Lecture05

Lecture05 - BIS101/Engebrecht Lecture05 4/8/10...

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BIS101/Engebrecht Lecture05 4/8/10 Announcements: Review Quiz due on line tomorrow, April 9. I understand that there is a problem with the grading of question number 3. Please be patient – I will check every test to make sure it is graded correctly. Complementation: Before we began our discussion of complementation, I went back over a dihybrid cross with the following configuration of markers putting it into the context of mutant and wild type: P: RRyy (mutant for seed color) x rrYY (mutant for seed shape) F1: RrYy – double heterozygous, therefore wild type for both phenotypes. In the F1, the progeny are all wild type since one parent contributed a good copy of the R gene and the other parent contributed a good copy of the Y gene. I hope this is helpful when we think about the idea of complementation. With respect to mutants, I told you that a single gene, when mutated, can affect many pathways in the cell, resulting in a pleiotropic phenotype. My example was Xeroderma pigmentosum (XP). This disease is caused by a single mutation in a DNA repair enzyme yet the people harboring this mutation have multiple phenotypes such as cancer predisposition, developmental defects, neurological abnormalities and skin abnormalities. Conversely, mutations in multiple genes can have the same phenotype: our example was eye color in Drosophila. There are ~ 100 genes that when mutated affect eye color. I then asked you to help me to design a genetic experiment to dissect a process. We decided to look at reproduction in C. elegans. First, we decided to identify mutants that were defective in reproduction (we decided to name them “unfit” mutants). We will make the assumption that the mutant worms each have one recessive mutation. The next question we wanted to address is how many different genes do our mutants represent? To determine this, we have to perform complementation tests. This entails crossing two different mutants and determining the phenotype of the progeny. It they are wild type, then the 2 mutations are in 2 different genes. The mutations are said to complement each other. In a way, this is no different than what Mendel saw in his dihybrid cross looking at two different genes segregating and seeing in the F1 that the progeny are wild type for both traits (i.e., are heterozygous for both traits). The difference is that instead of looking at two different traits, we are looking at the same trait and trying to determine if there is one gene or two genes affected, both of which are important for the trait we are looking at. Here, I am designating the mutants as unfit1 and unfit2 (remember lowercase indicates mutant; I will write the wild-type gene with uppercase letter, UNFIT1). We set up crosses between unfit1 mutants and unfit2 mutants. Lets assume that the mutants are in 2 different genes: P: unfit1/unfit1 UNFIT2/UNFIT2 x
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Lecture05 - BIS101/Engebrecht Lecture05 4/8/10...

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