The Direct Effect of X-Irradiation on HeLa S3 Deoxyribonucleic Acid Synthesis

1962 ◽  
Vol 16 (6) ◽  
pp. 846 ◽  
Author(s):  
Robert B. Painter
1959 ◽  
Vol 150 (941) ◽  
pp. 486-496 ◽  

An examination of the properties of T 2 coliphage, after treatment with the nitrogen mustard di(2-chloroethyl)methylamine, revealed a remarkable similarity to those of T 2 after X-irradiation. In particular, the phage remained capable of adsorption to the host cells and of combining with specific antibody, whilst showing a progressive loss of ability to kill the host cells with increasing dose. Further, a small degree of multiplicity and cross-reactivation was manifested, commensurate with that shown by phage X-irradiated in vitro . It is considered that these facts are consistent with the view that loss of plaque-forming ability is largely due to a failure of injection of the deoxyribonucleic acid moiety of the virus into the host cells following adsorption, an explanation already put forward by other workers in respect of X-rayed phage. This failure could arise by internal cross-linking of the DNA by the chloroethylamine, or of the DNA with the protein membrane. The experimental evidence supports the former proposal. The term 'radiomimetic' used in respect of di(2-chloroethyl)methylamine in the general title of this series is thus justifiable so far as phage inactivation is concerned.


1959 ◽  
Vol 151 (942) ◽  
pp. 148-155 ◽  

The sensitivity of phage T 7 to epoxides and freshly prepared solutions of di(2-chloroethyl) methylamine ( HN 2) was identical with that of T 2. T 7, however, proved considerably the more sensitive to ethylenimine and to aged solutions of HN 2. It was considered that this was due to the cationic nature of these latter agents affecting the rate of penetration into the phage heads, and that the susceptibility of T 2 and resistance of T 7 to osmotic shock was a parallel phenomenon. Confirmation was afforded by the fact that a strain of T 4 sensitive to osmotic shock behaved like T 2, and a resistant strain of T 4 like T 7. These results, together with others previously reported, are believed to offer very strong evidence that inactivation of bacteriophage by alkylating agents derives from reaction with the deoxyribonucleic acid moiety, probably leading to a failure of the injection process.


1981 ◽  
Vol 1 (11) ◽  
pp. 1038-1047
Author(s):  
S Kawasaki ◽  
L Diamond ◽  
R Baserga

Sodium butyrate (3 mM) inhibited the entry into the S phase of quiescent 3T3 cells stimulated by serum, but had no effect on the accumulation of cellular ribonucleic acid. Simian virus 40 infection or manual microinjection of cloned fragments from the simian virus 40 A gene caused quiescent 3T3 cells to enter the S phase even in the presence of butyrate. NGI cells, a line of 3T3 cells transformed by simian virus 40, grew vigorously in 3 mM butyrate. Homokaryons were formed between G1 and S-phase 3T3 cells, Butyrate inhibited the induction of deoxyribonucleic acid synthesis that usually occurs in B1 nuclei when G1 cells are fused with S-phase cells. However, when G1 3T3 cells were fused with exponentially growing NGI cells, the 3T3 nuclei were induced to enter deoxyribonucleic acid synthesis. In tsAF8 cells, a ribonucleic acid polymerase II mutant that stops in the G1 phase of the cell cycle, no temporal sequence was demonstrated between the butyrate block and the temperature-sensitive block. These results confirm previous reports that certain virally coded proteins can induce cell deoxyribonucleic acid synthesis in the absence of cellular functions that are required by serum-stimulated cells. Our interpretation of these data is that butyrate inhibited cell growth by inhibiting the expression of genes required for the G0 leads to G1 leads to S transition and that the product of the simian virus 40 A gene overrode this inhibition by providing all of the necessary functions for the entry into the S phase.


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