Effects of UV and Phototoxins on Selected Fungal Pathogens of Citrus

Photons in the UV region of the spectrum are important for organisms since they are energy-rich and strongly absorbed by biological molecules having the potential to react with membranes, enzymes, and nucleic acids. These wavelengths can also be absorbed by specific molecules that undergo conversion to a more reactive state (light activation) which can then cause damage to molecules of critical physiological function (phototoxicity). The importance of pigments in two genera of the Citrus pathogens, Fusarium and Penicillium, was assessed for ability to protect against inactivation by UV-A, B, and C and two phototoxins activated by UV-A. Pigment-deficient mutants of both genera were isolated following UV-C mutagenesis. Direct exposure of fungal spores in suspension of wild type and pigment-deficient mutants was carried out under the appropriate light source. The UV-A activated phototoxins investigated were: α-terthienyl (α-T), which produces predominantly singlet oxygen $({}^{1}{\rm O}{}_{2})$, an excited state of oxygen, which causes chiefly membrane damage; and 8-methoxypsoralen (8-MOP), which induces cycloadduct formation in DNA. For both genera, UV-A and UV-B alone were ineffective in causing inactivation of conidia at the fluences tested. Using appropriate Escherichia coli tester strains, it was demonstrated that the UV-B source was capable of inducing DNA lesions leading to lethality, presumably cyclobutane dimers in large measure. The carotenoids in one of the Fusarium species did not appreciably protect against lethal damage induced by UV-C, but the pigments of both Penicillium species were presumably able to screen UV-C and offer protection. It is assumed that the carotenoids in the wild type Fusarium species protected against UV-A activated α-T damage by quenching singlet oxygen. The blue-green pigment(s) in P. italicum prevent DNA damage caused by 8-MOP most probably by screening the UV-A wavelengths necessary to activate the phototoxin.

[1]  J. Heitz,et al.  Light-Activated Pesticides , 1987 .

[2]  R. W. Tuveson,et al.  SENSITIVITY OF HemA MUTANT Escherichia coli CELLS TO INACTIVATION BY NEAR‐UV LIGHT DEPENDS ON THE LEVEL OF SUPPLEMENTATION WITH δ‐AMINOLEVULINIC ACID , 1986, Photochemistry and photobiology.

[3]  A. Teramura Effects of ultraviolet‐B radiation on the growth and yield of crop plants , 1983 .

[4]  A. Clark,et al.  Analysis of the role of recombination and repair in mutagenesis of Escherichia coli by UV irradiation. , 1977, Genetics.

[5]  R. W. Tuveson,et al.  α‐TERTHIENYL PHOTOSENSITIZES DAMAGE TO pBR322 DNA , 1991 .

[6]  K. Ingold,et al.  beta-Carotene: an unusual type of lipid antioxidant. , 1984, Science.

[7]  R. W. Tuveson,et al.  Role of cloned carotenoid genes expressed in Escherichia coli in protecting against inactivation by near-UV light and specific phototoxic molecules , 1988, Journal of bacteriology.

[8]  M. Mathews COMPARATIVE STUDY OF LETHAL PHOTOSENSITIZATION OF SARCINA LUTEA BY 8-METHOXYPSORALEN AND BY TOLUIDINE BLUE , 1963, Journal of bacteriology.

[9]  D. Aylor,et al.  The Role of Solar Radiation, Especially Ultraviolet, in the Mortality of Fungal Spores , 1985 .

[10]  Y. Marchant Photodecomposition of Naturally Occurring Biocides , 1987 .

[11]  N. Krinsky Chapter 5 – THE PROTECTIVE FUNCTION OF CAROTENOID PIGMENTS , 1968 .

[12]  R. Hancock,et al.  MODE OF ACTION OF α‐TERTHIENYL ON ESCHERICHIA COLI: EVIDENCE FOR A PHOTODYNAMIC EFFECT ON MEMBRANES , 1982 .

[13]  Wolf Vishniac,et al.  Physiology of Fungi. , 1959 .

[14]  R. W. Tuveson,et al.  Inactivation of carotenoid-producing and albino strains of Neurospora crassa by visible light, blacklight, and ultraviolet radiation , 1976, Journal of bacteriology.

[15]  T. Árnason,et al.  Phototoxic substances from Flaveria trinervis and Simira salvadorensis , 1983 .

[16]  R. W. Tuveson,et al.  The isolation of ultraviolet sensitive mutants from Aspergillus rugulosus. , 1967, Radiation research.

[17]  G. Payne,et al.  The Role of Carotenoids in Resistance of Fungi to Cercosporin , 1989 .

[18]  R. W. Tuveson,et al.  MECHANISMS OF CITRAL PHOTOTOXICITY , 1992, Photochemistry and photobiology.

[19]  R. W. Tuveson,et al.  INACTIVATION BY MONOCHROMATIC NEAR‐UV RADIATION OF AN Escherichia coli hemA8 MUTANT GROWN WITH AND WITHOUT δ‐AMINOLEVULINIC ACID: THE ROLE OF DNA vs MEMBRANE DAMAGE , 1987, Photochemistry and photobiology.

[20]  B. Hug,et al.  Growing Escherichia coli mutants deficient in riboflavin biosynthesis with non-limiting riboflavin results in sensitization to inactivation by broad-spectrum near-ultraviolet light (320-400 nm). , 1990, Photochemistry and photobiology.

[21]  M. Berenbaum,et al.  Environmental phototoxicity: Solar ultraviolet radiation affects the toxicity of natural and man-made chemicals , 1988 .

[22]  G. Sandmann,et al.  Identification of carotenoids in Erwinia herbicola and in a transformed Escherichia coli strain. , 1990, FEMS microbiology letters.

[23]  Jeffrey H. Miller Experiments in molecular genetics , 1972 .

[24]  R. W. Tuveson,et al.  GENETIC CONTROL OF NEAR‐UV (300–400nm) SENSITIVITY INDEPENDENT OF THE recA GENE IN STRAINS OF ESCHERICHIA COLI K12 , 1979, Photochemistry and photobiology.

[25]  M. Caldwell,et al.  The changing solar ultraviolet climate and the ecological consequences for higher plants. , 1989, Trends in ecology & evolution.

[26]  R. W. Tuveson,et al.  THE EFFECTS OF EXOGENOUS CATALASE ON BROAD‐SPECTRUM NEAR‐UV (300‐400 nm) TREATEDEscherichia coli CELLS , 1984, Photochemistry and photobiology.

[27]  R. W. Tuveson,et al.  INACTIVATION OF NORMAL AND MUTANT NEUROSPORA CRASSA CONIDIA BY VISIBLE LIGHT AND NEAR‐UV: ROLE OF 1O2, CAROTENOID COMPOSITION AND SENSITIZER LOCATION , 1981, Photochemistry and photobiology.

[28]  S. Nemec,et al.  Light-activated antimicrobial chemicals from plants: their potential role in resistance to disease-causing organisms , 1987 .

[29]  D. Lilley,et al.  DNA Repair , 1998, Nucleic Acids and Molecular Biology.

[30]  M. Pathak,et al.  Molecular and genetic basis of furocoumarin reactions. , 1976, Mutation research.