TY - JOUR
T1 - The yeast eIF4E-associated protein Eap1p attenuates GCN4 translation upon TOR-inactivation
AU - Matsuo, Ryu
AU - Kubota, Hiroyuki
AU - Obata, Tohru
AU - Kito, Keiji
AU - Ota, Kazuhisa
AU - Kitazono, Takanari
AU - Ibayashi, Setsuro
AU - Sasaki, Takuma
AU - Iida, Mitsuo
AU - Ito, Takashi
N1 - Funding Information:
This work was partly supported by research grants from the Ministry of Education, Culture, Sports, Science and Technology (MEXT), Japan and from CREST, JST.
PY - 2005/4/25
Y1 - 2005/4/25
N2 - Amino acid-starved yeast activates the eIF2α kinase Gcn2p to suppress general translation and to selectively derepress the transcription factor Gcn4p, which induces various biosynthetic genes to elicit general amino acid control (GAAC). Well-fed yeast activates the target of rapamycin (TOR) to stimulate translation via the eIF4F complex. A crosstalk was demonstrated between the pathways for GAAC and TOR signaling: the TOR-specific inhibitor rapamycin activates Gcn2p. Here we demonstrate that, upon TOR-inactivation, the putative TOR-regulated eIF4E-associated protein Eap1p likely functions downstream of Gcn2p to attenuate GCN4 translation via a mechanism independent of eIF4E-binding, thereby constituting another interface between the two pathways.
AB - Amino acid-starved yeast activates the eIF2α kinase Gcn2p to suppress general translation and to selectively derepress the transcription factor Gcn4p, which induces various biosynthetic genes to elicit general amino acid control (GAAC). Well-fed yeast activates the target of rapamycin (TOR) to stimulate translation via the eIF4F complex. A crosstalk was demonstrated between the pathways for GAAC and TOR signaling: the TOR-specific inhibitor rapamycin activates Gcn2p. Here we demonstrate that, upon TOR-inactivation, the putative TOR-regulated eIF4E-associated protein Eap1p likely functions downstream of Gcn2p to attenuate GCN4 translation via a mechanism independent of eIF4E-binding, thereby constituting another interface between the two pathways.
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U2 - 10.1016/j.febslet.2005.03.043
DO - 10.1016/j.febslet.2005.03.043
M3 - Article
C2 - 15848184
AN - SCOPUS:20244365800
SN - 0014-5793
VL - 579
SP - 2433
EP - 2438
JO - FEBS Letters
JF - FEBS Letters
IS - 11
ER -