2026-08-29T14:07:36Zhttps://repisalud.isciii.es/rest/oai/requestoai:repisalud.isciii.es:20.500.12105/258542025-12-18T12:57:06Zcom_20.500.12105_19586com_20.500.12105_2202col_20.500.12105_19587
Repisalud
author
Mulet, Isabel
author
Grueso-Cortina, Carmen
author
Cortés-Cano, Mireia
author
Gerovska, Daniela
author
Wu, Guangming
author
Iakab, Stefania Alexandra
author
Jimenez-Blasco, Daniel
author
Curtabbi, Andrea
author
Hernansanz-Agustín, Pablo
author
Ketchum, Harmony
author
Manjarrés-Raza, Israel
author
Wunderlich, F Thomas
author
Bolaños, Juan Pedro
author
Dawlaty, Meelad M
author
Hopf, Carsten
author
Enríquez, José Antonio
author
Araúzo-Bravo, Marcos J
author
Tapia, Natalia
funder
Agencia Estatal de Investigación (España)
funder
Fundación BBVA
funder
Generalitat Valenciana (España)
funder
Unión Europea. Comisión Europea. H2020
funder
Ministerio de Ciencia e Innovación (España)
funder
Instituto de Salud Carlos III
funder
Unión Europea. Fondo Europeo de Desarrollo Regional (FEDER/ERDF)
funder
Fundación La Caixa
2024-12-04T11:36:06Z
2024-12-04T11:36:06Z
2024-11-18
Nat Commun. 2024 Nov 18;15(1):9749.
Nature Communications
39557858
https://hdl.handle.net/20.500.12105/25854
TET-family members play a critical role in cell fate commitment. Indeed, TET3 is essential to postnatal development due to yet unknown reasons. To define TET3 function in cell differentiation, we have profiled the intestinal epithelium at single-cell level from wild-type and Tet3 knockout mice. We have found that Tet3 is mostly expressed in differentiated enterocytes. In the absence of TET3, enterocytes exhibit an aberrant differentiation trajectory and do not acquire a physiological cell identity due to an impairment in oxidative phosphorylation, specifically due to an ATP synthase assembly deficiency. Moreover, spatial metabolomics analysis has revealed that Tet3 knockout enterocytes exhibit an unphysiological metabolic profile when compared with their wild-type counterparts. In contrast, no metabolic differences have been observed between both genotypes in the stem cell compartment where Tet3 is mainly not expressed. Collectively, our findings suggest a mechanism by which TET3 regulates mitochondrial function and, thus, terminal cell differentiation at the metabolic level.
eng
TET3 regulates terminal cell differentiation at the metabolic level.
research article
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TET3 regulates terminal cell_Nat Commun_2024.pdf