Berkeley STATISTICS 246 - Lecture Notes (20 pages)

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Lecture Notes



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Lecture Notes

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Lecture Notes


Pages:
20
School:
University of California, Berkeley
Course:
Statistics 246 - Statistical Genetics
Statistical Genetics Documents

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In Silico Mapping of Complex Disease Related Traits in Mice Stat 246 Spring 2002 Week 6 Lecture 2 Based on the paper with the same title by A Grupe et al Science 292 2001 1915 1918 Crosses of inbred strains of mice Here the grey scale denotes a quantitative trait Mapping genes for complex traits in crosses of inbred mouse strains I will refer you to the notes from Weeks 3 and 4 of my Stat 260 Spring 1998 There I describe mouse crosses and and linkage mapping methods for analyzing genome scans for localizing quantitative trait loci genes to regions of chromosomes We take up the problem from there The next step is quite time consuming and usually involve creating so called congenic strains which can take 1 2 years After this still more time consuming work is required physical mapping and genomic sequencing Of course you could get lucky sequencing candidate genes but this cannot be relied upon We now consider alternatives in silico and microarrays Chromosome 4 Congenic Strain 1 1 2 2 3 3 4 4 19 Strain 1 19 Strain 2 Achieved by repeated backcrossing following selection for the region to be retained Single Nucleotide Polymorphisms An Introduction Some people have blue eyes some are great artists or athletes and others are afflicted with a major disease before they are old Many of these kinds of differences among people have a genetic basis alterations in the DNA that change the way important proteins are made Sometimes the alterations involve a single base pair the smallest building block of DNA and are shared by many people Such single base pair differences are called single nucleotide polymorphisms or SNPs for short Nonetheless many SNPs perhaps the majority do not produce physical changes in people with affected DNA Why then are genetic scientists eager to identify as many SNPs as they can distributed on all 23 human chromosomes Two reasons Even SNPs that do not themselves change protein expression and cause disease may be close on the chromosome to deleterious



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