Various Levels of DNA Repair Synthesis in Xeroderma Pigmentosum Cells exposed to the Carcinogens N-Hydroxy and N-Acetoxy-2-acetyl-aminofluorene

1972 ◽  
Vol 238 (79) ◽  
pp. 9-10 ◽  
Author(s):  
H. F. STICH ◽  
R. H. C. SAN ◽  
J. A. MILLER ◽  
E. C. MILLER
Author(s):  
W.J. Kleijer ◽  
E.A. De Weerd-Kastelein ◽  
M.L. Sluyter ◽  
W. Keijzer ◽  
J. De Wit ◽  
...  

1985 ◽  
Vol 76 (1) ◽  
pp. 115-133
Author(s):  
R.T. Johnson ◽  
S. Squires ◽  
G.C. Elliott ◽  
G.L. Koch ◽  
A.J. Rainbow

Fusion between HeLa and fibroblasts from complementation group D xeroderma pigmentosum (XPD) followed by challenge with small doses of ultraviolet light (u.v.) results in the production of hybrid cells expressing either HeLa (HD1) or XPD-like (HD2) sensitivity to u.v. and related repair capacity. Assays used included unscheduled DNA synthesis (UDS), DNA break accumulation in the presence of inhibitors of DNA repair synthesis and host cell reactivation of irradiated adenovirus. Complementation assay in heterokaryons reveals limited ability of HD2 to restore UDS in XPD nuclei. We believe this complementation is more apparent than real since proliferating hybrids of HD2 and XPD parentage are without exception u.v.-sensitive and express limited excision repair. On the other hand hybrids between HD2 and XPC, XPE or XPF fibroblasts show true complementation resulting in a return to normal u.v. sensitivity and elevated repair ability.


1990 ◽  
Vol 18 (1) ◽  
pp. 35-40 ◽  
Author(s):  
Johan Hansson ◽  
Lawrence Grossman ◽  
Tomas Lindahl ◽  
Richard D. Wood

1989 ◽  
Vol 264 (36) ◽  
pp. 21788-21792
Author(s):  
J Hansson ◽  
M Munn ◽  
W D Rupp ◽  
R Kahn ◽  
R D Wood

1989 ◽  
Vol 264 (19) ◽  
pp. 11026-11034
Author(s):  
B Ramanathan ◽  
M J Smerdon

1983 ◽  
Vol 18 (1) ◽  
pp. 21-27 ◽  
Author(s):  
V. Bianchi ◽  
A. Zantedeschi ◽  
F. Ronchese ◽  
A.G. Levis

1984 ◽  
Vol 153 (2) ◽  
pp. 499-505 ◽  
Author(s):  
P. Orlando ◽  
P. Grippo ◽  
R. Geremia

1976 ◽  
Vol 20 (1) ◽  
pp. 207-213
Author(s):  
F. Giannelli ◽  
S.A. Pawsey

Patients with Xeroderma pigmentosum and defective DNA excision repair can be distinguished as a rapid (r-XP) and slow (s-XP) complementing variety. When fused with normal cells, fibroblasts from the r-XP are complemented rapidly and in the absence of protein synthesis while those from the s-XP are complemented slowly by a process partly, but not entirely, dependent on protein synthesis. Heterokaryons with different ratios of r-XP to s-XP nuclei (i.e. 1:1-5 and 1-5:1) and control heterokaryons containing one normal and 1-5 r- or s-XP nuclei show that if cell fusion and incubation is conducted in medium preventing protein synthesis, the rXP cells do not complement the s-XP partner at all and, conversely, that the latter is not as effective as normal cells at complementing the rXP partner. On the contrary, if protein synthesis is permitted, the 2 types of XP cells complement each other in a gene dose-dependent manner and to an extent similar to that observed in the control heterokaryons. These findings indicate that the r- and s-XP varieties are caused by mutations at different loci and suggest that the products of these loci interact to produce a functional unit which is present in normal control cells but absent in the XP strains. The relationship between the complementation groups described here and those already reported in the literature being investigated.


Sign in / Sign up

Export Citation Format

Share Document