Concept 27 Mutations are changes in genetic information.

factoid Did you know ?

Hermann Muller's laboratory at Indiana University was underneath the soundproof labs of another Indiana professor — the sexologist Alfred Kinsey.

Hmmm...

As bacteria evolved on Earth, damaging ultraviolet light from the Sun passed unfiltered through the atmosphere. How could life evolve in the presence of such a powerful mutagen?

Hi, I'm Hermann Muller. When I worked with Thomas Hunt Morgan in the early 1900s, we occasionally found mutant flies – including the famous white-eyed fly. We knew the mutants must be due to spontaneous mutations in genes. Although mutations are essential to understanding normal gene function, they are extremely rare events. I searched the literature and found hints that X-rays damage the chromosomes. I figured X-rays must cause mutations and might be used to quickly induce new mutations in fruit flies. In the 1920s, I set up an experiment to look for lethal mutations induced by X-rays. I used a special strain of female flies that carried a lethal recessive mutation – called – on one X chromosome. The females live because their other X chromosome has a normal copy of the gene. In the first cross, I mated these females with males whose sperm had been bombarded with X-rays. I designed the experiment to detect a mutation ( ) induced by X-rays in the X chromosome, but mutations can occur anywhere. The male progeny that inherit the gene die because they don't have another X chromosome to carry a normal copy of the gene. In the second cross, I mated daughters containing the gene with wild-type males. Like the previous cross, males with the gene died. Males that inherited the X-rayed chromosome also died if was a lethal mutation. When I found no males in the second cross, I showed that X-rays could induce mutations. Using different levels of X-ray exposure, we could make mutants that didn't die, but we still didn't know what a mutation was, or even what a gene looked like. Using different levels of X-ray exposure we could make mutants that didn't die, but we still didn't know what a mutation was, or even what a gene looked like. Hi, I'm Seymour Benzer. Until the 1950s, most people thought genes resembled beads in a string. That is, genes were indivisible, and crossing over could only occur between the genes. After Watson and Crick published their DNA model, I realized that if a gene were a sequence of bases it could be divisible at many different locations. And crossing over could occur within a gene. This is shown on the right where the chromosomes crossed over within the 'E' gene. In bead theory, shown on the left, the chromosomes crossed over between the 'E' and 'F' genes. I demonstrated the gene's divisibility by crossing different virus mutants. Each mutant came from a different viral culture, but all had a defective rII gene. I demonstrated the gene's divisibility by crossing different virus mutants. Each mutant came from a different viral culture, but all had a defective rII gene. After both mutants inject their DNA into a bacteria cell, some DNA from mutant #104 crosses over with DNA from mutant #51, and the bacterium replicates the viral DNA. In the gene-as-a-bead theory, all of the recombinant DNA would get a defective rII gene. But I found recombinant DNA that did not have a mutated rII gene. This happened because the DNA crossed over in the middle of the rII gene. In this example,crossing over occurred between the two adenines in the rII gene. The recombinant that didn't receive the mutations from its "parents" ended up with a wildtype rII sequence. I made a map of the locations of these mutations in the rII gene by counting the number of wild-type offspring produced in many different crosses – the same method Alfred Sturtevant used to map the location of different genes. I made a map of the locations of these mutations in the rII gene by counting the number of wildtype offspring produced in many different crosses – the same method Alfred Sturtevant used to map the location of different genes. With this map of mutations in the rII gene, I tried to discover the minimum number of altered nucleotides that is required to make one mutation. My map, combined with other work, showed that only one nucleotide change is needed to make a mutation. These single changes are called point mutations. For example, virus mutant #104 has a point mutation where adenine replaces cytosine. Point mutations cause only one amino acid change in the protein made from the gene. Other base changes cause frameshift mutations. Insertions or deletions of one or more bases alter the reading frame in the DNA sequence and cause changes in many amino acids.