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Physiology and Biochemistry

The Role of Carotenoids in Resistance of Fungi to Cercosporin. Margaret E. Daub, Assistant professor, Department of Plant Pathology, North Carolina State University, Box 7616, Raleigh 27695-7616; Gary A. Payne, Associate professor, Department of Plant Pathology, North Carolina State University, Box 7616, Raleigh 27695-7616 Phytopathology 79:180-185. Accepted for publication 16 August 1988. Copyright 1989 The American Phytopathological Society. DOI: 10.1094/Phyto-79-180.

Cercospora spp. produce large quantities of the singlet-oxygen-generating toxin cercosporin and are not harmed by it. We investigated carotenoid production by these fungi to determine if carotenoids (which quench singlet oxygen) play a role in resistance. Cercospora spp. produce high concentrations of Beta-carotene at early stages of the growth cycle, up to 12 μg/g dry weight. Three cercosporin-sensitive fungi differed in carotenoid production. Phytophthora cinnamomi and Phytophthora parasitica produced virtually no carotenoids, whereas Neurospora crassa produced carotenoids in amounts comparable to those found in C. nicotianae. Carotenoid-minus mutants of N. crassa and Phycomyces blakesleeanus were considerably more sensitive to cercosporin than carotenoid-producing strains. However, there was not a linear relationship between the amount of carotenoids produced by these strains and sensitivity to cercosporin. Three carotenoid inhibitors, norflurazon, mevinolin, and Beta-ionone, did not inhibit synthesis of carotenoids of C. nicotianae, and only low levels of inhibition were obtained with diphenylamine, whereas diphenylamine, norflurazon, and mevinolin effectively inhibited carotenoid synthesis in N. crassa. Equivalent amounts of carotenoids were isolated from protoplasts of N. crassa and C. nicotianae, suggesting that, in C. nicotianae, as in N. crassa, carotenoids are localized within the protoplast. Our data support the hypothesis that carotenoids play a role in resistance of fungi to cercosporin, but that they are not the only or even major mechanism of cercosporin resistance. This result was unexpected based on previous studies of photosensitizer resistance mechanisms in living organisms.