Barbara McClintock (1902–1992) was a remarkable scientist who made several very important discoveries in genetics dealing with chromosome structures. Her studies were carried out before the age of large interdisciplinary research teams and before the sophisticated tools of molecular genetics were available. Her tools consisted of a clear mind which could make sense of confusing and revolutionary observations, and a consuming curiosity that led her to work 12-hour days, six days a week in a small laboratory at Cold Spring Harbor on Long Island, New York.

In 1983, at age 81, McClintock received the Nobel Prize in Medicine or Physiology largely for her discovery of transposable elements, or transposons, popularly called "jumping genes" which she had made 40 years earlier. Her experimental system consisted of ears of corn. She observed various colored kernels which were produced by different enzymes (see figure 8.5). If the gene coding for an enzyme responsible for color formation was inactivated, the kernel was not pigmented. If the enzyme was only partially inactivated, then the kernel was partially pigmented. Thus by looking at kernel colors, McClintock was able to observe changes in genes by their effect on pigment production. She concluded that fragments of DNA must be capable of moving from one site on the chromosome to another, because the colors of the kernels changed. A transposable element moving into a gene would inactivate it. When the element left a gene and the gene was restored, it would function properly.

At the time she published her results, most scientists believed that chromosomes were very stable and unchanging. Consequently, most geneticists were very skeptical of McClintock’s heretical ideas. As a result, she stopped publishing many of her observations. It was not until the late 1970s that her ideas were accepted. By that time, transposable elements had been discovered in many organisms, including bacteria. Although transposons were first discovered in plants, once they were discovered in bacteria, the field moved ahead very quickly. The techniques of molecular biology, biochemistry and genetics made it possible to isolate, characterize and understand the movement of these remarkable pieces of DNA.

At the end of World War II, bacterial dysentery (caused by members of the genus Shigella) was a common disease in Japan. With the introduction of the sulfa drugs, the number of cases of dysentery decreased, as this antibacterial medicine proved highly successful. However, after 1949, the incidence of dysentery began to rise again, and many of the Shigella strains causing dysentery were resistant to sulfa. Fortunately, these organisms remained susceptible to such antibiotics as streptomycin, chloramphenicol, and tetracycline. However, a new problem arose. In 1955, a Japanese woman returning from Hong Kong developed Shigella dysentery that did not respond to any antibiotic treatment.

In the next several years, a number of dysentery epidemics developed in Japan. In some patients, the causative organisms were sensitive to antibiotics; in others, they were resistant. Curiously, bacteria isolated from certain patients who had been treated with a single antibiotic abruptly became resistant not only to that antibiotic but also to other antibiotics to which the patients had not been exposed. In addition, cells of Escherichia coli residing in the large intestine of many of the patients who carried antibiotic-resistant organisms were also resistant to the same antibiotics. How can these observations be explained? A reasonable conclusion is that the genes responsible for antibiotic resistance spread from one bacterium to another. The phenomenon of genes being able to jump from one site on DNA to anotyher discovered by McClintock play an important role in the movement of anitbiotic resistance genes between bacteria.

Antibiotics have reduced the incidence of many microbial infections. However, the development and spread of resistant strains of bacteria have created unique problems for the treatment of infectious diseases. Understanding the mechanisms by which organisms become resistant to antibiotics and how this resistance is transferred to sensitive cells may enable the medical community to keep one step ahead of disease-causing bacteria and maintain the usefulness of antibiotics.

Bacterial genetics encompasses the study of heredity; how genes function, how they can change and how they are transferred to other cells in the population. The functioning of genes was discussed in Chapter 7. In this chapter we will focus on how the chemical structure of DNA can change or mutate, thereby conferring new properties on the cell. These changes allow bacteria to adapt to changing environmental conditions. We will also discuss how genes are transferred from one bacterium to another, thereby changing the properties of cells into which the genes are transferred.