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Photomorphogenic light definitions were derived by mathematical determination of the estimated phytochrome photoequilibrium for each light treatment spectrum. A wide range of photomorphogenic light treatments represented by spectra with estimated phytochrome photoequilibria of0.45, 0.54, 0.60, 0.67, and 0.71 was utilized to determine the influence of photomorphogenicafly defined light on resistance of Poa pratensis L. to pathogenesis by Drechsera sorokiniana. Accurate resolution of D. sorokiniana leaf spot development required evaluation of separate leaf ages due to the sequential appearance, development, and senescence of P. pratensis leaves. Disease development (all Ught treatments) was greatest on leaf 4 (oldest, postmature) foHlowed by leaf 1 (youngest, premature). Low levels of disease occurred on leaves 2 and 3 (mature). Photomorphogenic light defined by estimated phytochrome photoequilibria greater than 0.60 (natural light = 0.60) was most disease promotive on leaf 1. Conversely, photomorphogenic light defined by estimated phytochrome photoequilibria of less than 0.60 was most disease promotive on leaf 4. These responses indicate that inherent resistance or susceptibility expressed by P. pratensis to pathogenesis by D. sorokiniana is regulated in part by leaf age (developmental senescent stage) and by photomorphogenically defined light quality. A hypothesis is presented and discussed which integrates and speculates on these observations with respect to the literature.

A controlled atmospheric-environment system (CAES) designed to sustain normal or hypobaric ambient growing conditions was partial pressures were maintained at levels approximating normal ambient availability.An unexpected increase in endogenous ethylene was detected within nontreated control leaves 48 hours subsequent to relocation from winter greenhouse conditions (latitude, 42°00" N) to the CAES operating at normal ambient pressure. The longer photoperiod and/or higher temperature utilized within the CAES are hypothesized to influence ethylene metabolism directly and growth-promotive processes (e.g. response thresholds) indirectly.