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@article{1361568,
author = {MolinaandSerrano, Diego and Schiza, Vassia and Demosthenous, Christis and Stavrou, Emmanouil and Oppelt, Jan and Kyriakou, Dimitris and Liu, Wei and Zisser, Gertrude and Bergler, Helmut and Dang, Weiwei and Kirmizis, Antonis},
article_location = {Hoboken},
article_number = {12},
doi = {http://dx.doi.org/10.15252/embr.201642540},
keywords = {Nat4; Pnc1; calorie restriction; histone N-terminal acetylation; lifespan},
language = {eng},
issn = {1469-221X},
journal = {EMBO reports},
title = {Loss of Nat4 and its associated histone H4 N-terminal acetylation mediates calorie restriction-induced longevity},
url = {http://embor.embopress.org/content/early/2016/10/31/embr.201642540.long},
volume = {17},
year = {2016}
}
TY - JOUR
ID - 1361568
AU - Molina-Serrano, Diego - Schiza, Vassia - Demosthenous, Christis - Stavrou, Emmanouil - Oppelt, Jan - Kyriakou, Dimitris - Liu, Wei - Zisser, Gertrude - Bergler, Helmut - Dang, Weiwei - Kirmizis, Antonis
PY - 2016
TI - Loss of Nat4 and its associated histone H4 N-terminal acetylation mediates calorie restriction-induced longevity
JF - EMBO reports
VL - 17
IS - 12
SP - 1829-1843
EP - 1829-1843
PB - Wiley-Blackwell
SN - 1469221X
KW - Nat4
KW - Pnc1
KW - calorie restriction
KW - histone N-terminal acetylation
KW - lifespan
UR - http://embor.embopress.org/content/early/2016/10/31/embr.201642540.long
L2 - http://embor.embopress.org/content/early/2016/10/31/embr.201642540.long
N2 - Changes in histone modifications are an attractive model through which environmental signals, such as diet, could be integrated in the cell for regulating its lifespan. However, evidence linking dietary interventions with specific alterations in histone modifications that subsequently affect lifespan remains elusive. We show here that deletion of histone N-alpha-terminal acetyltransferase Nat4 and loss of its associated H4 N-terminal acetylation (N-acH4) extend yeast replicative lifespan. Notably, nat4-induced longevity is epistatic to the effects of calorie restriction (CR). Consistent with this, (i) Nat4 expression is downregulated and the levels of N-acH4 within chromatin are reduced upon CR, (ii) constitutive expression of Nat4 and maintenance of N-acH4 levels reduces the extension of lifespan mediated by CR, and (iii) transcriptome analysis indicates that nat4 largely mimics the effects of CR, especially in the induction of stress-response genes. We further show that nicotinamidase Pnc1, which is typically upregulated under CR, is required for nat4-mediated longevity. Collectively, these findings establish histone N-acH4 as a regulator of cellular lifespan that links CR to increased stress resistance and longevity.
ER -
MOLINA-SERRANO, Diego, Vassia SCHIZA, Christis DEMOSTHENOUS, Emmanouil STAVROU, Jan OPPELT, Dimitris KYRIAKOU, Wei LIU, Gertrude ZISSER, Helmut BERGLER, Weiwei DANG and Antonis KIRMIZIS. Loss of Nat4 and its associated histone H4 N-terminal acetylation mediates calorie restriction-induced longevity. \textit{EMBO reports}. Hoboken: Wiley-Blackwell, 2016, vol.~17, No~12, p.~1829-1843. ISSN~1469-221X. Available from: https://dx.doi.org/10.15252/embr.201642540.
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