TY - JOUR
T1 - DNA TURNOVER IN BUFFER‐HELD ESCHERICHIA COLI AND ITS EFFECT ON REPAIR OF UV DAMAGE
AU - Tang, Moon‐Shong ‐S
AU - Wang, Tzu‐chien V.
AU - Patrick, Michael H.
PY - 1979/3
Y1 - 1979/3
N2 - Abstract— Continuous DNA degradation and resynthesis, without a net change in cellular DNA content, were observed in buffer‐held, non‐irradiated E. coli B/r. This constant DNA turnover probably involves most of the genome and reflects random sites of DNA repair due to the polA‐dependent excision‐resynthesis repair pathway. Under these non‐growth conditions, it appears that at any given time there is a minimum of one repair site per 6.5 × 106 daltons DNA, each of which is at least 160 nucleotides long. While the amount of DNA degradation is not influenced by prior exposure to UV radiation, the synthetic activity decreases with increasing UV fluence. We suggest that when sites of DNA turnover occur opposite to cyclobutyl dipyrimidines in UV‐irradiated cells, repair of the latter damage can be prevented. This implies that both beneficial and deleterious processes take place in irradiated buffer‐held cells, and that cell survival depends on the delicate balance between DNA turnover and repair of UV‐damage. Based on these findings, we propose a model to explain the limited repair observed during post‐irradiation liquid‐holding and to account for the large difference in cell survival between irradiation at low fluence rates (fluence‐rate dependent recovery) and at high fluence rates followed by liquid‐holding (liquid‐holding recovery).
AB - Abstract— Continuous DNA degradation and resynthesis, without a net change in cellular DNA content, were observed in buffer‐held, non‐irradiated E. coli B/r. This constant DNA turnover probably involves most of the genome and reflects random sites of DNA repair due to the polA‐dependent excision‐resynthesis repair pathway. Under these non‐growth conditions, it appears that at any given time there is a minimum of one repair site per 6.5 × 106 daltons DNA, each of which is at least 160 nucleotides long. While the amount of DNA degradation is not influenced by prior exposure to UV radiation, the synthetic activity decreases with increasing UV fluence. We suggest that when sites of DNA turnover occur opposite to cyclobutyl dipyrimidines in UV‐irradiated cells, repair of the latter damage can be prevented. This implies that both beneficial and deleterious processes take place in irradiated buffer‐held cells, and that cell survival depends on the delicate balance between DNA turnover and repair of UV‐damage. Based on these findings, we propose a model to explain the limited repair observed during post‐irradiation liquid‐holding and to account for the large difference in cell survival between irradiation at low fluence rates (fluence‐rate dependent recovery) and at high fluence rates followed by liquid‐holding (liquid‐holding recovery).
UR - http://www.scopus.com/inward/record.url?scp=0018449190&partnerID=8YFLogxK
U2 - 10.1111/j.1751-1097.1979.tb07083.x
DO - 10.1111/j.1751-1097.1979.tb07083.x
M3 - 文章
C2 - 375250
AN - SCOPUS:0018449190
SN - 0031-8655
VL - 29
SP - 511
EP - 520
JO - Photochemistry and Photobiology
JF - Photochemistry and Photobiology
IS - 3
ER -