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Pathogenesis of Drechslera sorokiniana leaf spot on progressively older leaves of Poa pratensis as influenced by photoperiod and light quality
Physiological
Plant Pathology
(1979)
15, 171-176
Pathogenesis of Drechslera sorokiniana leaf spot on progressively older leaves of Poa pratensis as influenced by photoperiod and light qualityt K. N. NILSEN,
C.
F. HODGES
Departments of Horticulture, Ames, IA 5001 I, U.S.A. (Accepted for publication
Botany January
and J. P. MADSEN and Plant
Pathology,
Iowa State University,
1979)
Drechslera sorokiniana leaf spot on Poa pratensis was investigated relative to photoperiod, light quality and sequential leaf development and senescence. Leaf spot expression was enhanced on each older leaf when subjected to blue-biased, far-red-rich light irrespective of photoperiod and when subjected to “balanced” light in combination with a short photoperiod (10 h). Leaf spot expression on progressively older leaves subjected to “balanced” light in combiLeaf spot expression on progressively nation with a long photoperiod (14 h) was inhibited. older leaves in response to orange-red-biased light in combination with a long photoperiod (14 h) was similar to that of “balanced” light, but orange-red-biased light uniquely promoted leaf spot expression on younger leaves in combination with a short photoperiod (10 h). The relationship between the calculated and projected phytochrome photoequilibrium (4) and disease expression suggests that pathogenesis on progressively older leaves can be influenced by a light-phytochrome-pathogen interaction. Spectral and photoperiodic conditions associated with retardation or stimulation of leaf sensescence also seem to retard or stimulate pathogenesis, especially on progressively older leaves.
INTRODUCTION The expression of symptoms sorokiniana (Sacc.) Subram. with seasonal environmental
on leaves of Poa pratensis L. infected by Drechslera and Jain (Helminthosporium sativum P. K. &. B.) changes conditions. The symptoms produced by this pathogen include leaf spot, leaf blight and root rot of P. pratensis and other species of grasses and cereals [I, 2, 8, 181. Leaf spot is predominant on P. pratensis and, in spring and early summer, is characterized by small lesions with or without chlorotic halos. The leaf spot symptoms of late fall and early winter are characterized by enlarged necrotic areas sometimes interconnected by chlorotic streaks or by complete chlorosis or straw-coloured blighting of infected leaves. The chlorosis and strawing are suggestive of premature senescence of infected leaves [13] and can be observed in monocultures of P. pratensis in late fall and early winter, primarily on undercover leaves below a canopy of green leaves. Recent studies have revealed that the chlorosis and strawing of P. pratensis leaves infected by D. sorokiniana in late fall and early winter can be induced by manipulation of photoperiod and light quality [ 131. D isease severity on leaves of P. pratensis infected by D. sorokiniana and subjected to a low level “balanced” spectrum, or to a low level IA
t Journal Paper 50011. Projects
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No. J-9271 of the Agriculture 2308 and 2038. 17 1 + 06$02.00/O
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@ 1979 Academic
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172
K. N. Nilsen, C. F. Hodges and J. P. Madsen
orange-red-biased spectrum, was increased under short days (10 h) and decreased under long days (14 h). This observation suggests that the chlorosis and strawing of infected leaves in the late fall and early winter under natural light of short-days are, in part, controlled by photoperiod. Chlorosis and strawing of infected leaves are also induced independent of photoperiod by subjecting the leaves to a low-level blue-biased, far-red-rich spectrum [ 131. This reaction is suggestive of a phytochrome-mediated interaction involving host, pathogen and light. The calculated and projected phytochrome photoequilibrium (4) [12] of the blue-biased, far-red-rich spectrum is relatively low, and low 4 values under low light levels are promotive of senescence [4, 5, 161; conversely, red-biased light may retard senescence [3,1.5, IS, 171. It also is of interest that spectral measurements taken within plant canopies describe relatively low-level far-red-rich irradiances [7, 10, II]. The enhancement of disease on leaves of P. pratensis infected by D. sorokiniana by blue-biased, far-red-rich light independent of the short days needed in combination with a “balanced” or orange-red-biased spectrum to produce the same symptoms suggest that symptom expression may be light mediated via phytochrome enhancement of leaf senescence [13]. This hypothesis is further supported by the observation that delaying either light treatment until after infection occurred had no effect on disease expression [13]. Hence, disease expression is in response to light-mediated changes in the host plant and is not due to any direct effect on the pathogen. The original host-pathogen-light interaction studies were conducted with the entire shoot of P.pratens;S, irrespective of leaf age [13]. If pathogenesis of D. sorokiniana leaf spot on P. pratensis is promoted via far-red light by stimulating premature leaf senescence, it is probable that such disease enhancement would be most pronounced on progressively older infected leaves. The research presented here was initiated to evaluate the influence of photoperiod and light quality relative to pathogenesis of D. sorokiniana leaf spot on progressively older leaves of P. pa&n&s. MATERIALS
AND
METHODS
The production and maintenance of Poa ~ratensis cv. “Newport” and Drechslera sorokiniana and the growth chamber lighting and inoculation facilities utilized in this study have been described in detail previously [13]. Inoculated plants were exposed to three separate spectral regimes in combination with a 14 h or 10 h photoperiod. The spectral regimes used produced an orange-red-biased spectrum (Spectrum A), a “balanced” spectrum (Spectrum B) and a blue-biased, far-red-rich spectrum (Spectrum C), respectively. All spectral determinations were made with a spectroradiometer (International Light IL 680), with subsequent action-spectra-based computer analysis [12] and were graphically displayed in a previous study (13). The calculated and projected phytochrome photoequilibrium of P,JPtotal (4) was O-73, 0.66 and 0.53 for spectrums A, B and C, respectively. The calculated phytochrome photoequilibrium of natural light was 0.60 [13]. The light level of all spectral regimes was adjusted to a photosynthetic photon flux density (PPFD) of 100 ( + 5) PE m--2 s-l with a quantum flux meter (Lambda Model LI-185). Temperatures within inoculation chambers were maintained at 20 “C ( f 1) during light and dark periods.
Drechslera sorokiniana
on
Pea pratensis
173
Inoculated leaves were subjected to six separate light treatments (spectrums A, B and C in combination with a 14 h or a 10 h photoperiod.) Each treatment consisted of two plants (two leaves of each of the four differently aged leaves per shoot) and was replicated five times (10 leaves of each age evaluated per treatment), and all data were analyzed statistically. Inoculations were conducted for each treatment on the four youngest, visible leaf blades of individual shoots by placing each leaf in a separate Pyrex glass inoculating tube of a specially designed inoculation apparatus [14]. Plant and inoculating apparatuses were placed within a plastic refrigerator crisper (9.5 x 27 x 19.5 mm). The four differently aged leaves were then inoculated with conidia through five inoculation ports (c. 2 mm diam.) spaced 1 cm apart over the upper epidermis of the leaf. Each leaf blade was inoculated by placing 10 conidia in a O-02 ml droplet of distilled water on the surface of the leaf through each of the five inoculating ports (conidia concentration was prepared with an automatic particle counter, High Accuracy Products Corp.). The refrigerator crispers were then covered with the appropriate shading and filtering materials to provide the desired spectral regime [13]. Disease severity was determined on the four differently aged leaves of each shoot, after 6 days of incubation under the appropriate treatment, by harvesting 10 cm lengths of leaf blades from the inoculating tubes, estimating the total leaf area of the specimen, and expressing the estimated disea.sed area as a percentage of the estimated total area of the leaf specimen [13]. RESULTS
Inoculated plants subjected to the various spectral r&imes in combination with the 14 h or 10 h photoperiod produced distinct differences in disease severity on progressively older leaves. Disease increased progressively from the youngest to the oldest leaf on plants subjected to spectrum A [Fig. l(a) and (b)]. Disease severity was not significantly different among the three oldest leaves of plants subjected to spectrum A in combination with the 14 h photoperiod, but the disease severity on each of the three oldest leaves was significantly greater than that on the youngest leaf [Fig. 11. No significant differences occurred in disease from the youngest to the oldest leaves on plants subjected to spectrum A in combination with the 10 h photoperiod [Fig. 1(b)]. Disease severity on leaves of all ages of plants subjected to spectrum A and the 10 h photoperiod was significantly greater than that on leaves of all ages of plants subjected to spectrum A and the 14 h photoperiod. Inoculated plants subjected to spectrum B in combination with the 14 h photoperiod resulted in the least severe disease, with no differences between leaf ages [Fig. 1(a)]. Leaves one and two of plants subjected to spectrum B in combination with the 10 h photoperiod showed no difference in disease; however, leaves 3 and 4 showed a significant increase in disease expression [Fig. 1 (b)]. Disease severity on leaves 1 and 2 subjected to spectrum B did not differ between the 14 h and 10 h photoperiods; leaves 3 and 4 subjected to the 10 h photoperiod, however, showed significantly greater disease than that produced on the same leaves subjected to the 14 h photoperiod. Disease expression on leaves of all ages exposed to the various spectral rCgimes in combination with the 14 h photoperiod was greatest in response to spectrum C [Fig. 1 (a)]. Disease severity on leaves 3 and 4 was significantly different and both
K. N. Nilsen,
C. F. Hodges
and J. P. Madsen
17-(a)
1615-
Leaf I (Youngest)
Leaf 2
Leaf3
Leaf 4 (Oldest) Leaf
Leaf I (Youngest)
Leaf 2
Leaf 3
Leaf 4 (Oldest)
age
FIG. 1. The influence of photoperiod and light quality on pathogenesis of Drechdera sorokiniuaa leaf spot on progressively older leaves of Poa pratcn.rsU: (a) 14 h photoperiod; (b) 10 h photoperiod. Differences in disease expression on progressively older leaves subjected to the same spectral treatment and followed by the same letter (a/) are not significantly different. Differences in disease expression on leaves of the same age between spectral treatments and followed by the same letter ( /a) are not significantly different. Duncan’s multiple range test, P = 0.05. 0, Spectrum A; @, spectrum B; l , spectrum C.
leaves showed greater levels of disease than that on leaves 1 and 2 [Fig. 1(a)]. The expression of disease on leaves of all ages subjected to spectrum C in combination with the 10 h photoperiod was similar to that in combination with the 14 h photoperiod [Fig. l(a) and (b)], with no significant differences between the two photoperiods. Spectral regimes and photoperiods interact with specific leaf-age groups to produce differing levels of disease. The differences in disease on each leaf-age group subjected to spectrums A and B in combination with the 14 h photoperiod were not different [Fig. l(a)]. Spectrum C in combination with the same photoperiod, however, produced significantly greater levels of disease on all leaf-age groups than that on leaves subjected to spectra A and B [Fig. 1(a)]. Th e interaction between leaf-age, spectral regimes and the 10 h photoperiod was more complex than that of the 14 h photoperiod. Among the three youngest leaf groups, disease was significantly
Drechslera
sorokiniana
on Poa pratensis
175
different among all spectral regimes (except leaf 3, spectra A and C), with disease severity greatest on leaves exposed to spectrums A, C and B in descending order [Fig. 1(b)]. Disease was greatest on leaf 4 in response to spectrums B and C, both of which resulted in significantly more disease than that produced in response to spectrum A [Fig. 1 (b)].
DISCUSSION
Disease enhancement under spectrum B (4 = O-66), which most closely approximates the photomorphogenic quality of “natural” light [13], seems to be a photoperiodic effect. The two youngest leaves of plants subjected to this spectrum show the lowest level of disease expression, irrespective of photoperiod [Fig. l(a) and (b)]. Leaves 3 and 4 show no difference in disease on plants subjected to the 14 h photoperiod [Fig. 1(a)] ; however, leaves 3 and 4 of plants subjected to the 10 h photoperiod show a sharp increase in disease severity [Fig. 1 (b)]. This suggests that the “balanced” light quality characteristics of “natural” light in combination with a long photoperiod (14 h) may retard pathogenesis [Fig. 1 (a)] and that increased disease under a short photoperiod [Fig. 1 (b)] is a consequence of enhanced sequential senescence due to a short photoperiod-leaf age-pathogen interaction [N]. Any deviation in light quality from a “balanced” spectrum influences pathogenesis of D. sorokiniana leaf spot on differently aged leaves of P. pratensis. The orange-redbiased light of spectrum A in combination with either the 14 h or 10 h photoperiod generally increased disease expression on leaves of all ages, but the only significant increases in disease on the various leaf ages above that of the “balanced” spectrum occurred under the 10 h photoperiod [Fig. 1(a) and (b)]. Only the oldest leaf showed significantly less disease in response to spectrum A and the 10 h photoperiod [Fig. l(b)]. These results show that the progressive increase in disease expression associated with increasing leaf age in response to a “balanced” spectrum and short photoperiod is minimized under orange-red-biased light on the oldest leaf and is enhanced on younger leaves. The relatively high phytochrome photoequilibrium (+ = O-73) generated by orange-red-biased light is associated with increased levels of gibberellins, cytokinins, photosynthate-sink activity and senescence retardation [3, 9, 15, IS, 17, 191. These characteristics of a high 4 value may delay senescence of older leaves and also inhibit pathogenesis; it does not, however, explain the increase in disease on the youngest leaves [Fig. 1 (b)]. The blue-biased, far-red rich light of spectrum C increased disease on progressively older leaves independent of photoperiod and generated the lowest 4 value (O-53) of the spectral regimes employed [Fig. 1 (a) and (b)]. In general, far-red-biased light produces lower 4 values and contributes to increases in auxin and ethylene levels and is senescence promoting [4,5,15]. Also, spectral measurements within plant canopies show low light levels relatively rich in far-red light [7, 10, II]. Consequently, under natural environmental conditions, D. sorokiniana disease expression may be enhanced by a combination of low-level light, by progressively shorter photoperiods of fall (northern temperate climates), and by a~relatively dense plant canopy likely to generate Iow + values promotive of sequential leaf senescence and subsequent stimulation of disease on older leaves. Experimentation is in progress to evaluate
176
K. N. Nilsen,
C. F. Hodges
and J. P. Madsen
further the relationship between red and far-red-enriched light treatments and the influence of phytochrome photoequilibrium on disease severity. REFERENCES 1. BEAN, G. A. & WILCOXSON, R. D. (1964). Helminthosporium leaf spot of bluegrass. Phytopatholoa 54, 1065-1070. 2. BEAN, G. A. & WILCOXSON, R. D. (1964). Pathogenicity of three species of Helminthosporium on roots of bluegrass. PhytopathologV 54, 1684-1085, 3. BISWALL. V. C.. & SHARMA R. (1976). Phvtochrome rezulation of senescence in detached barlev I lea&. zei&hriyt ftir Pflan.&hys&gie b, 71-75. 4. DE GREEP, J. A. & FREDERICQ, H. (1972). Enhan cement of senescence by far-red light. Plantu 104,272-274. 5. EREZ, A. (1971). The effect of different portions of the sunlight spectrum on ethylene evolution in peach (Prunus firsica) apices. Physiologia Plantarum 39, 285-289. 6. FLETCHER, R. A. (1969). Retardation of leaf senescence by benzyladenine in intact bean plants. Planta 89, l-7. 7. GATES, D. M., DEEGAN, H. J., SCHLETER, J. C. & WEIDNER, V. R. (1965). Spectral properties of plants. Applied Optics 4, 1 l-20. 8. HODGES, C. F. & WATSCHKE, G. A. (1975). Pathogenicity of soil-borne Bipolaris sorokiniuna on seed and roots of three perennial grasses. Phytoputholo~ 65, 398-400. 9. HOLMES, M. G. & SMITH, H. (1975). The function of phytochrome in plants growing in the natural environment. .Nature 254, 512-514. 10. HOLMES, M. G. & MCCARTNEY, H. A. (1976). Spectral energy distribution in the natural environment and its implications for phytochrome function. In Light and Plant Development, Ed. by H. Smith, pp. 467476. Butterworths, London. 11. HOLMES, M. G. & SMITH, H. (1977). The function of phytochrome in the natural environment. II. The influence of vegetation canopies on the spectral energy distribution of natural daylight. Photochemistry and Photobiology 25, 539-545. 12. NILSEN, K. N. & NILSEN, N. S. (1977). Photosynthetic and photomorphogenic efficacies of light sources: Spectroradiometric measurement with computer analysis. Hart. Science 12 (4), 405. 13. NILSEN, K. N., MADSEN, J. P. & HODGES, C. F. (1978). Enhanced Drechslera sorokiniuna leaf spot expression on Poa pratensis in response to photoperiod and blue-biased light. Physiological Plant Pathology 14, 57-69. 14. ROBINSON, P. W. & HODGES, C. F. (1976). An inoculation apparatus for evaluation of Bipolaris sorokiniana lesion development on progessively older leaves of Poa pratensis. Phytopathology 66, 360-362. 15. SATTER, R. C. & GALSTON, A. W. (1976). The physiological functions of phytochrome. In &m&y and Biochemistry of Plant Pigments, 2nd edn., Vol. 1, Ed. by T. W. Goodwin, pp. 680-735. Academic Press, London, New York. 16. SUQIURA, M. (1963). Effect of red and far-red light on protein and chloroplast metabolism in tobacco leaf discs. Botanical Magazine 76, 174-180. 17. WAREING. P. F. & THOMPSON, A. G. (1976). RaDid effects of red lirrht on hormone levels. In Light ind Plant Dcvclopment,‘Ed. by lk S&h, pp. 285-294. ButteGorths, London. 18. WEIHING, J. L., JENSEN, S. G. & HAMILTON, R. I. (1957). Helminthosporium sativum, a destructive pathogen of bluegrass. Phytopathology 47, 744746. 19. WOOLHOUSE, H. W. (1967). The nature of senescence in plants. In Aspects of the Biology of Ageing, Symposia of the Society for Experimental Biology, Vol. 2 1, Ed. by H. W. Woolhouse, pp. 179213. Academic Press, London, New York. 20. WOOLHOUSE, H. W. (1974). Longevity and senescence in plants. Science Progress 61, 123-147.
Plant Pathology
(1979)
15, 171-176
Pathogenesis of Drechslera sorokiniana leaf spot on progressively older leaves of Poa pratensis as influenced by photoperiod and light qualityt K. N. NILSEN,
C.
F. HODGES
Departments of Horticulture, Ames, IA 5001 I, U.S.A. (Accepted for publication
Botany January
and J. P. MADSEN and Plant
Pathology,
Iowa State University,
1979)
Drechslera sorokiniana leaf spot on Poa pratensis was investigated relative to photoperiod, light quality and sequential leaf development and senescence. Leaf spot expression was enhanced on each older leaf when subjected to blue-biased, far-red-rich light irrespective of photoperiod and when subjected to “balanced” light in combination with a short photoperiod (10 h). Leaf spot expression on progressively older leaves subjected to “balanced” light in combiLeaf spot expression on progressively nation with a long photoperiod (14 h) was inhibited. older leaves in response to orange-red-biased light in combination with a long photoperiod (14 h) was similar to that of “balanced” light, but orange-red-biased light uniquely promoted leaf spot expression on younger leaves in combination with a short photoperiod (10 h). The relationship between the calculated and projected phytochrome photoequilibrium (4) and disease expression suggests that pathogenesis on progressively older leaves can be influenced by a light-phytochrome-pathogen interaction. Spectral and photoperiodic conditions associated with retardation or stimulation of leaf sensescence also seem to retard or stimulate pathogenesis, especially on progressively older leaves.
INTRODUCTION The expression of symptoms sorokiniana (Sacc.) Subram. with seasonal environmental
on leaves of Poa pratensis L. infected by Drechslera and Jain (Helminthosporium sativum P. K. &. B.) changes conditions. The symptoms produced by this pathogen include leaf spot, leaf blight and root rot of P. pratensis and other species of grasses and cereals [I, 2, 8, 181. Leaf spot is predominant on P. pratensis and, in spring and early summer, is characterized by small lesions with or without chlorotic halos. The leaf spot symptoms of late fall and early winter are characterized by enlarged necrotic areas sometimes interconnected by chlorotic streaks or by complete chlorosis or straw-coloured blighting of infected leaves. The chlorosis and strawing are suggestive of premature senescence of infected leaves [13] and can be observed in monocultures of P. pratensis in late fall and early winter, primarily on undercover leaves below a canopy of green leaves. Recent studies have revealed that the chlorosis and strawing of P. pratensis leaves infected by D. sorokiniana in late fall and early winter can be induced by manipulation of photoperiod and light quality [ 131. D isease severity on leaves of P. pratensis infected by D. sorokiniana and subjected to a low level “balanced” spectrum, or to a low level IA
t Journal Paper 50011. Projects
0048-4059/79/050
No. J-9271 of the Agriculture 2308 and 2038. 17 1 + 06$02.00/O
and
Home
Economics
@ 1979 Academic
Experiment Press
Inc.
Station, (London)
Ames, Limited
172
K. N. Nilsen, C. F. Hodges and J. P. Madsen
orange-red-biased spectrum, was increased under short days (10 h) and decreased under long days (14 h). This observation suggests that the chlorosis and strawing of infected leaves in the late fall and early winter under natural light of short-days are, in part, controlled by photoperiod. Chlorosis and strawing of infected leaves are also induced independent of photoperiod by subjecting the leaves to a low-level blue-biased, far-red-rich spectrum [ 131. This reaction is suggestive of a phytochrome-mediated interaction involving host, pathogen and light. The calculated and projected phytochrome photoequilibrium (4) [12] of the blue-biased, far-red-rich spectrum is relatively low, and low 4 values under low light levels are promotive of senescence [4, 5, 161; conversely, red-biased light may retard senescence [3,1.5, IS, 171. It also is of interest that spectral measurements taken within plant canopies describe relatively low-level far-red-rich irradiances [7, 10, II]. The enhancement of disease on leaves of P. pratensis infected by D. sorokiniana by blue-biased, far-red-rich light independent of the short days needed in combination with a “balanced” or orange-red-biased spectrum to produce the same symptoms suggest that symptom expression may be light mediated via phytochrome enhancement of leaf senescence [13]. This hypothesis is further supported by the observation that delaying either light treatment until after infection occurred had no effect on disease expression [13]. Hence, disease expression is in response to light-mediated changes in the host plant and is not due to any direct effect on the pathogen. The original host-pathogen-light interaction studies were conducted with the entire shoot of P.pratens;S, irrespective of leaf age [13]. If pathogenesis of D. sorokiniana leaf spot on P. pratensis is promoted via far-red light by stimulating premature leaf senescence, it is probable that such disease enhancement would be most pronounced on progressively older infected leaves. The research presented here was initiated to evaluate the influence of photoperiod and light quality relative to pathogenesis of D. sorokiniana leaf spot on progressively older leaves of P. pa&n&s. MATERIALS
AND
METHODS
The production and maintenance of Poa ~ratensis cv. “Newport” and Drechslera sorokiniana and the growth chamber lighting and inoculation facilities utilized in this study have been described in detail previously [13]. Inoculated plants were exposed to three separate spectral regimes in combination with a 14 h or 10 h photoperiod. The spectral regimes used produced an orange-red-biased spectrum (Spectrum A), a “balanced” spectrum (Spectrum B) and a blue-biased, far-red-rich spectrum (Spectrum C), respectively. All spectral determinations were made with a spectroradiometer (International Light IL 680), with subsequent action-spectra-based computer analysis [12] and were graphically displayed in a previous study (13). The calculated and projected phytochrome photoequilibrium of P,JPtotal (4) was O-73, 0.66 and 0.53 for spectrums A, B and C, respectively. The calculated phytochrome photoequilibrium of natural light was 0.60 [13]. The light level of all spectral regimes was adjusted to a photosynthetic photon flux density (PPFD) of 100 ( + 5) PE m--2 s-l with a quantum flux meter (Lambda Model LI-185). Temperatures within inoculation chambers were maintained at 20 “C ( f 1) during light and dark periods.
Drechslera sorokiniana
on
Pea pratensis
173
Inoculated leaves were subjected to six separate light treatments (spectrums A, B and C in combination with a 14 h or a 10 h photoperiod.) Each treatment consisted of two plants (two leaves of each of the four differently aged leaves per shoot) and was replicated five times (10 leaves of each age evaluated per treatment), and all data were analyzed statistically. Inoculations were conducted for each treatment on the four youngest, visible leaf blades of individual shoots by placing each leaf in a separate Pyrex glass inoculating tube of a specially designed inoculation apparatus [14]. Plant and inoculating apparatuses were placed within a plastic refrigerator crisper (9.5 x 27 x 19.5 mm). The four differently aged leaves were then inoculated with conidia through five inoculation ports (c. 2 mm diam.) spaced 1 cm apart over the upper epidermis of the leaf. Each leaf blade was inoculated by placing 10 conidia in a O-02 ml droplet of distilled water on the surface of the leaf through each of the five inoculating ports (conidia concentration was prepared with an automatic particle counter, High Accuracy Products Corp.). The refrigerator crispers were then covered with the appropriate shading and filtering materials to provide the desired spectral regime [13]. Disease severity was determined on the four differently aged leaves of each shoot, after 6 days of incubation under the appropriate treatment, by harvesting 10 cm lengths of leaf blades from the inoculating tubes, estimating the total leaf area of the specimen, and expressing the estimated disea.sed area as a percentage of the estimated total area of the leaf specimen [13]. RESULTS
Inoculated plants subjected to the various spectral r&imes in combination with the 14 h or 10 h photoperiod produced distinct differences in disease severity on progressively older leaves. Disease increased progressively from the youngest to the oldest leaf on plants subjected to spectrum A [Fig. l(a) and (b)]. Disease severity was not significantly different among the three oldest leaves of plants subjected to spectrum A in combination with the 14 h photoperiod, but the disease severity on each of the three oldest leaves was significantly greater than that on the youngest leaf [Fig. 11. No significant differences occurred in disease from the youngest to the oldest leaves on plants subjected to spectrum A in combination with the 10 h photoperiod [Fig. 1(b)]. Disease severity on leaves of all ages of plants subjected to spectrum A and the 10 h photoperiod was significantly greater than that on leaves of all ages of plants subjected to spectrum A and the 14 h photoperiod. Inoculated plants subjected to spectrum B in combination with the 14 h photoperiod resulted in the least severe disease, with no differences between leaf ages [Fig. 1(a)]. Leaves one and two of plants subjected to spectrum B in combination with the 10 h photoperiod showed no difference in disease; however, leaves 3 and 4 showed a significant increase in disease expression [Fig. 1 (b)]. Disease severity on leaves 1 and 2 subjected to spectrum B did not differ between the 14 h and 10 h photoperiods; leaves 3 and 4 subjected to the 10 h photoperiod, however, showed significantly greater disease than that produced on the same leaves subjected to the 14 h photoperiod. Disease expression on leaves of all ages exposed to the various spectral rCgimes in combination with the 14 h photoperiod was greatest in response to spectrum C [Fig. 1 (a)]. Disease severity on leaves 3 and 4 was significantly different and both
K. N. Nilsen,
C. F. Hodges
and J. P. Madsen
17-(a)
1615-
Leaf I (Youngest)
Leaf 2
Leaf3
Leaf 4 (Oldest) Leaf
Leaf I (Youngest)
Leaf 2
Leaf 3
Leaf 4 (Oldest)
age
FIG. 1. The influence of photoperiod and light quality on pathogenesis of Drechdera sorokiniuaa leaf spot on progressively older leaves of Poa pratcn.rsU: (a) 14 h photoperiod; (b) 10 h photoperiod. Differences in disease expression on progressively older leaves subjected to the same spectral treatment and followed by the same letter (a/) are not significantly different. Differences in disease expression on leaves of the same age between spectral treatments and followed by the same letter ( /a) are not significantly different. Duncan’s multiple range test, P = 0.05. 0, Spectrum A; @, spectrum B; l , spectrum C.
leaves showed greater levels of disease than that on leaves 1 and 2 [Fig. 1(a)]. The expression of disease on leaves of all ages subjected to spectrum C in combination with the 10 h photoperiod was similar to that in combination with the 14 h photoperiod [Fig. l(a) and (b)], with no significant differences between the two photoperiods. Spectral regimes and photoperiods interact with specific leaf-age groups to produce differing levels of disease. The differences in disease on each leaf-age group subjected to spectrums A and B in combination with the 14 h photoperiod were not different [Fig. l(a)]. Spectrum C in combination with the same photoperiod, however, produced significantly greater levels of disease on all leaf-age groups than that on leaves subjected to spectra A and B [Fig. 1(a)]. Th e interaction between leaf-age, spectral regimes and the 10 h photoperiod was more complex than that of the 14 h photoperiod. Among the three youngest leaf groups, disease was significantly
Drechslera
sorokiniana
on Poa pratensis
175
different among all spectral regimes (except leaf 3, spectra A and C), with disease severity greatest on leaves exposed to spectrums A, C and B in descending order [Fig. 1(b)]. Disease was greatest on leaf 4 in response to spectrums B and C, both of which resulted in significantly more disease than that produced in response to spectrum A [Fig. 1 (b)].
DISCUSSION
Disease enhancement under spectrum B (4 = O-66), which most closely approximates the photomorphogenic quality of “natural” light [13], seems to be a photoperiodic effect. The two youngest leaves of plants subjected to this spectrum show the lowest level of disease expression, irrespective of photoperiod [Fig. l(a) and (b)]. Leaves 3 and 4 show no difference in disease on plants subjected to the 14 h photoperiod [Fig. 1(a)] ; however, leaves 3 and 4 of plants subjected to the 10 h photoperiod show a sharp increase in disease severity [Fig. 1 (b)]. This suggests that the “balanced” light quality characteristics of “natural” light in combination with a long photoperiod (14 h) may retard pathogenesis [Fig. 1 (a)] and that increased disease under a short photoperiod [Fig. 1 (b)] is a consequence of enhanced sequential senescence due to a short photoperiod-leaf age-pathogen interaction [N]. Any deviation in light quality from a “balanced” spectrum influences pathogenesis of D. sorokiniana leaf spot on differently aged leaves of P. pratensis. The orange-redbiased light of spectrum A in combination with either the 14 h or 10 h photoperiod generally increased disease expression on leaves of all ages, but the only significant increases in disease on the various leaf ages above that of the “balanced” spectrum occurred under the 10 h photoperiod [Fig. 1(a) and (b)]. Only the oldest leaf showed significantly less disease in response to spectrum A and the 10 h photoperiod [Fig. l(b)]. These results show that the progressive increase in disease expression associated with increasing leaf age in response to a “balanced” spectrum and short photoperiod is minimized under orange-red-biased light on the oldest leaf and is enhanced on younger leaves. The relatively high phytochrome photoequilibrium (+ = O-73) generated by orange-red-biased light is associated with increased levels of gibberellins, cytokinins, photosynthate-sink activity and senescence retardation [3, 9, 15, IS, 17, 191. These characteristics of a high 4 value may delay senescence of older leaves and also inhibit pathogenesis; it does not, however, explain the increase in disease on the youngest leaves [Fig. 1 (b)]. The blue-biased, far-red rich light of spectrum C increased disease on progressively older leaves independent of photoperiod and generated the lowest 4 value (O-53) of the spectral regimes employed [Fig. 1 (a) and (b)]. In general, far-red-biased light produces lower 4 values and contributes to increases in auxin and ethylene levels and is senescence promoting [4,5,15]. Also, spectral measurements within plant canopies show low light levels relatively rich in far-red light [7, 10, II]. Consequently, under natural environmental conditions, D. sorokiniana disease expression may be enhanced by a combination of low-level light, by progressively shorter photoperiods of fall (northern temperate climates), and by a~relatively dense plant canopy likely to generate Iow + values promotive of sequential leaf senescence and subsequent stimulation of disease on older leaves. Experimentation is in progress to evaluate
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and J. P. Madsen
further the relationship between red and far-red-enriched light treatments and the influence of phytochrome photoequilibrium on disease severity. REFERENCES 1. BEAN, G. A. & WILCOXSON, R. D. (1964). Helminthosporium leaf spot of bluegrass. Phytopatholoa 54, 1065-1070. 2. BEAN, G. A. & WILCOXSON, R. D. (1964). Pathogenicity of three species of Helminthosporium on roots of bluegrass. PhytopathologV 54, 1684-1085, 3. BISWALL. V. C.. & SHARMA R. (1976). Phvtochrome rezulation of senescence in detached barlev I lea&. zei&hriyt ftir Pflan.&hys&gie b, 71-75. 4. DE GREEP, J. A. & FREDERICQ, H. (1972). Enhan cement of senescence by far-red light. Plantu 104,272-274. 5. EREZ, A. (1971). The effect of different portions of the sunlight spectrum on ethylene evolution in peach (Prunus firsica) apices. Physiologia Plantarum 39, 285-289. 6. FLETCHER, R. A. (1969). Retardation of leaf senescence by benzyladenine in intact bean plants. Planta 89, l-7. 7. GATES, D. M., DEEGAN, H. J., SCHLETER, J. C. & WEIDNER, V. R. (1965). Spectral properties of plants. Applied Optics 4, 1 l-20. 8. HODGES, C. F. & WATSCHKE, G. A. (1975). Pathogenicity of soil-borne Bipolaris sorokiniuna on seed and roots of three perennial grasses. Phytoputholo~ 65, 398-400. 9. HOLMES, M. G. & SMITH, H. (1975). The function of phytochrome in plants growing in the natural environment. .Nature 254, 512-514. 10. HOLMES, M. G. & MCCARTNEY, H. A. (1976). Spectral energy distribution in the natural environment and its implications for phytochrome function. In Light and Plant Development, Ed. by H. Smith, pp. 467476. Butterworths, London. 11. HOLMES, M. G. & SMITH, H. (1977). The function of phytochrome in the natural environment. II. The influence of vegetation canopies on the spectral energy distribution of natural daylight. Photochemistry and Photobiology 25, 539-545. 12. NILSEN, K. N. & NILSEN, N. S. (1977). Photosynthetic and photomorphogenic efficacies of light sources: Spectroradiometric measurement with computer analysis. Hart. Science 12 (4), 405. 13. NILSEN, K. N., MADSEN, J. P. & HODGES, C. F. (1978). Enhanced Drechslera sorokiniuna leaf spot expression on Poa pratensis in response to photoperiod and blue-biased light. Physiological Plant Pathology 14, 57-69. 14. ROBINSON, P. W. & HODGES, C. F. (1976). An inoculation apparatus for evaluation of Bipolaris sorokiniana lesion development on progessively older leaves of Poa pratensis. Phytopathology 66, 360-362. 15. SATTER, R. C. & GALSTON, A. W. (1976). The physiological functions of phytochrome. In &m&y and Biochemistry of Plant Pigments, 2nd edn., Vol. 1, Ed. by T. W. Goodwin, pp. 680-735. Academic Press, London, New York. 16. SUQIURA, M. (1963). Effect of red and far-red light on protein and chloroplast metabolism in tobacco leaf discs. Botanical Magazine 76, 174-180. 17. WAREING. P. F. & THOMPSON, A. G. (1976). RaDid effects of red lirrht on hormone levels. In Light ind Plant Dcvclopment,‘Ed. by lk S&h, pp. 285-294. ButteGorths, London. 18. WEIHING, J. L., JENSEN, S. G. & HAMILTON, R. I. (1957). Helminthosporium sativum, a destructive pathogen of bluegrass. Phytopathology 47, 744746. 19. WOOLHOUSE, H. W. (1967). The nature of senescence in plants. In Aspects of the Biology of Ageing, Symposia of the Society for Experimental Biology, Vol. 2 1, Ed. by H. W. Woolhouse, pp. 179213. Academic Press, London, New York. 20. WOOLHOUSE, H. W. (1974). Longevity and senescence in plants. Science Progress 61, 123-147.