Two Photolyases Repair Distinct DNA Lesions and Reactivate UVB-Inactivated Conidia of an Insect Mycopathogen under Visible Light

Fungal conidia serve as active ingredients of fungal insecticides but are sensitive to solar UV irradiation, which impairs double-stranded DNA (dsDNA) by inducing the production of cytotoxic cyclobutane pyrimidine dimers (CPDs) and (6-4)-pyrimidine-pyrimidine photoproducts (6-4PPs). This study aims...

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Bibliographic Details
Published in:Applied and environmental microbiology 2019-02, Vol.85 (4)
Main Authors: Wang, Ding-Yi, Fu, Bo, Tong, Sen-Miao, Ying, Sheng-Hua, Feng, Ming-Guang
Format: Article
Language:English
Subjects:
Animals
Beauveria bassiana
Cell Nucleus
Conidia
Cyclobutane
Cyclobutane pyrimidine dimers
Cytotoxicity
Deoxyribodipyrimidine Photo-Lyase - genetics
Deoxyribonucleic acid
Dimers
DNA
DNA - radiation effects
DNA damage
DNA Damage - radiation effects
DNA Repair
Fungi
Gene Expression Regulation, Fungal
Genes
Insecta - microbiology
Insecticide resistance
Insecticides
Insects
Invertebrate Microbiology
Irradiation
Lesions
Light
Mutants
Photolyase
Photoreactivation
Pyrimidine Dimers
Radiation damage
Radiation Tolerance
Repair
Spores, Fungal - genetics
Spores, Fungal - radiation effects
Spotlight
Ultraviolet radiation
Ultraviolet Rays - adverse effects
Virulence
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Summary:Fungal conidia serve as active ingredients of fungal insecticides but are sensitive to solar UV irradiation, which impairs double-stranded DNA (dsDNA) by inducing the production of cytotoxic cyclobutane pyrimidine dimers (CPDs) and (6-4)-pyrimidine-pyrimidine photoproducts (6-4PPs). This study aims to elucidate how CPD photolyase (Phr1) and 6-4PP photolyase (Phr2) repair DNA damage and photoreactivate UVB-inactivated cells in , a main source of fungal insecticides. Both Phr1 and Phr2 are proven to exclusively localize in the fungal nuclei. Despite little influence on growth, conidiation, and virulence, singular deletions of and resulted in respective reductions of 38% and 19% in conidial tolerance to UVB irradiation, a sunlight component most harmful to formulated conidia. CPDs and 6-4PPs accumulated significantly more in the cells of Δ and Δ mutants than in those of a wild-type strain under lethal UVB irradiation and were largely or completely repaired by Phr1 in the Δ mutant and Phr2 in the Δ mutant after optimal 5-h exposure to visible light. Consequently, UVB-inactivated conidia of the Δ and Δ mutants were much less efficiently photoreactivated than were the wild-type counterparts. In contrast, overexpression of either or in the wild-type strain resulted in marked increases in both conidial UVB resistance and photoreactivation efficiency. These findings indicate essential roles of Phr1 and Phr2 in photoprotection of from UVB damage and unveil exploitable values of both photolyase genes for improved UVB resistance and application strategy of fungal insecticides. Protecting fungal cells from damage from solar UVB irradiation is critical for development and application of fungal insecticides but is mechanistically not understood in , a classic insect pathogen. We unveil that two intranuclear photolyases, Phr1 and Phr2, play essential roles in repairing UVB-induced dsDNA lesions through respective decomposition of cytotoxic cyclobutane pyrimidine dimers and (6-4)-pyrimidine-pyrimidine photoproducts, hence reactivating UVB-inactivated cells effectively under visible light. Our findings shed light on the high potential of both photolyase genes for use in improving UVB resistance and application strategy of fungal insecticides.
ISSN:0099-2240
1098-5336
DOI:10.1128/AEM.02459-18