Abstract:
:The Tor pathway mediates cell growth in response to nutrient availability, in part by inducing ribosomal protein (RP) gene expression via an unknown mechanism. Expression of RP genes coincides with recruitment of the Esa1 histone acetylase to RP gene promoters. We show that inhibition of Tor with rapamycin releases Esa1 from RP gene promoters and leads to histone H4 deacetylation without affecting promoter occupancy by Rap1 and Abf1. Genetic and biochemical evidence identifies Rpd3 as the major histone deacetylase responsible for reversing histone H4 acetylation at RP gene promoters in response to Tor inhibition by rapamycin or nutrient limitation. Our results illustrate that the Tor pathway links nutrient sensing with histone acetylation to control RP gene expression and cell growth.
journal_name
Mol Cell Bioljournal_title
Molecular and cellular biologyauthors
Rohde JR,Cardenas MEdoi
10.1128/mcb.23.2.629-635.2003subject
Has Abstractpub_date
2003-01-01 00:00:00pages
629-35issue
2eissn
0270-7306issn
1098-5549journal_volume
23pub_type
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