1206 Current Trends in Biotechnology and Pharmacy Vol. 5 (3) 1206-1232 July 2011, ISSN 0973-8916 (Print), 2230-7303 (Online) Abstract Nowadays, a great amount of pathogenic bacteria has been identified such as Mycobacterium sp. and Helicobacter pylori and have become a serious health problem around the world. These bacteria have developed several DNA repair mechanisms as a strategy to neutralize the effect of the exposure to endogenous and exogenous agents that will lead to two different kinds of DNA damage: single strand breaks (SSBs) and double strand breaks (DSBs). For SSBs repair, bacteria use the base excision repair (BER) and nucleotide excision repair (NER) mechanisms, which fix the damaged strand replacing the damaged base or nucleotide. DSBs repair in bacteria is performed by homologous recombination repair (HRR) and non-homologous end-joining (NHEJ). HRR uses the homologous sequence to fix the two damaged strand, while NHEJ repair does not require the use of its homologous sequence. The use of unspecific antibiotics to treat bacterial infections has caused a great deal of multiple resistant strains making less effective the current therapies with antibiotics. In this review, we emphasized the mechanisms mentioned above to identify molecular targets that can be used to develop novel and more efficient drugs in future. Key words: DNA damage, antibiotic resistance, SSB, DSB, antimicrobial drugs, drug-resistant mutants, BER, NER, HRR, NHEJ. 1. Introduction During the last decades, our knowledge of DNA structure and function has increased dramatically. For example, a recent publication of Wolfe-Simon et al. (1) shows a bacterium strain “GFAJ-1” of the Halomonadaceae, can use arsenic, a substance that is highly toxic to almost all life on this planet, instead of phosphorus to sustain its growth and incorporate it to its DNA. It is predicted that these bacteria may have formed more than 760,000 years ago. Until now, O 2 , C, H, N, P and S have been the basic ingredients of the chemistry of life. However, the present evidence shows this bacterium uses arsenic to maintain its life machinery (1). This information has allowed us to gain a better understanding of life in general, as well as of human diseases (2,3,4). As a matter of fact, with the rise of molecular biotechnology and genetic engineering, scientists have started to develop more effective tools against diseases, targeting key components of molecular mechanisms and even targeting the origin of any living process: the genes. Nevertheless, our knowledge about DNA still remains limited, as well as the options that we need to explore on the path to developing drugs and vaccines against infectious diseases (5). One aspect that could help us in our fight against infectious diseases is to understand DNA DNA Repair Mechanisms as Drug Targets in Prokaryotes Lorena M. Coronado*, Carolina I. De La Guardia, Yisett S. González, Carlos M. Restrepo and Nicole M. Tayler Center for Cellular & Molecular Biology of Diseases Institute for Scientific Research and Technology Services (INDICASAT) Building 219, City of Knowledge, Clayton, Republic of Panama (All authors contributed equally) *For Correspondence - lcoronado@indicasat.org.pa DNA repair mechanisms in prokaryotes