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. 2023 Jul 14;14:4129. doi: 10.1038/s41467-023-39672-2

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© The Author(s) 2023

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 7 — Glycolysis-derived lactate possesses non-metabolic functions that contribute to transcriptional regulation through epigenetic pathways involving histone H3 acetylation writer and eraser. Higher glucose uptake begins in the anterior neural plate (ANP) prior to optic vesicle (OV) morphogenesis. While the activity of Glut1 and Ldha is required for canonical glycolysis, the final product of glycolysis, lactate, acts as a signaling molecule being likely an endogenous HDAC inhibitor during eye morphogenesis. This non-canonical regulation is ATP-production independent and pivotal for specific eye developmental programs. cyto cytoplasm, nuc nucleus, enh enhancers, prom promoters.