%0 Journal Article
%T Impact of AtNHX1, a vacuolar Na+/H+ antiporter, upon gene expression during short- and long-term salt stress in Arabidopsis thaliana
%A Jordan B Sottosanto
%A Yehoshua Saranga
%A Eduardo Blumwald
%J BMC Plant Biology
%D 2007
%I BioMed Central
%R 10.1186/1471-2229-7-18
%X 147 transcripts showed both salt responsiveness and a significant influence of AtNHX1. Fifty-seven of these genes showed an influence of the antiporter across all salt treatments, while the remaining genes were influenced as a result of a particular duration of salt stress. Most (69%) of the genes were up-regulated in the absence of AtNHX1, with the exception of transcripts encoding proteins involved with metabolic and energy processes that were mostly down-regulated.While part of the AtNHX1-influenced transcripts were unclassified, other transcripts with known or putative roles showed the importance of AtNHX1 to key cellular processes that were not necessarily limited to the salt stress response; namely calcium signaling, sulfur metabolism, cell structure and cell growth, as well as vesicular trafficking and protein processing. Only a small number of other salt-responsive membrane transporter transcripts appeared significantly influenced by AtNHX1.The AtNHX1 gene encodes the most abundant vacuolar Na+/H+ antiporter in Arabidopsis thaliana, and mediates the transport of both K+ and Na+ into the vacuole [1,2]. Constitutive over-expression of AtNHX1 and homologues from other plants have been shown to confer significant salt tolerance in a variety of plant species as a result of increased vacuolar sequestration of sodium ions ([3], and references therein). The importance of AtNHX1 to salt stress tolerance was further demonstrated when T-DNA insertional mutant nhx1 'knockout' plants lacking a functional antiporter were shown to be more salt sensitive than wild-type Arabidopsis [4]. Additionally, it was found that nhx1 mutants exhibit an altered phenotype under normal growth conditions, including smaller cells, smaller leaves, and other developmental irregularities, associated with altered K+ homeostasis brought about by the lack of AtNHX1. These results suggested that AtNHX1 is associated with other cellular processes that are not necessarily related to salt tolerance.
%U http://www.biomedcentral.com/1471-2229/7/18