The Beauty of Clustered DNA Lesion

Dear Colleagues,

Local multi-damage sites (LMDS) such as DNA double-strand breaks (DSBs), inter-, or intra-strand cross-links are repaired by homologous recombination (HR) and non-homologous end-joining (NHEJ) systems. The mentioned repair mechanisms have been well recognized in the case of isolated lesions, while the repair process of clustered DNA lesions still requires further study. The isolated DSB, which has been known for 70 years, is well recognized, but multi-DSB sites or clustered lesions (CL) composed of different types of damage, are not, especially in the context of the cellular response. Clustered DNA lesion has been defined as two or more cases of DNA damage per one or two helix turn. The significance of CL was discerned by Ward and Goodhead, whereas Price identified their presence and significance in E. coli. Additionally, it has been confirmed that clustered lesions are induced in mammalian cells. It is estimated that 80% of all LMDS sites contain damage that is not caused by DSBs. It should be pointed out that CLs are composed of DNA damage subunits, which are recognized and removed mainly by BER or the more complicated NER system. Moreover, using the Monte Carlo approach, it has been predicted that high-LET radiation is able to generate up to 25 clustered lesions at a distance of 200 nucleobase pairs. Based on the Bragg peak, it is not surprising that low-LET possesses the ability to induce LMDS too.

It is a great pleasure to invite fellow members of the scientific community to submit a manuscript (regular articles, communications, reviews) to this Special Issue.

Prof. Dr. Boleslaw Karwowski
Guest Editor

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