Mitochondrial heredity: a determinant in the toxic response of maize to the insecticide methomyl

Abstract

Mitochondria isolated from etiolated Texas male-sterile (TMS) cytoplasm maize (Zea mays L.) seedlings were adversely affected by methomyl (Lannate, 90 wettable powder), while those isolated from normal-fertile seedlings were not. In a manner analogous to that reported for Bipolaris (Helminthosporium) maydis (race T) toxin, experiments with TMS mitochondria showed that 1 to 3 millimolar methomyl inhibited the state 4 oxidation rate of combined malate and pyruvate while stimulating that of succinate or exogenous reduced nicotinamide adenine dinucleotide. Similar concentrations of methomyl effected an inhibition of phosphorylation, an increase in the percentage of transmittance of light through mitochondrial suspensions, and a decrease in the density of the mitochondrial matrix. Methomyl (15 millimolar) had little effect on the physiological activity or ultrastructure of isolated normal-fertile mitochondria. These observations provide the opportunity to specifically assess the homogeneity, or lack of it, of a cytoplasmic heritable characteristic in a widely divergent group of higher plants.