DNA breakage is intimately associated with meiotic recombination in the fission yeast Schizosaccharomyces pombe. Sites of prominent DNA breakage were found approximately 25 to approximately 200 kb apart in the genomic regions surveyed. We examined in detail a 501 kb region of chromosome I and found six sites, or tight clusters of sites, at which approximately 2%-11% of the DNA accumulated breaks in a rad50S mutant. In contrast to the discrete, widely spaced distribution of prominent break sites, recombination in this region was more uniformly distributed (0.7-1.6 cM/10 kb) whether the genetic interval tested contained no, one, or more such sites. We infer that although recombination depends upon DNA breakage, recombination often occurs remote from these sites (tens of kilobases away); we discuss mechanisms by which this may occur.
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http://dx.doi.org/10.1016/s1097-2765(02)00452-5 | DOI Listing |
Nucleic Acids Res
December 2024
Department of Biology, Tufts University, Suite 4700, 200 Boston Ave, Medford, MA 02155, USA.
Long AT repeat tracts form non-B DNA structures that stall DNA replication and cause chromosomal breakage. AT repeats are abundant in human common fragile sites (CFSs), genomic regions that undergo breakage under replication stress. Using an in vivo yeast model system containing AT-rich repetitive elements from human CFS FRA16D, we find that DNA polymerase zeta (Pol ζ) is required to prevent breakage and subsequent deletions at hairpin and cruciform forming (AT/TA)n sequences, with little to no role at an (A/T)28 repeat or a control non-structure forming sequence.
View Article and Find Full Text PDFFood Sci Nutr
December 2024
Department of Biochemistry and Biotechnology, School of Health Sciences University of Thessaly Larissa Greece.
Previous studies have shown that seaweed extracts (HMEs) possess antioxidant properties, but the molecular mechanisms accounting for this activity are not known. Thus, the present study investigated the molecular mechanisms through which HME exerted its antioxidant activity in human mesenchymal stem cells (WJ-MSCs). After the isolation of HME, its chemical composition was analyzed with gas chromatography mass spectrometry, indicating that it contained amino acids, organic acids, organic amides, sugar alcohols, saturated fatty acids, hydrogenated diterpene alcohols, and other organic compounds.
View Article and Find Full Text PDFMol Biol Cell
December 2024
Department of Environmental and Biological Sciences, University of Eastern Finland, P.O. Box 111, 80101 Joensuu, Finland.
Mirin, a chemical inhibitor of MRE11, has been recently reported to suppress immune response triggered by mitochondrial DNA (mtDNA) breakage and release during replication stalling. We show that while Mirin reduces mitochondrial replication fork breakage in mitochondrial 3´-exonuclease MGME1 deficient cells, this effect occurs independently of MRE11. We also discovered that Mirin directly inhibits cellular immune responses, as shown by its suppression of STAT1 phosphorylation in Poly(I:C)-treated cells.
View Article and Find Full Text PDFJ Nanobiotechnology
December 2024
NHC Key Laboratory of Radiobiology, School of Public Health, Jilin University, Chang Chun, 130021, China.
Background: Cancer radiotherapy (RT) still has limited clinical success because of the obstacles including radioresistance of hypoxic tumors, high-dose X-ray-induced damage to adjacent healthy tissue, and DNA-damage repair by intracellular PD-L1 in tumor.
Results: Therefore, to overcome these obstacles multifunctional core-shell BMS@PtAu nanoparticles (NPs) are prepared using nanoprecipitation followed by electrostatic assembly. PtAu clusters are released from BMS@PtAu NPs to alleviate tumor hypoxia by catalyzing the decomposition of endogenous HO to generate O as well as by enhancing X-ray deposition at the tumor site, which thereby reduce the required X-ray dose.
J Genet Eng Biotechnol
December 2024
Medical Molecular Genetics Dpt., Human Genetics and Genome Research Institute, National Research Centre, Cairo, Egypt. Electronic address:
Background: Fanconi anemia is a genetically heterogeneous recessive disorder distinguished by cytogenetic instability, hypersensitivity to DNA crosslinking agents, increased chromosomal breakage, and disturbed DNA repair. To date, Fanconi anemia complementation group (FANC) includes 23 FANC genes identified of which, FANCA gene is the most commonly mutated. The mutation spectrum of the FANCA gene is highly heterogeneous with large intragenic deletions due to Alu elements-mediated recombination.
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