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Volume 7, Issue 2 (Suppl)

J Ecosyst Ecography, an open access journal

ISSN:2157-7625

September 18-20, 2017

September 18-20, 2017 Toronto, Canada

Joint Conference

International Conference on

Environmental Microbiology and Microbial Ecology

Ecology and Ecosystems

J Ecosyst Ecography 2017, 7:2 (Suppl)

DOI: 10.4172/2157-7625-C1-030

UV induced DNAdamage repair in bacteria

Khalil A El Halfawy

University of Sadat City, Egypt

he “Dogma” that has been accepted for many years in the field of mutagenesis and lethal of effect in bacteria was non-selective in

the nature of its repair mechanism, as well as, non-special and rather primitive. We studied the influence of a temporary specific

inhibition of post-radiation macromolecular syntheses and of preliminary UV irradiation on the kinetics of accumulation of fixed

mutations, that is mutations insensitive to MFD, in UV-irradiate

B. subtilis

cells. From experimental results, it is deduced that the

entry of pre-mutagenic lesion into a round of replication, initiated before irradiation, is not a fixing event in UV mutagenesis. For

performance of fixation, the proceeding of replication, initiated after irradiation, and protein synthesis are necessary. In irradiate

cells incubated in medium with lowered concentration of nitrogen sources, the anti-mutagenic activity of UVR-dependent repair

system competes with the process of fixation for pre-mutagenic lesions and reduce the efficiency of mutagenesis. The most efficient

fixation and mutagenesis occur at high concentration of nitrogen sources in post-radiation medium, when the manifestation of anti-

mutagenic activity appears to be blocked. The possible nature of a process leading to mutation fixation in the detection of specific

pathway-dependent mechanisms being conferred only to the acquired post-irradiation metabolism. It had also long been believed

that both pre-mutagenic as well as pre-lethal lesions are same pathways function until the adaptive repair mechanisms come into

actions. However, this simplistic sight, in which DNA repair performs, could not explain how bacterial cell recognize and trigger

different repair pathways cascades responses.