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Biomedical subjects

H Bernstein

Publications and source records attributed to H Bernstein.

At least 91 records · Page 5Linked to original sources
PubMed1978

Recombinational repair of alkylation lesions in phage T4. I. N-methyl-N'-nitro-N-nitrosoguanidine.

Treatment of phage T4-host adsorption complexes by MNNG increased recombination between two rII markers by about three-fold. Temperature sensitive mutants defective in genes 32, 46 and 47, which cause reductions in recombination at semirestrictive temperature, proved to be substantially more sensitive to MNNG at such temperatures than wild-type phage. In addition, the recombination defective mutants xm(uvsX) and y10(y) were sensitive to MNNG than wild-type, whereas mutants defective in genes 45 and denV, which are apparently not involved in recombination, were not MNNG sensitive. These findings suggest that a recombination pathway involving the products of genes 32, 46, 47, uvsX and y is employed in repairing MNNG-induced lethal lesions. This mechanism is effective in cells infected by single phage, implying post-replication recombinational repair between daughter chromosomes. MNNG-induced lesions are subjects to multiplicity reactivation, but mutants defective in genes 46 to 47 showed the same degree of multiplicity reactivation as wild-type phage. The gene 32 and gene 47 recombination defective mutants were tested for their effects of MNNG-induced reversion of an rII marker. No reduction in induced reversion was found. Thus, it appears that the postulated recombinational repair pathway employing the products of genes 32 and 47 does not contribute substanitally to induced mutagenesis.

Alkylation↗
PubMed1978

Recombinational repair of alkylation lesions in phage T4. II. Ethyl methanesulfonate.

Treatment of bacteriophage T4 by ethyl methanesulfonate (EMS) caused more than a doubling in recombination between two rII markers. The functions of genes 47, 46, 32, 30, uvsX and y are known to be required for genetic recombination, and mutants defective in these genes were found to be more sensitive to inactivation by EMS than wild-type phage. This suggests that a recombinational pathway involving the products of these genes may be employed in repairing EMS induced lethal lesions. Genes 45 and denV are apparently not involved in recombination, and mutants defective in these genes were not EMS-sensitive. Gene 47, 46 and y mutants which were defective in the repair of EMS induced lethal lesions had no detectable deficiency in their ability to undergo EMS-induced mutation. This implies that recombinational repair of EMS lesions does not contribute substantially to EMS mutagenesis. The results obtained here with EMS are general similar to the results reported in the preceding paper with MNNG, suggesting that the lesions caused by both of these monofunctional alkylating agents may be eliminated by similar recombinational repair processes.

Alkylation↗
PubMed1977

Suppressors of gene 32 am mutants that specifically overproduce P32 (unwinding protein) in bacteriophage T4.

A gene 32 amber (am) mutant, amNG364, fails to grow on Escherichia coli Su3+ high temperatures, suggesting that the tyrosine residue inserted at the am codon by Su3+ leads to a temperature-sensitive gene 32 protein (P32). By plating amNG364 on E. coli Su3+ 45 degrees C, several pseudorevertants were found that proved to contain a suppressor (su) mutant in addition to the original am mutation. Crosses of two of these amNG364su strains to am+ phage indicated that the suppressors themselves are in or close to gene 32. Phage strains carrying either of the two su mutations, without amNG364, grew normally. When cells were infected by these su mutants and the proteins produced were examined by sodium dodecyl sulfate-gel electrophroesis, specific overproduction of P32 was found. Maximum overproduction compared to am+ phage was 6.6-fold for one su mutant and 2.4-fold for the other. Other proteins were produced in normal amounts and in normal time sequence. When amNG364su phage were allowed to infect E. coli S/6/5(Su-), the gene 32 am fragments produced were present at the same derepressed levels as in an infection by amNG364 without a suppressor. The suppressor mutations are interpreted as causing derepression of P32 by altering sites in this autogenously regulated protein involved in template recognition. Previously, specific derepression of gene 32 had only been shown using gene 32 conditional lethal mutants grown under restrictive conditions. We have shown that P32 can also be derepressed under permissive conditions, indicating that loss of P32 function is not necessary for specific derepression.

Coliphages↗
PubMed1977

Wide-field resolution in radiography.

Multiple star test objects were placed so as to record the entire field covered on a 35 X 43-cm (14 X 17-in.) film and radiographed to determine the apparent shape of the focal spot and the directions in which degradation is maximum and minimum. It was found that geometric unsharpness decreases along lines radiating outward from the center of the anode shadow. The small focal spots used in magnification may be anticipated to behave in a similar fashion. It was also shown experimentally that truly lateral resolution is approximately constant over the field. A theoretical explanation for this finding is offered.

Radiographic Image Enhancement↗
PubMed1976

Genes 46 and 47 of phage T4: possible compensation for loss of their function.

The gene 46 and 47 functions of phage T4 are required for normal DNA replication, recombination, u.v. repair and host DNA breakdown, and yet am mutants defective in these genes characteristically form tiny plaques on Escherichia coli strains lacking an am suppressor. Our results imply that this limited growth is not due to misreading of am codons or partial function of nearly complete poly-peptides terminated at the am mutation. Thus it appears that genes 46 and 47 are not entirely essential, perhaps because other phage or host products can partially compensate for their loss.

Chromosome Mapping↗
PubMed1976

Wide-field X-ray tube comparisons.

X-ray tubes having similar resolution capabilities along the central ray were compared for their wide-field characteristics. It has been suggested that focal spot size, and therefore resolution capability, along the cathode-anode axis may vary in a manner which is dependent upon the tube target angle. The authors show that differences beyond the effects of target angle occur, the extent of those differences varying from tube to tube. Although 2 different-sized focal spots may be adjusted to have equivalent central beam resolution capabilities, they can exhibit different imaging capabilities at wide-angle (off central axis) position. More than one parameter (equivalent focal spot size) is needed to characterize the behavior of a focal spot.

Mathematics↗
PubMed1974

Coiled rings of DNA released from cells infected with bacteriophages T7 or T4 or from uninfected Escherichia coli.

The replicating intracellular DNA of phage T7 was labeled at high specific activity with tritiated thymidine. The DNA of uninfected Escherichia coli was similarly labeled. Portions of cells which contained replicating phage T7 or E. coli DNA were lysed by a lysozyme, freeze-thaw, sodium lauryl sulfate procedure, and the DNA was spread on Millipore membranes for visualization by autoradiography. The DNA of phage T7 appeared to be highly concatenated reaching lengths of up to 721 mum. Much of the DNA of phage T7 and E. coli was retained in compact globular structures. In addition, orderly coiled rings of varying diameter up to about 43 mum were regularly observed. Similar coiled ring structures were also observed in autoradiographs of replicating phage T4 DNA which had been prepared in previous experiments. Worcel and Burgi (27) have presented evidence that E. coli chromosomes, when gently extracted from cells, are in a multilooped and superhelically twisted configuration. The coiled rings which we have observed may correspond to the relaxed, multilooped configurations which they find when the superhelical twists have been relieved by one or more nicks in each loop.

Autoradiography↗
PubMed1974

The DNA-delay mutants of bacteriophage T4.

Mutants of phage T4 defective in genes 39, 52, 58-61, and 60 (the DNA delay or DD genes) are characterized by a delay in phage DNA synthesis during infection of a nonpermissive Escherichia coli host. Amber (am) mutants defective in these genes yield burst sizes varying from 30 to 110 at 37 C in E. coli lacking an am suppressor. It was found that when DD am mutants are grown on a non-permissive host at 25 C, rather than at 37 C, phage yield is reduced on the average 61-fold. At 25 C incorporation of labeled thymidine into phage DNA is also reduced to 3 to 10% of wild-type levels. Mutants defective in the DD genes were found to promote increased recombination as well as increased base substitution and addition-deletion mutation. These observations indicate that the products of the DD genes are necessary for normal DNA synthesis. The multiplication of the DD am mutants on an Su(-) host at 37 C is about 50-fold inhibited if prior to infection the host cells were grown at 25 C. This suggests that a compensating host function allows multiplication of DD am mutants at 37 C in the Su(-) host, and that this function is active in cells grown at 37 C prior to infection, but is inactive when the prior growth is at 25 C. Further results are described which suggest that the products of genes 52, 60, and 39 as well as a host product interact with each other.

Coliphages↗