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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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