By G. Obe (Editor), A. T. Natarajan (Editor)
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Extra resources for Chromosome Aberrations (Reprint of Cytogenetic and Genome Research 2004)
Inappropriate repair is a hallmark of clastogenicity, mutagenesis and carcinogenicity, but living cells have an alternative pathway, here referred to as death pathway, to escape from the effects of genotoxic insult. The death pathway seems to have considerable weight in tolerating ICL damage. The life-or-death decision with its signaling mechanism may vary among types of damage and cell types, and should constitute a significant determinant of the chromosomal manifestation of the response to DNA damage, in particular to ICLs.
Excluding this rapid component from consideration, the repair rates observed in DNA from the three chromosomal compartments are in the relation Alu-probed 1 Fig. 2. A CPD repair panel from 20 J/m2 UVC-irradiated human fibroblasts. 7 % agarose and stained with ethidium bromide. Southern blots from this gel were sequentially probed with 32[P]-Alu, 32[P]-L1, and 32[P]-Satellite DNA. The M of full length Ï phage DNA and HindIII-digested Ï phage DNA are shown at the left. The mobility of r 800-kb DNA was estimated as the mobility of uncut DNA when the signal on the well-proximal side of the peak of undigested DNA was 30 % of maximum.
1 for all sizes and plots the log of b on the X axis and Wx, along the Y axis, then a sigmoidal curve is obtained with Y values that vary from 0 to 1. Such a plot describes the cumulative weight fraction of DNA less than size “b” bases. This equation was used along with gel electrophoresis by Hamer and Thomas (1975) and by Peterson (2000) to show that restriction endonucleases cleave genomic DNA in a random fashion. With modern computers, one can create small polymer-length intervals and determine the weight fraction expected in each small interval.
Chromosome Aberrations (Reprint of Cytogenetic and Genome Research 2004) by G. Obe (Editor), A. T. Natarajan (Editor)