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. 2024 Nov 5;15:9553. doi: 10.1038/s41467-024-53636-0

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© The Author(s) 2024

Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by-nc-nd/4.0/.

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Fig. 7 — a Distribution of DDX3X mutants in this study across cBioPortal samples and ten studies of DDX3X-related neurodevelopmental disorders. The number of patient samples in which the mutations at the position of each mutant appeared, in addition to mutations at positions within three amino acids of our selected mutants, were counted. b Proposed working model. DDX3X mutants that disrupt ATPase and strand release activities form hollow condensates in cells without external stress, while mutants that do not disrupt those catalytic steps remain diffuse. The severity of disease related to these mutations is correlated with the dynamics of these condensates. When coexpressed with WT DDX3X, hollow condensates are more dynamic than when coexpressed with DDX3Y, which may explain sex bias in DDX3X-related diseases. Created in BioRender. Owens (2023) BioRender.com/j70v272.