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Title: Boron stress activates the general amino acid control mechanism and inhibits protein synthesis
Authors: Uluışık, İrem
Kaya, Alaattin
Fomenko, Dmitri E.
Karakaya, Hüseyin Çağlar
Carlson, Bradley A.
Gladyshev, Vadim N.
Koç, Ahmet
Keywords: Boron
ATR1 protein
Biological marker
Transfer RNA
Chemical stress
Amino acid synthesis
Issue Date: Nov-2011
Publisher: Public Library of Science
Source: Uluışık, İ., Kaya, A., Fomenko, D. E., Karakaya, H. Ç., Carlson, B. A., Gladyshev, V. N., and Koç, A. (2011). Boron stress activates the general amino acid control mechanism and inhibits protein synthesis. PLoS ONE, 6(11). doi:10.1371/journal.pone.0027772
Abstract: Boron is an essential micronutrient for plants, and it is beneficial for animals. However, at high concentrations boron is toxic to cells although the mechanism of this toxicity is not known. Atr1 has recently been identified as a boron efflux pump whose expression is upregulated in response to boron treatment. Here, we found that the expression of ATR1 is associated with expression of genes involved in amino acid biosynthesis. These mechanisms are strictly controlled by the transcription factor Gcn4 in response to boron treatment. Further analyses have shown that boron impaired protein synthesis by promoting phosphorylation of eIF2α in a Gcn2 kinase dependent manner. The uncharged tRNA binding domain (HisRS) of Gcn2 is necessary for the phosphorylation of eIF2α in the presence of boron. We postulate that boron exerts its toxic effect through activation of the general amino acid control system and inhibition of protein synthesis. Since the general amino acid control pathway is conserved among eukaryotes, this mechanism of boron toxicity may be of general importance.
ISBN: 1932-6203
ISSN: 1932-6203
Appears in Collections:Molecular Biology and Genetics / Moleküler Biyoloji ve Genetik
PubMed İndeksli Yayınlar Koleksiyonu / PubMed Indexed Publications Collection
Scopus İndeksli Yayınlar Koleksiyonu / Scopus Indexed Publications Collection
WoS İndeksli Yayınlar Koleksiyonu / WoS Indexed Publications Collection

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