Role of the YWHAG gene mutations in Developmental and Epileptic Encephalopathy

Violet Vilmont^*Richard S. Nowakowski^*Yi Zhou

• Florida State University, Tallahassee, United States

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The publisher apologizes for this mistake. The original version of this article has been updated. In the published article, there was a mistake in the Funding statement. The funding statement for the Key Development Project of the Department of Science and Technology was displayed as '2015CBd051'. The correct statement is 'Key Development Project of Department of Science and Technology (2015C03Bd051)'. Correction: INSERT Template continues on the next page Role of the YWHAG gene mutations in Developmental and Epileptic Encephalopathy Correction on: Vilmont V, Nowakowski RS and Zhou Y (2025) Role of the YWHAG gene mutations in developmental and epileptic encephalopathy. Front. Neurosci. 19:1641250. doi: 10.3389/fnins.2025.1641250 Error in figure/table legend 1) In the published article, there was an error in the legend for [Figure 6] as published. [In the published article, there was a mistake at the end of the Figure 6 legend, stating the Source of the Figure 6. The statement "Source: Logue et al. (2024)" is incorrect, and must be replaced with "Created in Biorender"]. The corrected legend appears below. [Figure 6: Impact of heterozygous truncating and missense YWHAG mutations on 14-3-3γ dimer formation and function. (A) The wildtype YWHAG gene produces normal 14-3-3γ subunits, which assemble into functional 14-3-3γ dimers, able to bind phosphorylated ligands. (B) A truncating mutation produces non-functional mutant 14-3-3γ subunits that are shorter and smaller, which are unable to dimerize and to bind phosphorylated ligands. (C) A missense mutation produces non-functional mutant 14-3-3γ subunits that are the same size as the wildtype subunits, which are able to dimerize but unable to bind two phosphorylated ligands. WT, wildtype; MT, mutant. Created in Biorender.] 2) In the published article, there was an error in the legend for [Figure 7] as published. [In the published article, there was a mistake at the end of the Figure 7 legend, stating the how Figure 7 was created. The statement "Created in Biorender" is incorrect, and must be removed. Figure 7 was not created in Biorender, it was a reference figure taken from Logue et al. (2024)]. The corrected legend appears below. [Figure 7: 14-3-3 FKO hippocampal CA1 neurons fire more APs than WT neurons in the presence and absence of synaptic blockers. (A) Hippocampal slice images captured using phase contrast and fluorescence microscopy show 14-3-3 FKO neurons (left) identified by their YFP fluorescence, indicating difopein expression. (B) Traces of spontaneous AP firing in 14-3-3 FKO and WT neurons under whole-cell configuration, before and after synaptic blocker application. (C) Group data showing a higher AP firing rate for 14-3-3 FKO cells (n = 9 before blockers, 6 after blockers) than WT cells (n = 9 before blockers, 8 after blockers). AP, Action Potential; FKO, Functional Knockout; WT, Wildtype; CA1, one of four hippocampal subfields that make up hippocampus structure. Source: Figure 1 from Logue et al. (2024).] The authors apologize for this error and state that this does not change the scientific conclusions of the article in any way. The original article has been updated. 1) In the published article, there was an error in [Figure 1] as published. [Figure 1 and Figure 2 are swapped, and must be switched with each other]. The corrected [Figure 1] should be original Figure 2 as published, and its caption as published appear below; the figure captions and legends are correct as published. Original caption: [Figure 1. Functional interaction network of 14-3-3γ encoded by YWHAG. Network nodes are labeled with the name of the individual genes which encode the represented proteins. Protein interactions are represented by color coded lines, based on known and predicted interactions, as indicated by the legend. Source: https://stringdb.org/cgi/network?taskId=bMYGzw1kOtuv&sessionId=bMliKFIeKj5g. Screenshot image obtained from the STRING database (string-db.org). Licensed under the Creative Commons Attribution 4.0 International License (CC BY 4.0).] 2) In the published article, there was an error in [Figure 2] as published. [Figure 2 and Figure 1 are swapped, and must be switched with each other]. The corrected [Figure 2] should be original Figure 1 as published and its caption as published appear below; the figure captions and legends are correct as published. Original caption: [Figure 2. RNA tissue specificity expression of 14-3-3γ. Normalized RNA expression levels (nTPM) shown for 55 tissue types. Color coding is based on tissue groups, each consisting of tissues with functional features in common. RNA tissue specificity expression is enhanced in brain (yellow bars) and skeletal muscle cells (brown bars). Source: https://www.proteinatlas.org/ENSG00000170027-YWHAG/tissue. Screenshot image obtained from the Human Protein Atlas (proteinatlas.org). Licensed under the Creative Commons Attribution-ShareAlike 4.0 International License (CC BY-SA 4.0).] 3) In the published article, there was an error in [Figure 6] as published. [Figure 6 and Figure 7 are swapped, and must be switched with each other]. The corrected [Figure 6] should be original Figure 7 as published and its caption as published appear below; a correction for the Figure 6 legend has been requested on Page 2 of this document. Original caption: [Figure 6. Impact of heterozygous truncating and missense YWHAG mutations on 14-3-3γ dimer formation and function. (A) The wildtype YWHAG gene produces normal 14-3-3γ subunits, which assemble into functional 14-3-3γ dimers, able to bind phosphorylated ligands. (B) A truncating mutation produces non-functional mutant 14-3-3γ subunits that are shorter and smaller, which are unable to dimerize and to bind phosphorylated ligands. (C) A missense mutation produces non-functional mutant 14-3-3γ subunits that are the same size as the wildtype subunits, which are able to dimerize but unable to bind two phosphorylated ligands. WT, wildtype; MT, mutant. Source: Logue et al. (2024).] 4) In the published article, there was an error in [Figure 7] as published. [Figure 7 and Figure 6 are swapped, and must be switched with each other]. The corrected [Figure 7] should be original Figure 6 as published and its caption as published appear below; a correction for the Figure 7 legend has been requested on Page 2 of this document. Original caption: [Figure 7. 14-3-3 FKO hippocampal CA1 neurons fire more APs than WT neurons in the presence and absence of synaptic blockers. (A) Hippocampal slice images captured using phase contrast and fluorescence microscopy show 14-3-3 FKO neurons (left) identified by their YFP fluorescence, indicating difopein expression. (B) Traces of spontaneous AP firing in 14-3-3 FKO and WT neurons under whole-cell configuration, before and after synaptic blocker application. (C) Group data showing a higher AP firing rate for 14-3-3 FKO cells (n = 9 before blockers, 6 after blockers) than WT cells (n = 9 before blockers, 8 after blockers). AP, Action Potential; FKO, Functional Knockout; WT, Wildtype; CA1, one of four hippocampal subfields that make up hippocampus structure. Source: Figure 1 from Logue et al. (2024). Created in Biorender.] The authors apologize for this error and state that this does not change the scientific conclusions of the article in any way. The original article has been updated. Reminder: Figures, tables, and images will be published under a Creative Commons CC-BY licence and permission must be obtained for use of copyrighted material from other sources (including re-published/adapted/modified/partial figures and images from the internet). 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