TOLERANCE OF RICE PLANTS TO A RESPIRATION-INHIBITING BLASTICIDE, METOMINOSTROBIN (SSF126)
A MIZUTANI, N MIKI and M MASUKO
Aburahi Laboratories, Shionogi & Co., Ltd., 1405 Gotanda, Koka, Shiga 520-34, Japan
Background and objectives
Metominostrobin (SSF1 26) has been developed as a systemic fungicide and the efficacy is remarkable in control of rice blast caused by Pyricularia grisea. It is able to bind to the Qo site of the mitochondhal cytochrome c reductase and inhibits fungal respiration. However, the mycelial cells of P. grisea have the ability to induce a cyanide-resistant respiration in response to the blockage of cytochrome-mediated electron transport by metominostrobin and recover from respiratory inhibition . Superoxide anion (O2) generated by blockage of electron flux through the cytochrome pathway mediates the metominostrobin-dependent induction of the cyanide-resistant respiration i n the fungus However, flavonoids found in plants have the ability to scavenge 02 and inhibit metominostrobin-dependent induction of the cyanide-redstant respiration. These indicate that metominostrobin controls rice blastin conjunction with rice plant components . Rice plants also prevent severe injury caused by blockage of the cytochrome pathway through utilization of the cyanide-resistant respiration. However, the regulatory mechanism of the cyanide-resistant respiration is quite different from that indicated for P. grisea. Here, we describe a mechanism by which rice plants survive exposure to metominostrobin.
Results and conclusions
The oxygen uptake by mitochondria from control rice roots (Oryza sativa) was partially susceptible to salicyihydroxamic acid (inhibitor of cyanide-resistant respiration). With mitochondha from rice roots treated with metominostrobin, most of oxygen uptake became susceptible to salicyihydroxamic acid, indicating that metominostrobin augmented the capacity of the cyanide-resistant respiration. The mitochondrial protein was immunoblotted with a monocional antibody against the alternative oxidase protein in an attempt to determine whether expression of the alternative oxidase protein is closely linked to the augmentation of the cyanide-resistant respiration. In control mitochondha, bands were detected in 72- to 88-KDa range, in addition to molecular mass species of 36- to 40-KDa. Quantification of high and low molecular mass species revealed an increase in the amount of the lower molecular mass species (active form) approximately equivalent to the decrease in the amount of higher molecular mass species (inactive form) after incubation with metominostrobin. The conversion correlated with the enhancement of the cyanide-resistant respiration. Consequently, the tolerance of rice plants to metominostrobin could be produced through activation of the cyanide-resistant pathway by interconversion of the alternative oxidase protein when the cytochrome pathway is limiting respiration.
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