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Study Guide

Biology 3592A- Final Exam Guide - Comprehensive Notes for the exam ( 45 pages long!)Premium

45 pages135 viewsFall 2017

Department
Biology
Course Code
Biology 3592A
Professor
Kathleen Hill
Study Guide
Final

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Western
Biology 3592A
FINAL EXAM
STUDY GUIDE
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Clonal Mosaicism
September 14, 2017
Lecture 1
The Rise of de novo Mutations & Mosaicism
Clonal Mosaicism: arises when a postzygotic mutational event is detectable in
subpopulations of cells as an alternative genotype while not present in the germline
genome
Was undetectable until recent technological advances
DNA Damage: lesion or broken bond
The first thing that happens to DNA; reversible
Mutation: DNA damage that’s been replicated & proliferated; irreversible
Clonal Expansion: proliferation of mutated cells
Drives it to detectable; more easily detected when cells are expanded
Detectable:
1. Genotypically lots of cells to a single cell with better tech
2. Phenotypically what you can see
Purifying Selection: detecting mutations as being aberrant; cause loss of mutation
i.e. immune system gets rid of necrosis from mutation
works on the molecular, inter/intracellular, & systemic level
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Penetrance: proportion of individuals carrying a particular allele of a gene that also
express an associated trait (the phenotype)
Creates a phenotype that’s recognizable
Driver mutation: oncogenic or mutated tumor suppressors
Have genes that drive cells to grow, divide and proliferate
Main component that the positive selection is working on
Very delicate balance if driver mutation is knocked out,
passenger/hitchhiker mutation can take over & mutations can become worse
Fitness: mutations either increase/decrease fitness of individual
Concept Diagram of Somatic Mosaicism i.e. Cancer
Mosaicism: the whole tissue (i.e. normal cell + subpopulation of mutated cells)
Different colours different subclones of cell phenotypes
Adhesion, mutator, apoptotic, angiogenesis
Mutators can increase mutation frequency
Each cell has a distinctive pattern of mutation
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