HERBICIDE MEDIATED UV-RESISTANCE IN CYANOBACTERIA: ON THE ROLE OF PHOTOSYNTHETIC ELECTRON TRANSPORT SYSTEM RATHER THAN REPLICATIVE DNA AS LETHAL TARGET DETERMINING DARK-SURVIVAL OF Anacystis nidulans

Abstract— The role of the replicative state of DNA and of the photosynthetic electron transport system in determining UV-sensitivity of A. nidulans under conditions of non-photoreactivation (by incubating the cells for 24 h in the dark following UV-irradiation) has been investigated. Both the DNA synthesis data and the data on survival levels during cell cycle synchrony forced by light to dark and dark to light transitions showed that the differential UV-sensitivity was not correlated with the replicative state of the DNA as suggested earlier. However, incubation in the light with the herbicides 2/3-4, dichlorophenyl/-l, 1-dimethyl urea (DCMU) and 2-chloro-4-ethylamino-6-isopropylamino-s-triazine (atrazine) which are known to inhibit electron transport by specifically binding to the high turnover B protein of photosynthetic electron transport system II (PSII), enhanced the UV-resistance with kinetics similar to those of a culture transferred from light to dark. We interpret this result as implicative of PSII as the second lethal target in the case of cyanobacteria. The inactivation of electron transport activity of PSII as measured by the fall in DCMU-sensitive fluorescence yield during post-UV dark incubation supports this hypothesis. It is proposed that in wild type cells the survival under conditions of non-photoreactivation following UV-irradiation is essentially determined by the level of dark-repair of damage to PSII and that the 32 kD B protein may have a role in dark-repair of damage to the electron transport system. This hypothesis explains the paradox of negative liquid holding recovery phenomenon under conditions which promote excision-repair of damaged DNA in cyanobacteria.