Transcript profiling in the chl1-5 mutant of Arabidopsis reveals a role of the nitrate transporter NRT1.1 in the regulation of another nitrate transporter, NRT2.1.

摘要: Arabidopsis thaliana mutants deficient for the NRT1.1 NO(3)(-) transporter display complex phenotypes, including lowered uptake, altered development of nascent organs, and reduced stomatal opening. To obtain further insight at molecular level on multiple physiological functions NRT1.1, we performed large-scale transcript profiling by serial analysis gene expression in roots chl1-5 deletion mutant Columbia wild type. Several hundred genes were differentially expressed between two genotypes, when plants grown NH(4)NO(3) as N source. Among these genes, satiety-repressed NRT2.1 gene, encoding a major component root high-affinity transport system (HATS), was found to be strongly derepressed (as well other mutants). This associated with marked stimulation HATS activity mutant, suggesting adaptive response possible limitation resulting from mutation. However, derepression NH(4)NO(3)-fed could not attributed production metabolites. Rather, results show that normal regulation is where this no more repressible high provision plant. indicates plays an unexpected but important role both activity. Overexpression also wild-type supplied 1 mM NH(4)(+) plus 0.1 NO(3)(-), situation likely mediate very low transport. Thus, suggest it lack activity, rather than absence transporter, derepresses presence NH(4)(+). Two hypotheses are discussed explain results: (1) upregulated demand signaling, indirectly triggered NRT1.1-mediated which overrides feedback repression metabolites, (2) direct signaling role, its generates unknown signal required Both mechanisms would warrant either or ensure significant uptake external medium, crucial prevent detrimental effects pure nutrition.