Literature DB >> 31949314

GATAD2B-associated neurodevelopmental disorder (GAND): clinical and molecular insights into a NuRD-related disorder.

Christine Shieh1, Natasha Jones2, Brigitte Vanle3,4, Margaret Au5, Alden Y Huang6, Ana P G Silva2, Hane Lee7, Emilie D Douine8, Maria G Otero9, Andrew Choi9, Katheryn Grand10, Ingrid P Taff11, Mauricio R Delgado12, M J Hajianpour13, Andrea Seeley14, Luis Rohena15,16, Hilary Vernon17, Karen W Gripp18, Samantha A Vergano19, Sonal Mahida20, Sakkubai Naidu21,22, Ana Berta Sousa23, Karen E Wain24, Thomas D Challman24, Geoffrey Beek25, Donald Basel26, Judith Ranells27, Rosemarie Smith28, Roman Yusupov29, Mary-Louise Freckmann30, Lisa Ohden31, Laura Davis-Keppen32, David Chitayat33,34, James J Dowling35, Richard Finkel36, Andrew Dauber37, Rebecca Spillmann38, Loren D M Pena39,40, Kay Metcalfe41, Miranda Splitt42, Katherine Lachlan43,44, Shane A McKee45, Jane Hurst46, David R Fitzpatrick47, Jenny E V Morton48,49,50, Helen Cox48,49,50, Sunita Venkateswaran51, Juan I Young52, Eric D Marsh53, Stanley F Nelson8, Julian A Martinez54, John M Graham55, Usha Kini56, Joel P Mackay2, Tyler Mark Pierson57,58,59.   

Abstract

PURPOSE: Determination of genotypic/phenotypic features of GATAD2B-associated neurodevelopmental disorder (GAND).
METHODS: Fifty GAND subjects were evaluated to determine consistent genotypic/phenotypic features. Immunoprecipitation assays utilizing in vitro transcription-translation products were used to evaluate GATAD2B missense variants' ability to interact with binding partners within the nucleosome remodeling and deacetylase (NuRD) complex.
RESULTS: Subjects had clinical findings that included macrocephaly, hypotonia, intellectual disability, neonatal feeding issues, polyhydramnios, apraxia of speech, epilepsy, and bicuspid aortic valves. Forty-one novelGATAD2B variants were identified with multiple variant types (nonsense, truncating frameshift, splice-site variants, deletions, and missense). Seven subjects were identified with missense variants that localized within two conserved region domains (CR1 or CR2) of the GATAD2B protein. Immunoprecipitation assays revealed several of these missense variants disrupted GATAD2B interactions with its NuRD complex binding partners.
CONCLUSIONS: A consistent GAND phenotype was caused by a range of genetic variants in GATAD2B that include loss-of-function and missense subtypes. Missense variants were present in conserved region domains that disrupted assembly of NuRD complex proteins. GAND's clinical phenotype had substantial clinical overlap with other disorders associated with the NuRD complex that involve CHD3 and CHD4, with clinical features of hypotonia, intellectual disability, cardiac defects, childhood apraxia of speech, and macrocephaly.

Entities:  

Keywords:  GATAD2B; NuRD complex; apraxia of speech; chromatin remodeling; macrocephaly

Mesh:

Substances:

Year:  2020        PMID: 31949314      PMCID: PMC7920571          DOI: 10.1038/s41436-019-0747-z

Source DB:  PubMed          Journal:  Genet Med        ISSN: 1098-3600            Impact factor:   8.822


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