RecAX53 is a chimeric variant of the Escherichia coli RecA protein (RecAEc) that contains a part of the central domain of Pseudomonas aeruginosa RecA (RecAPa), encompassing a region that differs from RecAEc at 12 amino acid positions. Like RecAPa, this chimera exhibits hyperrecombination activity in E. coli cells, increasing the frequency of recombination exchanges per DNA unit length (FRE). RecAX53 confers the largest increase in FRE observed to date. The contrasting properties of RecAX53 and RecAPa are manifested by in vivo differences in the dependence of the FRE value on the integrity of the mutS gene and thus in the ratio of conversion and crossover events observed among their hyperrecombination products. In strains expressing the RecAPa or RecAEc protein, crossovers are the main mode of hyperrecombination. In contrast, conversions are the primary result of reactions promoted by RecAX53. The biochemical activities of RecAX53 and its ancestors, RecAEc and RecAPa, have been compared. Whereas RecAPa generates a RecA presynaptic complex (PC) that is more stable than that of RecAEc, RecAX53 produces a more dynamic PC (relative to both RecAEc and RecAPa). The properties of RecAX53 result in a more rapid initiation of the three-strand exchange reaction but an inability to complete the four-strand transfer. This indicates that RecAX53 can form heteroduplexes rapidly but is unable to convert them into crossover configurations. A more dynamic RecA activity thus translates into an increase in conversion events relative to crossovers.
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http://dx.doi.org/10.1128/JB.01006-07 | DOI Listing |
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MOE Key Laboratory of Biosystems Homeostasis and Protection, College of Life Sciences, Zhejiang University, No.866 Yuhangtang Road, 310058, Hangzhou, China.
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Department of Biology of Bacteria, Institute of Microbiology, Biotechnology and Immunology, Faculty of Biology and Environmental Protection, University of Lodz, 90-237 Lodz, Poland.
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January 2025
Jiangsu Key Laboratory for Pathogens and Ecosystems, College of Life Sciences, Nanjing Normal University, Nanjing, China.
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View Article and Find Full Text PDFSci Rep
January 2025
Reproductive Biology Laboratory, Centre for Reproductive Medicine, Amsterdam UMC, University of Amsterdam, Amsterdam, 1105AZ, The Netherlands.
Radiation therapy is a common treatment modality for lung cancer, and resistance to radiation can significantly affect treatment outcomes. We recently described that lung cancer cells that express more germ cell cancer genes (GC genes, genes that are usually restricted to the germ line) can repair DNA double-strand breaks more rapidly, show higher rates of proliferation and are more resistant to ionizing radiation than cells that express fewer GC genes. The gene encoding TRIP13 appeared to play a large role in this malignant phenotype.
View Article and Find Full Text PDFCell Rep
January 2025
Laboratory of Biochemistry, Wageningen University, 6708 WE Wageningen, the Netherlands. Electronic address:
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