The role of growth regulators in Puccinia striiformis accelerated senescence of the wheat leaf

Abstract

The earlier appearance of senescence characteristics in yellow-rust infected wheat leaves was investigated to determine whether senescence started earlier and proceeded at a faster rate, or both, and whether the physiological changes were the same as in naturally senescing leaves. Measurement of such different senescence processes as the decline in chlorophyll, total protein and organic-nitrogen levels, and the movement of potassium phosphorus and sodium show that infection results in the decline in levels beginning earlier in some senescence changes such as chlorosis, and later in others, such as potassium decline. Further examination of the changes in these compounds shows that the second way in which infection accelerates senescence, is by an effect on the rate at which senescence proceeds. Therefore the results show that infection not only induces chlorophyll decline to begin earlier, but that the rate of decline is faster than in healthy leaves. Conversely, whilst infection results in the earlier decline in total protein levels, the rate at which proteolysis subsequently proceeds, is slower than in healthy senescirti leaves. Quantitative and qualitative estimation of the major endogenous plant growth regulators in the infected and healthy third leaf blades, roots and remaining parts of the plant was also undertaken. This analysis demonstrates that whilst there are significant hormonal changes in the directly infected tissues, there are also many significant hormonal alterations in the uninfected tissues. Since many of these infection induced changes in the induction and rate of senescence symptoms occur before any hormonal changes and as one of the major effects of infection is the delay in the pattern of hormonal changes exhibited by healthy leaves, the hypothesis that the acceleration of senescence is controlled by a quantitative change in endogenous growth regulators is rejected, though a role for hormones as an integral factor in the induction of senescence (which is altered by infection) can be formulated. The results also indicate that hormonal changes resulting from infection may be responsible for the differences in rate at which the various processes proceed.It can be concluded therefore, that infection has a differential effect on senescence processes, inducing some senescence reactions to occur earlier or proceed faster than in healthy senescing leaves, whilst causing other senescence reactions to proceed at a slower rate.

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