An amino acid ester of menthol elicits defense responses in plants.

KEY MESSAGE: Valine menthyl ester (ment-Val) acts as a plant defense potentiator for several crop species including soybean. Terpenoids, including menthol, exhibit potent abilities as plant defense potentiators in agriculture and horticulture. In the current study, we developed new terpene derivatives that consisted of menthol and various amino acids and that were expected to act as powerful plant defense potentiators. We used 6 amino acids possessing low-reactive sidechains to synthesize an array of amino acid ester of menthol (ment-aa) compounds. Transcript levels of two defense genes (pathogenesis-related protein 1 [PR1] and trypsin inhibitor [TI]) were evaluated in leaves of soybean plants 24 h after application of aquatic solution of menthol or menthol-aa, and revealed that the valine menthyl ester (ment-Val) alone elevated the transcript level of defense genes, and it did so only at the low dose of 1 µM, not at higher or lower doses tested. Moreover, it appeared that histone acetylation was involved in this effect. Application of ment-Val enabled soybean plants to sustain the increased transcript levels in their leaves for up to 3 days. Moreover, when ment-Val was additionally applied at day 4, at which time the transcript level had declined to the basal level, the transcript level was re-elevated, indicating the possibility that ment-Val could be repeatedly used to sustain pest control. Ment-Val was found to be chemically stable and effective for defense of several crop species. Collectively, these data show that terpenoid conjugates are useful for pest control instead of or in addition to pesticides.

Induction of Nickel Accumulation in Response to Zinc Deficiency in Arabidopsis thaliana.

Excessive accumulation of nickel (Ni) can be toxic to plants. In Arabidopsis thaliana, the Fe²âº transporter, iron (Fe)-regulated transporter1 (IRT1), mediates Fe uptake and also implicates in Ni²âº uptake at roots; however, the underlying mechanism of Ni²âº uptake and accumulation remains unelucidated. In the present study, we found that zinc (Zn) deficient conditions resulted in increased accumulation of Ni in plants, particularly in roots, in A. thaliana. In order to elucidate the underlying mechanisms of Ni uptake correlating zinc condition, we traced 63Ni isotope in response to Zn and found that (i) Zn deficiency induces short-term Ni²âº absorption and (ii) Zn²âº inhibits Ni²âº uptake, suggesting competitive uptake between Ni and Zn. Furthermore, the Zrt/Irt-like protein 3 (ZIP3)-defective mutant with an elevated Zn-deficient response exhibited higher Ni accumulation than the wild type, further supporting that the response to Zn deficiency induces Ni accumulation. Previously, expression profile study demonstrated that IRT1 expression is not inducible by Zn deficiency. In the present study, we found increased Ni accumulation in IRT1-null mutant under Zn deficiency in agar culture. These suggest that Zn deficiency induces Ni accumulation in an IRT1-independen manner. The present study revealed that Ni accumulation is inducible in response to Zn deficiency, which may be attributable to a Zn uptake transporter induced by Zn deficiency.

AtIRT1, the primary iron uptake transporter in the root, mediates excess nickel accumulation in Arabidopsis thaliana.

Nickel (Ni) is an essential nutrient for plants, but excessive amounts can be toxic. Ni competes with iron (Fe) in vivo, raising the possibility that Ni is competitively taken up via the Fe uptake system in plants. Here, we show evidence that AtIRT1, the primary Fe(2+) uptake transporter in the root, mediates Ni accumulation in Arabidopsis thaliana. In hydroponic cultures, excess Ni exposure increased Fe accumulation and the relative transcription level of AtIRT1 in roots, indicating that excess Ni induces AtIRT1 expression in roots. An Fe-deficient treatment increased Ni accumulation in plants, suggesting that excess Ni was absorbed via the Fe uptake system, which was induced by Fe starvation. Moreover, Ni accumulation under Fe-deficient conditions was markedly lower in AtIRT1-defective mutants than in the wild-type, Col-0. Furthermore, AtIRT1 showed Ni(2+) uptake activity in a yeast expression system. These data demonstrate that AtIRT1 transports Ni(2+) in roots, and strongly suggest that Ni accumulation is further accelerated by AtIRT1 that is expressed in response to excess Ni.