Ultraviolet light

About: Ultraviolet light is a research topic. Over the lifetime, 49494 publications have been published within this topic receiving 843151 citations.

Induction of specific mutations with 5-bromouracil.

Abstract: The hereditary characteristics of an organism occasionally undergo abrupt changes (mutations), and genetic techniques have traced these to alterations at definite locations in the genetic structure. Recently, the fineness of this genetic mapping has been extended to the level where the finite molecular units (nucleotides) of the hereditary material limit further subdivision. At this level, local details of the hereditary material should exert their influence; the frequency of mutation at a particular point should depend upon the local molecular configuration. It is therefore feasible to try to correlate genetic observations with precise molecular models, such as the one proposed by Watson and Crick [1] for the structure of DNA. In a fine-structure study of spontaneous mutations in phage T4, the mutability at different points in the genetic structure was, in fact, found to be strikingly varied [2]. To relate mutability to actual chemical structure, it would seem promising to employ mutagenic agents of specific types, to act selectively on particular configurations. Since the initial discovery by Muller [3] and Stadler [4] on induct on of mutations with X-rays and the discovery of chemical mutagenesis by Auerbach and Robson [5] and by Oehlkers [6], many physical agents and chemical substances have been found to be mutagenic in many organisms. Some mutagens act selectively; in particular the induced reversion from biochemically dependent to independent strains has been shown to depend upon the mutant and the mutagen used. (For chemical mutagens in bacteria see Demerec [7].) A recent comprehensive review of this subject has been published by Westergaard [8]. Mutagens in some cases produce gross chromosomal aberrations; in others the alterations are so small as to be beyond the limited resolving power of genetic techniques for the organism used. The absence of this limitation makes phage a suitable organism for our purposes. There have been reports of induction of mutations in phage by ultraviolet light [9,10] nitrogen mustard [11], streptomycin [12], and proflavine [13]. A very provocative discovery is that analogues of the normal bases may be built into DNA in place of the usual ones and also raise the mutation rate. In particular, one such analogue, 5-bromouracil, has been proven by Dunn and Smith [14] to be incorporated into the DNA of phage (in place of thymine), and Litman and Pardee [15] have shown that it greatly increases the frequency with which phage mutants of various types arise. In the present work, this possibility of directly affecting the DNA structure is combined with a genetic analysis of high resolving power, to make a fine-structure study of mutagenesis. Our attention will be restricted to the rII region of the genome of phage T4. The mutational alterations arising by 5-bromouracil induction are compared to, and shown to differ from, those which occur spontaneously.

Disseminated Superficial Actinic Porokeratosis (DSAP)

Abstract: This study of 31 patients presents disseminated superficial actinic porokeratosis (DSAP) as a distinctive and recognizable entity characterized by many uniformly small, minimal, annular, anhidrotic, keratotic lesions developing during the third or fourth decade of life on sun-exposed areas of skin. It is not a rare condition. While many clinical features of DSAP differ from the classic type of porokeratosis (Mibelli), the histologic features are essentially the same including the typical cornoid lamella, but the features are often minimal. Of six attempts to autotransplant portions of lesions, three were successful. Exacerbation following natural or experimental ultraviolet light radiation, distribution of lesions limited to sun-exposed areas of skin, and frequent clinical and histologic similarities to true actinic keratoses indicate that actinic radiation plays an important role in the pathogenesis of DSAP.

The expression of genetic information: a study with hybrid animal cells.

Abstract: When the nucleus of a hen erythrocyte is introduced into the cytoplasm of a human or mouse cell in culture, it resumes the synthesis of RNA. The reactivated erythrocyte nucleus undergoes great enlargement, but it does not, for at least 2 or 3 days, develop nucleoli which can be discerned under the light microscope. During this period, the heterokaryon, although it may contain several active erythrocyte nuclei, does not synthesize any hen-specific surface antigens; and the hen-specific antigens introduced into the surface of the heterokaryon by the process of cell fusion are eliminated. But when, later, the erythrocyte nuclei do develop nucleoli, hen-specific antigens reappear on the surface of the heterokaryon and progressively accumulate. Before developing nucleoli, the erythrocyte nuclei synthesize little, if any, normal 28 S or 16 S RNA; but they do synthesize large amounts of the RNA which shows polydisperse sedimentation in conventional sucrose density gradients. Autoradiographic studies involving the use of a microbeam of ultraviolet light show, however, that this ‘polydisperse’ RNA is not transferred to the cytoplasm of the cell in detectable amounts so long as the erythrocyte nucleus lacks a definitive nucleolus. The inability of the erythrocyte nucleus at this stage to determine the synthesis of hen-specific surface antigens is thus attributable to the fact that it fails to transfer the RNA made on its chromosomes to the cytoplasm of the cell. When the erythrocyte nuclei develop nucleoli, however, the RNA which they make is transferred to the cytoplasm of the cell, and the synthesis of hen-specific surface antigens then begins. These experiments suggest that the nucleolus may play a decisive role in the transfer of information from nucleus to cytoplasm. The possible nature of this role is discussed.