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Non-homologous end joining (NHEJ) is a pathway that repairs double-strand breaks in DNA. It is called "non-homologous" because the break ends are directly ligated without the need for a homologous template, in contrast to homology directed repair (HDR), which requires a homologous sequence to guide repair.
At various steps of these recombination processes, heteroduplex DNA (double-stranded DNA consisting of single strands from each of the two homologous chromosomes which may or may not be perfectly complementary) is formed. During meiosis non-crossover recombinants occur frequently and these appear to arise mainly by the SDSA pathway.
[52] γH2AX (H2AX phosphorylated on serine 139) can be detected as soon as 20 seconds after irradiation of cells (with DNA double-strand break formation), and half maximum accumulation of γH2AX occurs in one minute. [52] The extent of chromatin with phosphorylated γH2AX is about two million base pairs at the site of a DNA double-strand break.
A double-strand break repair model refers to the various models of pathways that cells undertake to repair double strand-breaks (DSB). DSB repair is an important cellular process, as the accumulation of unrepaired DSB could lead to chromosomal rearrangements, tumorigenesis or even cell death. [ 1 ]
The MRN complex (MRX complex in yeast) is a protein complex consisting of Mre11, Rad50 and Nbs1 (also known as Nibrin [1] in humans and as Xrs2 in yeast). In eukaryotes, the MRN/X complex plays an important role in the initial processing of double-strand DNA breaks prior to repair by homologous recombination or non-homologous end joining.
During telomeric DNA replication in the S/G2 and G1 phases of the cell cycle, the 3' lagging strand leaves a short overhang called a G-tail. [4] [3] Telomeric DNA ends at the 3' G tail end because the 3' lagging strand extends without its complementary 5' C leading strand. The G tail provide a major function to telomeric DNA such that the G ...
Homology-directed repair (HDR) is a mechanism in cells to repair double-strand DNA lesions. [1] The most common form of HDR is homologous recombination . The HDR mechanism can only be used by the cell when there is a homologous piece of DNA present in the nucleus , mostly in G2 and S phase of the cell cycle .
Double-stranded breaks (DSBs) in regions of DNA related to neuronal activity are produced by a variety of mechanisms within and around the genome. The enzyme topoisomerase II , or TOPIIβ plays a key role in DSB formation by aiding in the demethylation or loosening of histones wrapped around the double helix to promote transcription . [ 85 ]