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Science 29 September 1978:
Vol. 201. no. 4362, pp. 1227 - 1229
DOI: 10.1126/science.201.4362.1227
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Articles

Mitochondrial Heredity: A Determinant in the Toxic Response of Maize to the Insecticide Methomyl

DAVID E. KOEPPE 1, JULIE K. COX 1, and CARL P. MALONE 1

1 Departments of Agronomy and Botany, University of Illinois, Urbana 61801

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.

Submitted on February 14, 1978
Revised on May 8, 1978


THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
The Texas Cytoplasm of Maize: Cytoplasmic Male Sterility and Disease Susceptibility.
C. S. Levings III (1990)
Science 250, 942-947
   Abstract »    PDF »
A 13-kilodalton maize mitochondrial protein in E. coli confers sensitivity to Bipolaris maydis toxin.
R. Dewey, J. Siedow, D. Timothy, and C. Levings 3rd (1988)
Science 239, 293-295
   Abstract »    PDF »


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