Involvement of cyclic nucleotide-gated channels in soybean cyst nematode chemotaxis and thermotaxis.

The soybean cyst nematode (SCN) is one of the most damaging pests affecting soybean production. SCN displays important host recognition behaviors, such as hatching and infection, by recognizing several compounds produced by the host. Therefore, controlling SCN behaviors such as chemotaxis and thermotaxis is an attractive pest control strategy. In this study, we found that cyclic nucleotide-gated channels (CNG channels) regulate SCN chemotaxis and thermotaxis and Hg-tax-2, a gene encoding a CNG channel, is an important regulator of SCN behavior. Gene silencing of Hg-tax-2 and treatment with a CNG channel inhibitor reduced the attraction of second-stage juveniles to nitrate, an attractant with a different recognition mechanism from the host-derived chemoattractant(s), and to host soybean roots, as well as their avoidance behavior toward high temperatures. Co-treatment of ds Hg-tax-2 with the CNG channel inhibitor indicated that Hg-tax-2 is a major regulator of SCN chemotaxis and thermotaxis. These results suggest new avenues for research on control of SCN.

Fenoxycarb, a carbamate insect growth regulator, inhibits brassinosteroid action.

Brassinosteroids (BRs) are steroid hormones that regulate plant growth, development, and stress resistance. In this study, we evaluated the effect of agrochemicals on dark-induced hypocotyl elongation, which is regulated by BRs, to identify novel chemicals that regulate BR action. We found that the juvenile hormone agonist fenoxycarb inhibited dark-induced hypocotyl elongation in Arabidopsis. Treatment with the same class of juvenile hormone agonist, pyriproxyfen, did not affect hypocotyl elongation. Co-treatment with fenoxycarb and BR partly canceled the fenoxycarb-induced hypocotyl suppression. In addition, gene expression analysis revealed that fenoxycarb altered the BR-responsive gene expression. These results indicate that fenoxycarb is a BR action inhibitor.