Brenner, "The genetics of Caenorhabditis elegans"

Date:
1974
Reference:
PP/CRI/I/3/9
Catalogue details

Licence: In copyright

Credit: Brenner, "The genetics of <i>Caenorhabditis elegans</i>". Source: Wellcome Collection.

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    WaUL )P-Qsu THE GENETICS OF CAENORHABDITIS ELEGANS S. BRENNER Medical Research Council Laboratory of Molecular Biology, Hills Road, Cambridge, CB2 2QH, England Manuscript received December 10, 1973 abstract Methods are described for the isolation, complementation and mapping of mutants of Caenorhabditis elegans, a small free-living nematode worm. About 300 EMS-induced mutants affecting behavior and morphology have been char acterized and about one hundred genes have been defined. Mutations in 77 of these alter the movement of the animal. Estimates of the induced mutation fre quency of both the visible mutants and X chromosome lethals suggests that, just as in Drosophila, the genetic units in C. elegans are large. T TOW genes might specify the complex structures found in higher organisms is a major unsolved problem in biology. Many of the molecular mechanisms involved in gene expression in prokaryotic microorganisms have already been found to exist in a relatively unmodified form in eukaryotic cells. The genetic code is universal and the mechanism of protein synthesis is much the same in both kinds of organisms. There are, by contrast, great differences in the organi zation of the genetic material. The chromosomes of higher organisms are com plex structures that contain histones and other proteins in addition to DNA and the genetic units are much larger than their counterparts in simple prokaryotes (Judd, Shen and Kaufman 1972). Although there are many theories suggest ing how the extra DNA might be used for complex genetic regulation ( Britten and Davidson 1969; Georgiev 1969; Crick 1971), the problem is still opaque. We know very little about the molecular mechanisms used to switch genes on and off in eukaryotes. We know nothing about the logic with which sets of genes might be connected to control the development of the assemblages of different cells that we find in multicellular organisms. These questions arise in a particularly acute form in elaborate structures like nervous systems. In one sense, all neurons resemble each other; they must be excitable, able to transmit electrical signals and produce and respond to chemical transmitters. They must be equipped with very similar, possibly commonly spe cified biochemical machinery. Yet, in another sense, they are all very different; cells are located at specific places and are connected to each other in definite ways. How is this complexity represented in the genetic program? Is it the outcome of a global dynamical system with a very large number of interactions? Or are there defined subprograms that different cells can get a hold of and execute for them selves? What controls the temporal sequences that we see in development? Genetics 77: 71-94 May 1974.