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Griffiths AJF, Miller JH, Suzuki DT, et al. An Introduction to Genetic Analysis. 7th edition. New York: W. H. Freeman; 2000.

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The physical nature of the gene fascinated scientists for many years. A series ofexperiments beginning in the 1920s finally revealed that DNA was the geneticmaterial.

Discovery of transformation

A puzzling observation was made by Frederick Griffith in the course ofexperiments on the bacterium Streptococcus pneumoniae in 1928.This bacterium, which causes pneumonia in humans, is normally lethal in mice.However, different strains of this bacterial species have evolved that differ invirulence (in the ability to cause disease or death). In his experiments,Griffith used two strains that are distinguishable by the appearance of theircolonies when grown in laboratory cultures. In one strain, a normal virulenttype, the cells are enclosed in a polysaccharide capsule, giving colonies asmooth appearance; hence, this strain is labeled S. InGriffith’s other strain, a mutant nonvirulent type that grows in mice but is notlethal, the polysaccharide coat is absent, giving colonies a rough appearance;this strain is called R.

Griffith killed some virulent cells by boiling them and injected the heat-killedcells into mice. The mice survived, showing that the carcasses of the cells donot cause death. However, mice injected with a mixture of heat-killed virulentcells and live nonvirulent cells did die. Furthermore, live cells could berecovered from the dead mice; these cells gave smooth colonies and were virulenton subsequent injection. Somehow, the cell debris of the boiled S cells hadconverted the live R cells into live S cells. The process is called transformation. Griffith’s experimentis summarized in Figure 8-1.


Figure 8-1

The first demonstration of bacterial transformation. (a) Mouse diesafter injection with the virulent S strain. (b) Mouse survives afterinjection with the R strain. (c) Mouse survives after injection withheat-killed S strain. (d) Mouse dies after injection (more...)

This same basic technique was then used to determine the nature of thetransforming principle—the agent in the cell debris that isspecifically responsible for transformation. In 1944, Oswald Avery, C. M.MacLeod, and M. McCarty separated the classes of molecules found in the debrisof the dead S cells and tested them for transforming ability, one at a time.These tests showed that the polysaccharides themselves do not transform therough cells. Therefore, the polysaccharide coat, although undoubtedly concernedwith the pathogenic reaction, is only the phenotypic expression of virulence. Inscreening the different groups, Avery and his colleagues found that only oneclass of molecules, DNA, induced the transformation of R cells (Figure 8-2). They deduced that DNA is theagent that determines the polysaccharide character and hence the pathogeniccharacter (see pages 219–220 for a description of the mechanism oftransformation). Furthermore, it seemed that providing R cells with S DNA wastantamount to providing these cells with S genes.


Figure 8-2

Demonstration that DNA is the transforming agent. DNA is the only agentthat produces smooth (S) colonies when added to live rough (R)cells.


The demonstration that DNA is the transforming principle was the firstdemonstration that genes are composed of DNA.

Hershey-Chase experiment

The experiments conducted by Avery and his colleagues were definitive, but manyscientists were very reluctant to accept DNA (rather than proteins) as thegenetic material. The clincher was provided in 1952 by Alfred Hershey and MarthaChase with the use of the phage (virus) T2. They reasoned that phage infectionmust entail the introduction (injection) into the bacterium of the specificinformation that dictates viral reproduction. The phage is relatively simple inmolecular constitution. Most of its structure is protein, with DNA containedinside the protein sheath of its “head.”

Phosphorus is not found in proteins but is an integral part of DNA; conversely,sulfur is present in proteins but never in DNA. Hershey and Chase incorporatedthe radioisotope of phosphorus (32P) into phage DNA and that ofsulfur (35S) into the proteins of a separate phage culture. They thenused each phage culture independently to infect E. coli withmany virus particles per cell. After sufficient time for injection to takeplace, they sheared the empty phage carcasses (called ghosts)off the bacterial cells by agitation in a kitchen blender. They usedcentrifugation to separate the bacterial cells from the phage ghosts and thenmeasured the radioactivity in the two fractions. When the 32P-labeledphages were used, most of the radioactivity ended up inside the bacterial cells,indicating that the phage DNA entered the cells. 32P can also berecovered from phage progeny. When the 35S-labeled phages were used,most of the radioactive material ended up in the phage ghosts, indicating thatthe phage protein never entered the bacterial cell (Figure 8-3). The conclusion is inescapable: DNA is thehereditary material; the phage proteins are mere structural packaging that isdiscarded after delivering the viral DNA to the bacterial cell.

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Figure 8-3

The Hershey-Chase experiment, which demonstrated that the geneticmaterial of phage is DNA, not protein. The experiment uses two setsof T2 bacteriophages. In one set, the protein coat is labeled withradioactive sulfur (35S), not found in DNA. In the (more...)

Why such reluctance to accept this conclusion? DNA was thought to be a rathersimple chemical. How could all the information about an organism’s features bestored in such a simple molecule? How could such information be passed on fromone generation to the next? Clearly, the genetic material must have both theability to encode specific information and the capacity to duplicate thatinformation precisely. What kind of structure could allow such complex functionsin so simple a molecule?

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