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 eIF2a in a Gcn2 kinase dependent manner. The uncharged tRNA binding domain (HisRS) of
Gcn2 is necessary for the phosphorylation of eIF2a 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.
