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Epigenetic modifications driving ground state pluripotency exit require an NF-κB-independent chromatin IκBα function
Epigenetic modifications driving ground state pluripotency exit require an NF-κB-independent chromatin IκBα function
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Length:
20 minutes
Released:
Jul 29, 2023
Format:
Podcast episode
Description
Link to bioRxiv paper:
http://biorxiv.org/cgi/content/short/2023.07.28.550934v1?rss=1
Authors: Galan, L., Alvarez-Villanueva, D., Maqueda, M., Barrero, M., IGLESIAS, A., Bertran, j., ALVAREZ, D., GARCIA-PRIETO, C., BALLARE, C., RODRIGUEZ-CORTEZ, V., BUENO, C., VIDAL, A., Villanueva, A., Menendez, P., Di Croce, L., Payer, B., Esteller, M., Espinosa, L., Bigas, A.
Abstract:
Inflammatory signals are key in development and cell differentiation but their orchestration with pluripotency and stemness signals is poorly understood. Our previous work identified a chromatin function of I{kappa}B, the NF-{kappa}B inhibitor, that is crucial for differentiation in different types of somatic stem cells. Here we demonstrate that deficiency of I{kappa}B imposes a profound chromatin rewiring defect that impacts on DNA methylation, histone post-translational modifications and transcriptional regulation, stabilizing mouse embryonic stem cells (ESCs) in a ground state of pluripotency while preventing them from pluripotency exit and differentiation. By engineering separation-of-function mutants of I{kappa}B with specific binding to either NF-{kappa}B or histones, we demonstrate that regulation of pluripotency state by I{kappa}B is independent of NF-{kappa}B but requires the chromatin-related I{kappa}B function.
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Podcast created by Paper Player, LLC
http://biorxiv.org/cgi/content/short/2023.07.28.550934v1?rss=1
Authors: Galan, L., Alvarez-Villanueva, D., Maqueda, M., Barrero, M., IGLESIAS, A., Bertran, j., ALVAREZ, D., GARCIA-PRIETO, C., BALLARE, C., RODRIGUEZ-CORTEZ, V., BUENO, C., VIDAL, A., Villanueva, A., Menendez, P., Di Croce, L., Payer, B., Esteller, M., Espinosa, L., Bigas, A.
Abstract:
Inflammatory signals are key in development and cell differentiation but their orchestration with pluripotency and stemness signals is poorly understood. Our previous work identified a chromatin function of I{kappa}B, the NF-{kappa}B inhibitor, that is crucial for differentiation in different types of somatic stem cells. Here we demonstrate that deficiency of I{kappa}B imposes a profound chromatin rewiring defect that impacts on DNA methylation, histone post-translational modifications and transcriptional regulation, stabilizing mouse embryonic stem cells (ESCs) in a ground state of pluripotency while preventing them from pluripotency exit and differentiation. By engineering separation-of-function mutants of I{kappa}B with specific binding to either NF-{kappa}B or histones, we demonstrate that regulation of pluripotency state by I{kappa}B is independent of NF-{kappa}B but requires the chromatin-related I{kappa}B function.
Copy rights belong to original authors. Visit the link for more info
Podcast created by Paper Player, LLC
Released:
Jul 29, 2023
Format:
Podcast episode
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