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Lecture 8

Notes Lecture 8.odt

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McGill University
Biology (Sci)
BIOL 202
Daniel Schoen

Solution manual (griffiths is online)------> he uploaded it au fur et a mesure The monday conference starts at 1400 now Phenotypes and Gene interactions 1 Interactions btween alleles of the same gene (biochemical basis of dominance and recessiveness) Interactions btween genes in pathways ( why do different genes affect the same phenotype) Chi squared test in linkage analysis Do a dihybrid cross , get a double heterozygote, and do a test cross....normally would expect 1:1:1:1 slight excess of big Aand B carrying gametes. To calculate the expected proportion of AB carrying gametes: =255/500 *254/500 *500 expected Ab = 255/500*246/500*500 (see chart for why these numbers, but you would do this individually with each 4 possibilities) only one degree of freedom, we removed 2 degrees of freedom when we tried to calculate the increased probability.....We reject the hypothesis of independant assortment while taking into account viability of certain genotypes. Therefore, we have weak linkage Physical maps of chromosomes (up till now, we've been looking at genetic/recombination maps) chromosome (have chromosomes with different colours)-->physical map, large clones--->physical map small clones--->DNAseq Physical map: entire DNAsequence of a chromosome, all the information that you have for that chromosome at the DNAlevel. If we have physical maps, why use recombinance maps? Suppose you dont know what causes a disease, but you don't know anything about a genetic basis, how are you going to pull it out of a physical map? Recombinant maps are good if you have a phenotype wtout ne idea about the gene responsible for it. Alignment of physical and recombination maps If you line up the 2 maps, then you can use proteinAand protein B flanking your unknown gene, then you can get a better idea which region of the genome it is in. You've narrowed it down to a region of what is called candidate genes, maybe spot which is the defective gene in that pedigree. These kind of approaches really help us find locii of genes wt mutant phenotype that we know naught about, genotypically wise. Lecture 8 what is the basis of a phenotype? Genetics andCell biology/biochem are connected by molecular biology and both contribute to biological function Why dominant vs recessive? Archibald Garrod and inborn errors of metabolism (homogentisic acid --> maleylactoacetic acid) he was a physician who believed research was important for practitioners, studied genetic diseases, specifically alkaptonuria (black urine, homogentisic acid, why builds up other tissues and joints) Garrod knew something about this disease at the biochemical level. Individuals who don't have the diseasise normally convert homogentisic acid-->maleylactoacetic acid. So he inferred that in diseased individuals, there must be an enzyme f*** up, not allowing that conversion to happen. Mechanism Precursor ------- Enzyme (GeneApost transcription and translation)--->product Gene B not transcribed ---------Regulatory protein (geneA)---->Gene B transcribed Ex: CYSTIC FIBROSIS=recessive, 25/1000 people carry at least 1 defective allele for this disease. You cough up a lot of thick mucous, your nose is blocked, you have digestive problems, abnormal transport of sodium and chloride ions. Cau
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