Transduction of linked genetic characters of the host by bacteriophage P1

The accumulating geochronologic evidence indicates more and more convincingly that tektites were formed from terrestrial rocks in large meteoritic impacts on the earth. Ivory Coast tektites were formed about 1.3 million years ago, simultaneously with the Bosumtwi crater, and from rocks 2000 million years old. The rocks around the crater are of the same age. Moldavites were formed 14.8 million years ago, simultaneously with the Ries crater, and from rocks now roughly 300 million years old. Crystalline rocks throughout Germany north of the Alps are about 300 million years old. North American tektites were formed 35 million years ago, but no crater is known to be associated with them. Their age, as determined by the strontium isochron method, would be compatible with an origin from Appalachian granites, volcanic rock, or sediments derived from them. Not much can be said about a parent rock for the Australasian tektites, except that it would be roughly 200 to 400 million years old. The principle of simplicity suggests that one might more profitably look for large concealed craters in that vast region than postulate an extraterrestrial origin for the tektites.

https://science.sciencemag.org/content/sci/152/3727/1345.full.pdf

Radiation-induced mutations and their repair.

[This corrects the article on p. 493 in vol. 32.].

https://mmbr.asm.org/content/mmbr/32/4_Pt_2/493.full.pdf

Antibiotic inhibitors of the bacterial ribosome.

Mechanism of Streptomycin Action on Bacteria: A Unitary Hypothesis

Several theories put forward to explain the biological mechanisms underlying the aging process are examined. The only ones which attack the problem from the point of view of basic biological mechanisms are the wear-and- tear theory and the somatic mutation theory. The finding that radiation accelerates the aging process is a potent tool for attacking the problem experimentally. Experiments with mice specifically designed to verify the wear- and-tear theory showed conclusively that stress per se does not contribute to aging, and no experimental evidence could be found to support the theory. On the other hand, a great deal of evidence now available indicates that mutations in somatic cells play a dominant role in aging. It is further shown that the organs having cells which frequently undergo cell division take part in the aging process very little, if at all. Organs having cells which seldom, if ever, divide have no opportunity to throw off either spontaneous or induced mutations, and it is these organs which are responsible for the aging of the animal. Spontaneous mutations build up at a rapid rate in these organs. A cell may continue to function normally long after it has suffered a deleterious mutation, and thismore » accounts for much of the delay in the expression of radiation damage. It is suggested that the mutation rates for somatic celis are very much higher than the rates for gametic cells, and that this circumstance insures the death of the individual and the survival of the species. (auth)« less

https://science.sciencemag.org/content/sci/141/3582/686.full.pdf

Biological mechanisms underlying the aging process.

Bacteria give promise of yielding quantitative information on the process of gene mutation, which could not be obtained from the clasical genetic materials (Luria, 1947). However, detailed studies have so far been confined almost entirely to a particular group of mutations, namely, those producing phage resistance (Demerec, 1946; Witkin, 1947b; Bryson, 1948; Beale, 1948; Newcombe, 1948; Newcombe and Scott, 1949). For this reason, the present investigation has been directed toward obtaining accurate data for a different kind of mutational change, na.nely, the development of drug resistance. The genetic origin of resistance to three of the most common ahtibacterial drugs has already been studied. These are penicillin (Demerec, 1945, using Staphylococcus aureus), sodium sulfathiazole (Oakberg and Luria, 1947, using S. aureus), and streptomycin (Klein andKimmelman, 1946; Alexander and Leidy, 1947; Demerec, 1947; Scott, 1949; using, respectively, Shigella spp., Hemophilus influenzae, S. aureus, and Escherichia coli). Of these, streptomycin was chosen since it appeared to be the only one to which a high degree of resistance could be developed in a single mutational step.

Spontaneous mutation to streptomycin resistance and dependence in escherichia coli.

The inheritance of streptomycin resistance and dependence in crosses of Escherichia coli.

When living cells are irradiated with ultraviolet, some of the individuals are killed and some are caused to mutate. Further, the ultraviolet wave lengths that are most active in producing the two effects are essentially the same and are those that are most readily absorbed by the nucleic acids. This implies a relationship between the induced killing and mutation, but the nature of the relationship is not known. Recently it has been found that both the lethal and the mutagenic effects of irradiation with 2,537 A ultraviolet (which is strongly absorbed by the nucleic acids) can be partially reversed by posttreatment with visible light and with near ultraviolet. The reversal of the lethal effect, which is termed \"photoreactivation,\" was demonstrated in Streptomyce8 griseus by Kelner (1949a) and was later shown to occur in a wide range of organisms including the bacterial viruses, bacteria, yeasts, molds, and protozoa (Kelner, 1949b; Novick and Szilard, 1949; Dulbecco, 1950; Goodgal, 1950; Kimball and Gaither, 1950). A corresponding reversal of the mutagenic effect has now been reported in bacteria (Novick and Szilard, 1949; Newcombe, 1950; see also Kelner, 1949b, 1950), in molds (Goodgal, 1950; Roegner, unpublished), and in Paramecium (Kimball and Gaither, 1950; Kimball, 1950). The present report deals with the probable nature of the relationship between the lethal and the mutagenic effects.

Photoreversal of ultraviolet-induced mutagenic and lethal effects in Escherichia coli.

Major malformations of the embryos of trout are substantially more frequent following exposure of the sperm or eggs to ionizing radiation. The response per unit dose falls off at high doses but at 200 rads, the lowest dose used, there is a yield of approx. 300 malformations per 10 6 embryos per rad, for irradiations of either kind of gamete. Assuming that the response varies linearly with dose at still lower levels, approx. 26 rads would be required to double the rate observed in the controls. Reasons for believing that the major malformations may be associated predominantly with gross chromosomal changes, such as those due to non-disjunction, are discussed. The advantages of this organism for studies of the dose-response relationships down to low doses, the current lack of such informations, and its possible bearing on both a theoretical problem and the practical task of assessing radiation risks in man, are noted.

Howard B. Newcombe

Papers

Spontaneous mutation to streptomycin resistance and dependence in escherichia coli.

The inheritance of streptomycin resistance and dependence in crosses of Escherichia coli.

Photoreversal of ultraviolet-induced mutagenic and lethal effects in Escherichia coli.

Major congenital malformations from irradiations of sperm and eggs

A comparison of spontaneous and induced mutations of Escherichia coli to streptomycin resistance and dependence.