Abstract:
:Changes in chromatin organization occur during aging. Overexpression of histones partially alleviates these changes and promotes longevity. We report that deletion of the histone H3-H4 minor locus HHT1-HHF1 extended the replicative life span of Saccharomyces cerevisiae. This longevity effect was mediated through TOR signaling inhibition. We present evidence for evolutionarily conserved transcriptional and phenotypic responses to defects in chromatin structure, collectively termed the chromatin architectural defect (CAD) response. Promoters of the CAD response genes were sensitive to histone dosage, with HHT1-HHF1 deletion, nucleosome occupancy was reduced at these promoters allowing transcriptional activation induced by stress response transcription factors Msn2 and Gis1, both of which were required for the life-span extension of hht1-hhf1Δ. Therefore, we conclude that the CAD response induced by moderate chromatin defects promotes longevity.
journal_name
Sci Advjournal_title
Science advancesauthors
Yu R,Sun L,Sun Y,Han X,Qin L,Dang Wdoi
10.1126/sciadv.aav1165subject
Has Abstractpub_date
2019-07-10 00:00:00pages
eaav1165issue
7issn
2375-2548pii
aav1165journal_volume
5pub_type
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