Alterations in mitochondria associated with cytoplasmic and nuclear genes concerned with male sterility in maize

Abstract

Mitochondria isolated from etiolated shoots of a range of maize genotypes with the "Texas" cytoplasm conferring cytoplasmically-inherited male sterility, are sensitive to a pathotoxin isolated from Helmintho-sporium maydis, race T. The pathotoxin inhibits oxidation of α ketoglutarate and malate and stimulates NADH oxidation. The time taken for the pathotoxin to induce these changes is a measure of the sensitivity of the mitochondria to the pathotoxin. A range of nine different pairs of genotypes, each pair differing principally in the presence of nuclear male fertility restorer alleles has been compared in their sensitivity to pathotoxin. In every case the line carrying the restorer alleles is more resistant to the pathotoxin. The restored genotypes can be quantitatively arranged into groups which correspond to the four different sources of the restorer genes in these lines. It is suggested that the restorer genes cause changes in mitochondria, which modify the functional aberration introduced by the cytoplasmically-inherited mutation causing sterility.