Bradyrhizobium japonicum FixK2, a Crucial Distributor in the FixLJ-Dependent Regulatory Cascade for Control of Genes Inducible by Low Oxygen Levels

Bradyrhizobium japonicum possesses a second fixK-like gene, fixK₂, in addition to the previously identified fixK₁ gene. The expression of both genes depends in a hierarchical fashion on the low-oxygen-responsive two-component regulatory system FixLJ, whereby FixJ first activates fixK₂, whose product then activates fixK₁. While the target genes for control by FixK₁ are unknown, there is evidence for activation of the fixNOQP, fixGHIS, and rpoN₁ genes and some heme biosynthesis and nitrate respiration genes by FixK₂. FixK₂ also regulates its own structural gene, directly or indirectly, in a negative way.     

Ammonia regulation of the Rhizobium meliloti nitrogenase structural and regulatory genes under free-living conditions: Involvement of the fixL gene product?

Summary The expression under microaerobic conditions of the Rhizobium meliloti nifA and consequently the nifHDK genes was found to be negatively regulated by ammonia and nitrate. Assimilation of the ammonia to glutamate and glutamine is not required for this regulation to occur. This indicates that ammonia itself, and not a product of its metabolism, may be regulating nif expression. Unlike the situation in Klebsiella pneumoniae, NtrC is apparently not involved in mediating the ammonia effect on nifA expression in R. meliloti. Neither does the fixK gene product, which is known to regulate nifA in R. meliloti, appear to be involved in mediating the ammonia effect. The regulation of nifA by ammonia is shown to be mediated through the FixL protein. A truncated fixJ gene, the product of which has been shown to induce nifA expression irrespective of the oxygen status of the cell, also circumvented the repressive effect of ammonia on nifA expression. This suggests that the ammonia effect is mediated through the FixLJ regulatory cascade. Interstingly no effect of ammonia on fixK expression was observed.     

Cytokinin regulates differentially expression of PAHK-GUS constructs in transgenic Arabidopsis thaliana plants

The expression regulation by cytokinin of genetic constructs P _AHK2 -GUS, P _AHK3 -GUS, and P _AHK4 -GUS in transgenic Arabidopsis thaliana (L.) Heynh plants bearing the gene encoding β-glucuronidase (GUS) under the control of the promoter of one of three genes encoding histidine protein kinases, which are membrane receptors of cytokinin was studied. In 4–5-day-old etiolated A. thaliana seedlings, treatment with cytokinin resulted in the strongest expression activation of the constructs P _AHK2 -GUS and P _AHK3 -GUS. The same constructs were activated by cytokinin also at the seedling transit from scoto- to photomorphogenesis. Long-term seedling growing in darkness on medium containing cytokinin resulted in the substantial promoter activation of the gene encoding the histidine kinase AHK2. In the leaves of three-week-old plants with actively functioning chloroplasts, treatment with cytokinin mainly stimulated expression of the construct P _AHK3 -GUS. In detached senescing leaves, treatment with cytokinin retarded the loss of chlorophyll but did not affect significantly GUS activity under both light and darkness conditions in either of tested lines containing GUS gene under the control of promoters of histidine kinase genes. At the same time, cytokinin activated the promoter of the gene of primary response to cytokinin in the construct P _ARR5 -GUS. Thus, in the studied test-system, treatment with cytokinin of A. thaliana plant grown in darkness or in the light affected differently the expression of histidine kinase genes in dependence of plant age, conditions of plant cultivation, and plant physiological state.     

Rice <Emphasis Type="Italic">PLASTOCHRON</Emphasis> genes regulate leaf maturation downstream of the gibberellin signal transduction pathway

Rice PLASTOCHRON 1 (PLA1) and PLA2 genes regulate leaf maturation and plastochron, and their loss-of-function mutants exhibit small organs and rapid leaf emergence. They encode a cytochrome P450 protein CYP78A11 and an RNA-binding protein, respectively. Their homologs in Arabidopsis and maize are also associated with plant development/organ size. Despite the importance of PLA genes in plant development, their molecular functions remain unknown. Here, we investigated how PLA1 and PLA2 genes are related to phytohormones. We found that gibberellin (GA) is the major phytohormone that promotes PLA1 and PLA2 expression. GA induced PLA1 and PLA2 expression, and conversely the GA-inhibitor uniconazole suppressed PLA1 and PLA2 expression. In pla1-4 and pla2-1 seedlings, expression levels of GA biosynthesis genes and the signal transduction gene were similar to those in wild-type seedlings. GA treatment slightly down-regulated the GA biosynthesis gene GA20ox2 and up-regulated the GA-catabolizing gene GA2ox4, whereas the GA biosynthesis inhibitor uniconazole up-regulated GA20ox2 and down-regulated GA2ox4 both in wild-type and pla mutants, suggesting that the GA feedback mechanism is not impaired in pla1 and pla2. To reveal how GA signal transduction affects the expression of PLA1 and PLA2, PLA expression in GA-signaling mutants was examined. In GA-insensitive mutant, gid1 and less-sensitive mutant, Slr1-d1, PLA1 and PLA2 expression was down-regulated. On the other hand, the expression levels of PLA1 and PLA2 were highly enhanced in a GA-constitutive-active mutant, slr1-1, causing ectopic overexpression. These results indicate that both PLA1 and PLA2 act downstream of the GA signal transduction pathway to regulate leaf development.