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A pair of ZFNs, each with three zinc fingers binding to target DNA, are shown introducing a double-strand break, at the FokI domain, depicted in yellow. Subsequently, the double strand break is shown as being repaired through either homology-directed repair or non-homologous end joining. [3]
Zinc fingers were first identified in a study of transcription in the African clawed frog, Xenopus laevis in the laboratory of Aaron Klug.A study of the transcription of a particular RNA sequence revealed that the binding strength of a small transcription factor (transcription factor IIIA; TFIIIA) was due to the presence of zinc-coordinating finger-like structures. [6]
In addition to histidine, a conserved arginine on the second beta strand of the zinc fingers makes contact with the phosphodiester oxygen on the DNA strand. [25] [26] [29] Also serine 75 on the third finger hydrogen bonds to the phosphate between base pairs 7 and 8, as the only backbone contact with the secondary strand of DNA. [25] [26] [29]
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 ]
MUS81/EME1 is a structure specific endonuclease involved in converting interstrand crosslinks to double-strand breaks in a DNA replication-dependent manner. [12] After introduction of a double-strand break, further steps are required to complete the repair process. If a crosslink is not properly repaired it can block DNA replication. [citation ...
Off-target genome editing refers to nonspecific and unintended genetic modifications that can arise through the use of engineered nuclease technologies such as: clustered, regularly interspaced, short palindromic repeats ()-Cas9, transcription activator-like effector nucleases (), meganucleases, and zinc finger nucleases (ZFN). [1]
Based on the findings that (1) several polypeptides in the NHEJ pathway are "potential targets of autoantibodies" and (2) "one of the autoimmune epitopes in XRCC4 coincides with a sequence that is a nexus for radiation-induced regulatory events", it has been suggested that exposure to DNA double-strand break-introducing agents "may be one of ...
Wee1 activity is high in early prophase I and the accumulation of Cdc25 activates M-Cdk by direct phosphorylation and marking Wee1 to be degraded. Meiotic recombination may begin with a double-strand break, either induced by Spo11 [2] or by other endogenous or exogenous causes of DNA damage. These DNA breaks must be repaired before metaphase I ...