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Plant Physiology Preview Published on March 7, 2008; 10.1104/pp.108.116137
OPEN ACCESS ARTICLE
Received January 9, 2008 The Central Role of a SNRK2 Kinase in Sulfur Deprivation Responses
Department of Plant Biology, The Carnegie Institution, 260 Panama Street, Stanford, CA 94305; Department of Biological Sciences, Louisiana State University, Baton Rouge, LA 70803; Department of Biological Sciences, Stanford University; Stanford, CA 94305 * Corresponding author; email: davidg3{at}stanford.edu.
In the absence of sulfur, Chlamydomonas reinhardtii increases the abundance of several transcripts encoding proteins associated with sulfur acquisition and assimilation, conserves sulfur amino acids and acclimates to suboptimal growth conditions. A positive regulator, SAC1, and a negative regulator, SAC3, were shown to participate in the control of these processes. In this study, we investigated two allelic mutants (ars11 and ars44) affected in a gene encoding a SNRK2 kinase designated SNRK2.1. Like the sac1 mutant, both snrk2.1 mutants were deficient in expression of sulfur-responsive genes. Furthermore, the mutant cells bleached more rapidly than wild-type cells during sulfur deprivation, although the phenotypes of ars11 and ars44 were not identical; ars11 exhibited a more severe phenotype than either ars44 or sac1. The phenotypic differences between the ars11 and ars44 mutants reflected distinct alterations of SNRK2.1 mRNA splicing caused by insertion of the marker gene. The ars11 phenotype could be rescued by complementation with SNRK2.1 cDNA. In contrast to the non-epistatic relationship between SAC3 and SAC1, characterization of the sac3 ars11 double mutant showed that SNRK2.1 is epistatic to SAC3. These data reveal the crucial regulatory role of SNRK2.1 in the signaling cascade critical for eliciting sulfur-deprivation responses in Chlamydomonas. The phylogenetic relationships and structures of the eight members of the SNRK2 family in Chlamydomonas are discussed.
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