NatB catalytic subunit depletion disrupts DNA replication initiation leading to senescence in MEFs
Keywords: 
Actin cytoskeleton
N-terminal acetylation
NatB
Cell cycle
DNA replication
senescence
N-degron pathway
N-recognins
Issue Date: 
2023
Project: 
info:eu-repo/grantAgreement/MINECO/Contratos Torres Quevedo/PTQ-13-06466/ES/RESULTADOS DE INVESTIGACIÓN PROYECTOS PTQ-13-06466
ISSN: 
1661-6596
Note: 
This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https:// creativecommons.org/licenses/by/ 4.0/).
Citation: 
Elurbide-Tardio, J. (Jasmin); Carte-Abad, B. (Beatriz); Guedes, J.; et al. "NatB catalytic subunit depletion disrupts DNA replication initiation leading to senescence in MEFs". International journal of molecular sciences. 24 (10), 2023, 8724
Abstract
Alpha-aminoterminal acetyltransferase B (NatB) is a critical enzyme responsible for acetylating the aminoterminal end of proteins, thereby modifying approximately 21% of the proteome. This post-translational modification impacts protein folding, structure, stability, and interactions between proteins which, in turn, play a crucial role in modulating several biological functions. NatB has been widely studied for its role in cytoskeleton function and cell cycle regulation in different organisms, from yeast to human tumor cells. In this study, we aimed to understand the biological importance of this modification by inactivating the catalytic subunit of the NatB enzymatic complex, Naa20, in non-transformed mammal cells. Our findings demonstrate that depletion of NAA20 results in decreased cell cycle progression and DNA replication initiation, ultimately leading to the senescence program. Furthermore, we have identified NatB substrates that play a role in cell cycle progression, and their stability is compromised when NatB is inactivated. These results underscore the significance of N-terminal acetylation by NatB in regulating cell cycle progression and DNA replication.

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