Aberrant gene expression in the Arabidopsis SULTR1; 2 mutants suggests a possible regulatory role for this sulfate transporter in response to sulfur nutrient status

Abstract

Sulfur is required for the biosynthesis of cysteine, methionine and numerous other metabolites, and thus iscritical for cellular metabolism and various growth and developmental processes. Plants are able to sensetheir physiological state with respect to sulfur availability, but the sensor remains to be identified. Here wereport the isolation and characterization of two novel allelic mutants of Arabidopsis thaliana, sel1-15 andsel1-16, which show increased expression of a sulfur deficiency-activated gene b-glucosidase 28 (BGLU28).The mutants, which represent two different missense alleles of SULTR1;2, which encodes a high-affinity sul-fate transporter, are defective in sulfate transport and as a result have a lower cellular sulfate level. How-ever, when treated with a very high dose of sulfate, sel1-15 and sel1-16 accumulated similar amounts ofinternal sulfate and its metabolite glutathione (GSH) to wild-type, but showed higher expression of BGLU28and other sulfur deficiency-activated genes than wild-type. Reduced sensitivity to inhibition of gene expres-sion was also observed in the sel1 mutants when fed with the sulfate metabolites Cys and GSH. In addition,a SULTR1;2 knockout allele also exhibits reduced inhibition in response to sulfate, Cys and GSH, consistentwith the phenotype of sel1-15 and sel1-16. Taken together, the genetic evidence suggests that, in additionto its known function as a high-affinity sulfate transporter, SULTR1;2 may have a regulatory role in responseto sulfur nutrient status. The possibility that SULTR1;2 may function as a sensor of sulfur status or a compo-nent of a sulfur sensory mechanism is discussed.