Abstract

The first leaves of resistant (Khapli) and susceptible (Little Club) species of wheat were heavily inoculated with stem rust (Race 15B). After infection, oxygen consumption per unit dry weight increased two- to three-fold and then fell off again. The R.Q. remained close to 1.0 until the respiratory peak was reached and then declined to 0.80 to 0.85, at least in Khapli. The INR/OR values (approximately 1.2) suggest the operation of a Pasteur effect in uninfected tissue. With infected tissue there was little or no increase in NR as oxygen uptake rose and the INR/OR values declined steadily to about 0.2 to 0.3. The oxygen uptake of rusted, mildewed, and uninfected tissue was stimulated by 2,4-dinitrophenol. The percentage stimulation was reduced by infection. The smallest percentage stimulations were observed, after the respiratory peak had been passed, with infected tissue of Khapli, in which chlorosis and other degenerative changes developed quickly. The actual increases in oxygen uptake obtained with 10−5 M dinitrophenol were about the same for infected as for uninfected tissue, but, in Khapli, fell sharply after the respiratory maximum. Leaf-disks were incubated separately with glucose-1-C14, glucose-6-C14, and glucose-UL-C14, and the relative activities of the carbon dioxide produced were measured. The C6/C1 ratio showed a significant negative correlation with the oxygen uptake of rusted tissue, suggesting that the pentose phosphate pathway is of increased importance in infected tissue. The C6/C1 ratio was also reduced in the host tissue at the loci of mildew infections. In short term experiments dinitrophenol raised the C6/C1 ratio. The significance of the results is discussed and it is concluded that infection with rust or mildew not only raises the respiration rate but alters the pathway of respiration in the host tissue.

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