TY - INPR UR - http://dx.doi.org/10.1038/s41431-024-01610-1 JF - European Journal of Human Genetics N2 - Bryant-Li-Bhoj syndrome (BLBS), which became OMIM-classified in 2022 (OMIM: 619720, 619721), is caused by germline variants in the two genes that encode histone H3.3 (H3-3A/H3F3A and H3-3B/H3F3B) [1-4]. This syndrome is characterized by developmental delay/intellectual disability, craniofacial anomalies, hyper/hypotonia, and abnormal neuroimaging [1, 5]. BLBS was initially categorized as a progressive neurodegenerative syndrome caused by de novo heterozygous variants in either H3-3A or H3-3B [1-4]. Here, we analyze the data of the 58 previously published individuals along 38 unpublished, unrelated individuals. In this larger cohort of 96 people, we identify causative missense, synonymous, and stop-loss variants. We also expand upon the phenotypic characterization by elaborating on the neurodevelopmental component of BLBS. Notably, phenotypic heterogeneity was present even amongst individuals harboring the same variant. To explore the complex phenotypic variation in this expanded cohort, the relationships between syndromic phenotypes with three variables of interest were interrogated: sex, gene containing the causative variant, and variant location in the H3.3 protein. While specific genotype-phenotype correlations have not been conclusively delineated, the results presented here suggest that the location of the variants within the H3.3 protein and the affected gene (H3-3A or H3-3B) contribute more to the severity of distinct phenotypes than sex. Since these variables do not account for all BLBS phenotypic variability, these findings suggest that additional factors may play a role in modifying the phenotypes of affected individuals. Histones are poised at the interface of genetics and epigenetics, highlighting the potential role for gene-environment interactions and the importance of future research. PB - Springer Science and Business Media LLC Y1 - 2024/04/27/ A1 - Layo-Carris, Dana E A1 - Lubin, Emily E A1 - Sangree, Annabel K A1 - Clark, Kelly J A1 - Durham, Emily L A1 - Gonzalez, Elizabeth M A1 - Smith, Sarina A1 - Angireddy, Rajesh A1 - Wang, Xiao Min A1 - Weiss, Erin A1 - Mendoza-Londono, Roberto A1 - Dupuis, Lucie A1 - Damseh, Nadirah A1 - Velasco, Danita A1 - Valenzuela, Irene A1 - Codina-Solà, Marta A1 - Ziats, Catherine A1 - Have, Jaclyn A1 - Clarkson, Katie A1 - Steel, Dora A1 - Kurian, Manju A1 - Barwick, Katy A1 - Carrasco, Diana A1 - Dagli, Aditi I A1 - Nowaczyk, MJM A1 - Han?árová, Miroslava A1 - Bendová, ?árka A1 - Prchalova, Darina A1 - Sedlá?ek, Zden?k A1 - Baxová, Alica A1 - Nowak, Catherine Bearce A1 - Douglas, Jessica A1 - Chung, Wendy K A1 - Longo, Nicola A1 - Platzer, Konrad A1 - Klöckner, Chiara A1 - Averdunk, Luisa A1 - Wieczorek, Dagmar A1 - Krey, Ilona A1 - Zweier, Christiane A1 - Reis, Andre A1 - Balci, Tugce A1 - Simon, Marleen A1 - Kroes, Hester Y A1 - Wiesener, Antje A1 - Vasileiou, Georgia A1 - Marinakis, Nikolaos M A1 - Veltra, Danai A1 - Sofocleous, Christalena A1 - Kosma, Konstantina A1 - Traeger Synodinos, Joanne A1 - Voudris, Konstantinos A A1 - Vuillaume, Marie-Laure A1 - Gueguen, Paul A1 - Derive, Nicolas A1 - Colin, Estelle A1 - Battault, Clarisse A1 - Au, Billie A1 - Delatycki, Martin A1 - Wallis, Mathew A1 - Gallacher, Lyndon A1 - Majdoub, Fatma A1 - Smal, Noor A1 - Weckhuysen, Sarah A1 - Schoonjans, An-Sofie A1 - Kooy, R Frank A1 - Meuwissen, Marije A1 - Cocanougher, Benjamin T A1 - Taylor, Kathryn A1 - Pizoli, Carolyn E A1 - McDonald, Marie T A1 - James, Philip A1 - Roeder, Elizabeth R A1 - Littlejohn, Rebecca A1 - Borja, Nicholas A A1 - Thorson, Willa A1 - King, Kristine A1 - Stoeva, Radka A1 - Suerink, Manon A1 - Nibbeling, Esther A1 - Baskin, Stephanie A1 - L E Guyader, Gwenaël A1 - Kaplan, Julie A1 - Muss, Candace A1 - Carere, Deanna Alexis A1 - Bhoj, Elizabeth JK A1 - Bryant, Laura M SN - 1018-4813 TI - Expanded phenotypic spectrum of neurodevelopmental and neurodegenerative disorder Bryant-Li-Bhoj syndrome with 38 additional individuals AV - public N1 - This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. ID - discovery10191954 ER -