Genetic engineering

Genetic engineering has to do with experiments that change genes so that different traits are inherited. These experiments are also called recombinant DNA experiments. Scientists have discovered enzymes that can change the genetic code in a DNA molecule. Such enzymes can “clip out” a whole section of a DNA molecule. This clipped – out section can then be transplanted into the DNA molecule of another species. Even through genetic engineers work with an ordinary microscope, they can cause changes that are dramatic.

Scientists may also be able to introduce new traits into plants and animals.

Genetic engineering can be useful to people. For example, useful materials such as human growth hormones, insulin, and other materials. As more skill is developed, scientists may be able to transplant a healthy section into a defective gene.

Genetics Problems

1. The sex of fishes is determined by the same X-Y system as in humans. An allele of one locus on the Y chromosome of the fish Lebistes causes a pigmented spot to appear on the dorsal fin. A male fish that has a spotted dorsal fin is mated with a female fish that has an unspotted fin. Describe the phenotypes of the F1 and the F2 generations from this cross.

2. In Drosophila melanogaster, the recessive allele p, when homozygous, determines pink eyes. Pp or PP results in wildtype eye color. Another gene, on another chromosome, has a recessive allele, sw, that produces short wings when homozygous.

Consider a cross between females of genotype PPSwSw and males of genotype ppswsw. Describe the phenotypes and genotypes of the F1 generation and of the F2 generation produced by allowing the F1 progeny to mate with one another.

3. On the same chromosome of Drosophila melanogaster that carries the p (pink eyes) locus, there is another locus that affects the wings. Homozygous recessives, byby, have blistery wings, while the dominant allele By produces wild-type wings. The P and By loci are very close together on the chromosome; that is, the two loci are tightly linked. In answering these questions, assume that no crossing over occurs. a. For the cross PPByBy X ppbyby, give the phenotypes and genotypes of the F1 and of the F2 generations produced by interbreeding of the F1 progeny. b. For the cross PPbyby X ppByBy, give the phenotypes and genotypes of the F1 and of the F2 generations. c. For the cross of Question 7b, what further phenotype(s) would appear in the F2 generation if crossing over occurred? d. Draw a nucleus undergoing meiosis, at the stage in which the crossing over (Question 7c) occurred. In which generation (P, F1, or F2) did this crossing over take place?

4. Consider the following cross of Drosophila melanogaster (allelesas described in Question 6): Males with genotype Ppswsw arecrossed with females of genotype ppSwsw. Describe the phenotypes and genotypes of the F1 generation.

 

 

2.2.3. From DNA to Protein: Genotype to Phenotype

 

 

This subchapter deals with the mechanisms by which genes are expressed as proteins. We will begin with evidence for the relationship between genes and proteins, and then fill in some of the details of the processes of transcription—the copying of the gene sequence of DNA into a sequence of RNA—and translation—the use of the sequence of RNA to make a polypeptide with a defined order of amino acids. Finally, we will define mutations and their phenotypes in specific molecular terms.

 

One Gene, One Polypeptide

There are many steps between genotype and phenotype. Genes cannot, all by themselves, directly produce a phenotypic result, such as a particular eye color, a specific seed shape or a cleft chin, any more than a compact disk can play a symphony without the help of a CD player. The first historical step in relating genes to phenotypes was to define phenotypes in molecular terms. The molecular basis of phenotypes was actually discovered before the discovery that DNA was the genetic material. Scientists had studied the chemical differences between individuals carrying wild-type and mutant alleles in organisms as diverse as humans and bread molds. They found that the major phenotypic differences were the result of differences in specific proteins. In the 1940s, a series of experiments by George W. Beadle and Edward L. Tatum at Stanford University showed that when an altered gene resulted in an altered phenotype, that altered phenotype was always associated with an altered enzyme. This finding was critically important in defining the phenotype in chemical terms. The roles of enzymes in biochemistry were being described at this time, and it occurred to Beadle and Tatum that the expression of a gene as phenotype could occur through an enzyme. They experimented with the bread mold Neurospora crassa. The nuclei in the body of this mold are haploid (n), as are its reproductive spores. (This fact is important because it means that even recessive mutant alleles are easy to detect in experiments.) Beadle and Tatum grew Neurospora on a minimal nutritional medium containing sucrose, minerals and a vitamin. Using this medium, the enzymes of wild-type Neurospora could catalyze the metabolic reactions needed to make all the chemical constituents of their cells, including proteins. These wild-type strains are called prototrophs (“original eaters”). Beadle and Tatum treated wild-type Neurospora with X rays, which act as a mutagen (something known to cause mutations). When they examined the treated molds, they found some mutant strains could no longer grow on the minimal medium, but needed to be supplied with additional nutrients. The scientists hypothesized that these auxotrophs (“increased eaters”) must have suffered mutations in genes that code for the enzymes used to synthesize the nutrients they now needed to obtain from their environment. For each auxotrophic strain, Beadle and Tatum were able to find a single compound that, when added to the minimal medium, supported the growth of that strain. This result suggested that mutations have simple effects, and that each mutation causes a defect in only one enzyme in a metabolic pathway described as the one-gene, one-enzyme hypothesis. One group of auxotrophs, for example, could grow only if the minimal medium was supplemented with the amino acid arginine. (Wild-type Neurospora makes its own arginine.). These mutant strains were designated arg mutants. Beadle and Tatum found several different arg mutant strains. They proposed two alternative hypotheses to explain why these different genetic strains had the same phenotype:

The different arg mutants could have mutations in the same gene, as in the case of the different eye color alleles of fruit flies. In this case, the gene might code for an enzyme involved in arginine synthesis.

The different arg mutants could have mutations in different genes, each coding for a separate function that leads to arginineproduction. These independent functions might bedifferent enzymes along the same biochemical pathway.

Some of the arg mutant strains fell into each of the two categories. Genetic crosses showed that some of the mutations were at the same chromosomal locus, and so were different alleles of the same gene. Other mutations were at different loci or on different chromosomes and so were not alleles of the same gene. Beadle and Tatum concluded that these different genes participated in governing a single biosynthetic pathway—in this case, the pathway leading to arginine synthesis. By growing different arg mutants in the presence of various compounds suspected to be intermediates in the synthetic metabolic pathway for arginine, Beadle and Tatum were able to classify each mutation as affecting one enzyme or another, and to order the compounds along the pathway. Then they broke open the wild-type and mutant cells and examined them for enzyme activities. The results confirmed their hypothesis: Each mutant strain was indeed missing a single active enzyme in the pathway. The gene–enzyme connection had been proposed 40 years earlier in 1908 by the Scottish physician Archibald Garrod, who studied the inherited human disease alkaptonuria. He linked the biochemical phenotype of the disease to an abnormal gene and a missing enzyme. Today we know of hundreds of examples of such hereditary diseases. The gene–enzyme relationship has undergone several modifications in light of our current knowledge of molecular biology. Many enzymes are composed of more than one polypeptide chain, or subunit (that is, they have a quaternary structure). In this case, each polypeptide chain is specified by its own separate gene. Thus, it is more correct to speak of a one-gene, one-polypeptide relationship: the function of a gene is to control the production of a single, specific polypeptide. Much later, it was discovered that some genes code for forms of RNA that do not become translated into polypeptides, and that still other genes are involved in controlling which other DNA sequences are expressed. While these discoveries have supplanted the idea that all genes code for proteins, they did not invalidate the relationship between genes and polypeptides. But how does this relationship work—that is, how is the information encoded in DNA used to specify a particular polypeptide?

 






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