other collaborators and lab members for making this possible!
We hope that our work will be a step toward a fuller understanding of interconnections between chromatin regulators and shed light on a disorder lacking mechanistic insight. We are also very interested in the possible interplay between ZMYND11 and KMT2A in regulating oncogenesis.
Many chromatin regulators have been linked to NDD and ASD, an expanding family of “chromatinopathies” with overlapping symptoms and convergence in gene misregulation. To understand the network-scale behaviour of these systems, we need to unravel the dense interconnections between regulatory nodes.
We link ZMYND11 function to KMT2A, a histone methyltransferase and transcriptional activator which is itself the cause of a neurodevelopmental disorder. We find that ZMYND11 binds and inhibits KMT2A, repressing non-neuronal developmental programs and safeguarding neuronal gene expression.
Very pleased to share this work from my time as a graduate student with the Greenberg lab. We investigate the molecular function of ZMYND11, a tumor suppressor and chromatin reader which is also a cause of syndromic intellectual disability. Preprint available now: www.biorxiv.org/content/10.1...
Mutations in the chromatin reader and tumor suppressor ZMYND11 are the cause of ZMYND11-related syndromic intellectual disability (ZRSID), a disorder characterized by symptoms such as language and mot...
