Inactivation of Normal and Mutant Neurospora Crassa Conidia by Visible Light and Near‐uv: Role of ¹o₂, Carotenoid Composition and Sensitizer Location

Inactivation of Neurospora crassa conidia from wild‐type and mutant strains by visible and near‐UV light has been investigated in the presence and absence of photosensitizing dyes. Inactivation by near‐UV is virtually unchanged by the presence of deuterium oxide or azide suggesting that, contrary to the situation with visible light and photosensitizing dyes, 1 O 2 is not involved in any substantial way in the formation of lethal lesions. The finding that carotenoid deficient strains are similar to wild‐type strains in sensitivity to near‐UV inactivation is consistent with 1 O 2 not being involved. Photodynamic inactivation of conidia by visible light occurs in the presence of methylene blue (MB), toluidine blue O (TB), or acridine orange (AO). Carotenoid deficient strains are more sensitive to such inactivation only when MB and TB are used. These results support the contention that MB and TB mediated damage involves the cell membrane where carotenoids are available for quenching, whereas AO mediated damage occurs in the nucleus sequestered from the protective influence of carotenoids. A newly isolated, lemon–yellow mutant, mapping to the al ‐1 locus, exhibits sensitivities to photodynamic inactivation similar to other pure‐white mutants at the same locus. The sensitivity of this pigmented mutant is apparently related to insufficient unsaturation (seven to nine double bonds) of the two colored carotenoids, zeta–carotene and neurosporene, produced by the mutant.