Popular in Course
verified elite notetaker
Popular in Department
This 24 page Reader was uploaded by email@example.com on Friday February 7, 2014. The Reader belongs to a course at a university taught by a professor in Fall. Since its upload, it has received 171 views.
Reviews for Genetics 310
Report this Material
What is Karma?
Karma is the currency of StudySoup.
You can buy or earn more Karma at anytime and redeem it for class notes, study guides, flashcards, and more!
Date Created: 02/07/14
January 22 Intro and What to Expect Course Overview Of ce hours on syllabus shared with other classes also don t hesitate to call Wants to meet us after class in lab in office hours Syllabus lt s online contact if there s trouble downloading Grade three midterms 100 pts each final 150 lab 150 Shared grade for lecture and lab percentage overall Will do a bit ethics presentation in lab a technical description of the technology that gives rise to the ethical controversy You write a technical paper then take a position on the controversy Make sure you are registered to Blackboard course There are practice exams worksheets lecture handouts etc Full lecture slides are posted after lecture Lab materials page lab manual released in pieces generally posted a week before the lab Worksheets are chapter oriented questions vocab important part of studying and preparing Problem sets usually old exam questions very good practice for exams Practice exams are from last semester Genetics Lab There will be some bumps as we figure out what works for USF 3 10L grade will be a percent score multiplied by 150 then incorporated into overall grade You are responsible for downloading the materials needed for the following week s lab and reading them Genetics Lab is out of 250 points two lab reports group presentation ethics paper quizzes quiz tests on how well you ve read the material for that day there will be one next Tuesday and summaries Tips for success This class will start out with some review that can lull you into complacency don t get behind on reviewing the material we need to really get this stuff Work on worksheets and problem sets during lab Attend class and make use of office hours Peer advising program everyone seems to think office hours are underutilized He thinks more of people who take initiative and are attempting to learn Please don t browse around on the intemet in class the poor people behind you Four every hour of seat time you are expected to spend a good two hours studying Recommendation schedule it in like a job Loves questions can be interrupted especially if something is not clear The class itself Genetics Punnett Squares are about phenotypic ratios in offspring heredity The other part is how traits arise pattems of gene expression Genetics in a nutshell is the study of heredity Aristotle and Hippocrates had different ideas of heredity Pangenesis said that the body send signals to the offspring about the state of the body but it didn t make sense in that a onearmed person doesn t have onearmed kids In Europe there was a battle between spermists and ovists One line of thinking was that the egg was an empty vessel and the sperm had all the information alternatively it was thought that the eggs had all the information and the sperm just gave it a spark of life There were fanciful drawings of sperm with little hermunculi inside Of course this didn t jive with the observation that we are part of each parent Darwin had thoughts about heredity too he had no clue He hand wavingly backed Aristotle on Pangenesis Mendel was the one who really nailed it He called what we now refer to as genes hereditary factors He figured out that alleles of each gene separated so each child got one copy from each parent he figured out that there s a nice mathematically predictable pattem It wasn t until later when Thomas Hunt Morgan put forward the Chromosomal Theory of Heredity studying fruit ies found the chromosomes within cells It wasn t clear then what the important part was note Chase and Hershey Next question was how the four bases encode traits Human genome project helped sequenced the whole human genome Genomics is the study of genome sized samples This is a useful tool not the end this is a whole lot of information and now we have to figure out what it means Heredity 1 The passing of genetic factors from parent to offspring 2 the genetic constitution of an individual Interested in understanding variable heritable traits and the molecular basis for inheritance Phenotypes are observable traits observation can be lots of things blood levels chemical tests Phenotypes are in uenced by the environment as well as genotype Random schocastic differences can be used A gene might be involved in synthesizing the pigment for your eye Different alleles different versions of that gene like for blue or brown pigment Mutations are changes to the sequence of DNA responsible for all genetic variation Mutations we have today have to have been in the germ line cells of our ancient ancestors Think about the link between the two different definitions of gene the molecular basis and the manifestation that is gene expression There is the proteome the collection of all the expressed proteins resulting from genes Discussion of point mutations and how one base change can change the RNA to have a different codon 9 different amino acid 9 improperly made protein Levels of genetic analysis molecular cellular organismal population Darwin and Alfred Wallace heritable variation competition for resources proposed that this could explain speciation even at a time we didn t understand the mechanism of heredity Look at a phylogenetic tree know that every modern living thing has been evolving for the same amount of time assuming the LUCA was real More complex does not equal more evolved January 24 Genetics and Evolution The original creation of phylogenetic trees was based on traits but big traits can be misleading due to convergent evolution Now we use protein and DNA Myoglobin is an important oxygen carrier in animals if you compare three different monkeys you can see a few differences amid much that s the same there are three ways of thinking about genetics Classical Transmission Genetics the way genes are passed on from parents to offspring or between organisms Molecular genetics structure and function of molecular and cellular level Population genetics frequency and fitness of alleles within a population concepts like Hardy Weinberg equilibrium This in biology and publicly is the age of genetics We see this when we think of things like GMO s However we have been doing genetics for a long time As far as we can see modern corn exists because humans messed with teosinte selecting for those with larger more edible grain The modern cow is related to species of bison and buffalo these things look like they do because of selective breeding We have been doing genetics as long as we have been doing modem agriculture Direct manipulation of genes is the next level For example we ve modi ed com to produce an insecticide and be resistant to infection Personal genetics it s becoming plausible for people to figure things out about their genotype that affect medical decisions this will only become more common Patemity tests are now available forensic genetics are more in the mainstream A serial killer was caught in 2010 because his SON was in the prison system The son was a 50 match with crime scene and his DNA was in their database The power raises questions of privacy and accuracy DNA and Chromosomes This is likely to be awful review What do we need from hereditary material What led people to the conclusion we have now Store all the information needed to make a complete organism Able to be expressed Able to be copied reproduced Must be capable of change to create variation within the population We knew chromosomes seem to condense around cell replication and had DNA and protein inside We knew DNARNA was composed of four bases believed to be short molecules seemed too simple to be hereditary material Proteins were more interesting with 20 main amino acids pretty large structures looking at thousands of amino acids strung together proteins were attractive as genetic material However protein could be found all over the place whereas DNA was only in the chromosomes which added credence to the DNA theory It wasn t until later that this was settled Fred Griffith was not as interested in the DNA question but trying to find a vaccine for pneumonia So he student virulence in strains of S pneumonia that killed mice The smooth strain was lethal the rough strain was mutant altered strain that formed little colonies didn t produce polysaccharide coat were easily picked off by organism immune system didn t kill mice on its own Vaccine expose someone to a nonlethal variant of a pathogen Grif th hoped the R strain would work but it wasn t a good vaccine He took the smooth strain and killed it injected it in mice and it didn t kill the mice but it didn t work as a vaccine Then he put in live rough cells and dead smooth cells 9 those mice got sick and died and he found live smooth cells in their bloodstream by looking at genetic markers he found that rough cells had been transformed by picking up the smooth trait He found that hereditary material was leaking out of the dead smooth cells and being picked up by rough cells So if rough cells picked up gene for capsule capsule was created Griffith never found the vaccine and was then killed in a London bombing Avery MacLeod and McCarty used enzymes that digested DNA RNA or protein to demonstrate that DNA was the transforming factor They found if they ground up dead S strain and mixed it with R cells transformation happens Then they found if they treated the S mixture with DNase no transformation happened transformation still happened with RNase and protease There were suspicions still people weren t sure all the proteins had been destroyed by protease Viruses take over host cell by turning it into a virus factory we knew that viruses had pretty much DNA and protein only The question was where was the hereditary information the blueprint for new viruses What part gets into the cells HersheyChase blender experiment Produced viruses under two conditions 35S that only labels protein and 32P that only labels DNA They infected some bacteria cells then put them in a blender and shook off whatever left cells They found that what got into cells was the DNA of the virus and proteins were always separable That pretty well closed the door on this question Mnemonic for Thornton was the UC Davis Aggies he remembered that the Aggies were always Pure even though it wasn t true The number of phosphates is varied found in name monophosphate one phosphate Phosphates are always almost of course a 5 3 linkage DNA is polar has 5 end and 3 end Chargaff s Rules Analyzed the base composition of DNA he broke apart DNA to find what percentage was each base E Coli had basically equal for each base but other bacteria varied The interesting thing was that these weird rules came up if you divide the purines by the pyrimidines you always had a ratio of about one something was balancing the purines and pyrimidines Any time adenine was variant thymine was by the same amount same with guanine and cytosine X ray diffraction done by crystallizing the substance so every molecule is perfectly aligned If you fry an egg the egg proteins all coalesce but that is not a crystal a crystal must be formed so that an X ray diffracts in a predictable pattern You can figure out the structure of the molecule from the X ray diffraction pattem mathematically Watson and Crick s stolen model found that the strands were anti parallel and the hbonds were following rules for base pairing This explained Chargaff s rules They called this a right handed double helix chiral purity had to do with the direction the helix turns as you go up your right hand would describe the curvature as it spirals up Watson Crick and Wilkinson did no wet lab work on this modeled it after Chargaffs and Franklin s data Franklin died The UC Davis Genome Center has a lefthanded helix in their logo Spend some time understanding how the base pairs are arranged where are the H bonds Bases are at from our perspective there is a column of space in the middle there are 34 nm per base and ten bases per turn so 34 nm per turn The backbones have a major groove and a minor groove UCD genome center logo also has perfectly symmetrical helix someone talk to that artist January 27 Replication and Chromosome Structure Week 2 Lab will be up Tuesday night Structure There are different ways to make two antiparallel strands in a helix Most DNA is in B form under most physiological conditions A form under high salt conditions Z form can potentially form in long strands of GC pairs it s not clear if it happens naturally Supercoiling has effects on the topography of DNA as well as the periodicity Tightening it up causes additional coils to form in neg supercoiling Why did DNA end up getting picked as the genetic material One reason is that ribose with its extra hydroxyl group is more reactive in solution Thus even RNARNA double helices are more easily broken up Spend some time on 221225 of the book reviewing the semi conservative method of DNA replication and how it was settled on Replication occurs at a 3000 nucmin rate Always extends off a 3 OH end without that no extension is possible Must use triphosphates cleaving off the two phosphates drives the energetically unfavorable reaction of lengthening a molecule Polarity problem DNA only extends from the 3 end Thus only one strand can extend directly in the 5 3 direction one strand seems to run backwards Replication of the other strand must happen discontinuously Initiation DNA helicases help stretch and open up DNA A bunch of proteins bend the DNA 9 mechanical stress 9 easier to open This happens at a specific site origin of replication For most bacteria this is just one spot The process of stabilizing unwound DNA is helped by singlestranded binding proteins SSBP s DNA can otherwise harm itself due to the hydrophobicity A problem occurs when you open the DNA supercoiling Positive supercoils occur ahead of the replication fork remember DNA is two long covalently bound molecules The positive supercoils can create enough torsional stress to mechanically cause breaks DNA topoisomerases deal with this there are classes 1 and 2 Topoisomerase 2 makes a break then passes the loop through Topoisomerase 1 is attracted to the supercoil and nicks one of the two strands so the other strand can rotate freely to let go of some of that pressure Topoisomerase stores the chemical energy it gets from making the nick and uses it to fix the nick so doesn t require energy from outside There s a very important class of anticancer drugs that inhibit topoisomerase makes cancer cells kill themselves of course so do your skin cells and the lining of your gut so you get really sick Primase extends RNA polymers RNA polymerases can start from scratch unlike DNA polymerases E Coli has a number of DNA polymerases involved in repair and fixing breaks and damages Replication done largely by DNA Polymerase III So far all the DNA polymerases we have require a template and a 3 OH Some of them have a 5 3 exonuclease function can remove nucleotides can chew away nucleotides from in front There s also a proofreading exonuclease activity chews backwards in a 3 5 direction to remove mistakes DNA Polymerase is a machine with multiple polypeptide parts It has two copies of the enzyme that catalyzes addition of nucleotides It has primase associated with it a lot of the time Additional subunits make the parts move together It also has a betasliding clamp which is donutshaped with a hole just big enough to clamp around the DNA keeps the polymerase tethered to the DNA DNA polymerase III can chew up primers ahead of it Laggingdiscontinuous strand each time a new segment of DNA is opened a new primer must be laid down replication starts again there How is this all organizedcoordinated We think that the DNA twists itself up to keep the site of replication the same on both strands See movie in lecture sliding clamp of lagging strand dissociates when it runs into the back end of the previous strand then new sliding clamp associates with new primase and DNA polymerase grabs on again DNA polymerase will grab on to the closest clamp to it this has to happen over and over at a very fast rate Polymerase cannot join the new segment to the old needs a triphosphate DNA ligase comes in and fixes the nick Most of this stuff has been modeled from E Coli Luckily it turns out that the way replication developed there says a lot about it in humans Differences more origins of replication more polymerase types restricted according to the cell cycle and the telomere problem Eukaryotic chromosomes are huge replication from a single origin would take a very long time it s been done in vitro but it took hours for budding yeast Forks from individual origins eventually collide mechanism of resolution is still not understood Telomeres Nucleases at the very end of the lagging strand can digest the primer so the new strand of DNA is a primer short This shortening happens again and again with each round of replication Eventually you could eat into genes that matter Because of semiconservative replication chromosomes are doomed to get shorter Telomerase is a DNA polymerase needs a 3 OH and a template However it carries its own template RNA in its own complex Telomerase recognizes a sequence at the very 3 end of the strand and lays down GGGTTA Then it lets go reanneals and extends over and over again tacking a bunch of repetitive junk at the end of the chromosome lengthening the telomere RNA primers can be laid down again and the chromosome is lengthened again Most cells have no telomerase activity so most human cells can stop replicating we think some of the effects of aging comes from telomere shortening We have active telomerase in a few locations in our body germline etc People that lack telomerase have premature aging Werner s syndrome is premature aging Companies have pursued the idea of re activating telomerase as antiaging mechanism The problem is that one of the first thing a cancer cell does is turn telomerase on Anything that activates telomerase is also a potent carcinogen Question to think on why does DNA replication need leading and lagging strands Jan 29 Chromosome Structure Print off Week 2 lab protocol Look at the sample exam Note that genome size varies Within groups Prokaryotic chromosomes Bacteria are generally monoploid Nucleoid DNA plus protein the DNA gets condensed Loops around a basic scaffold and is negatively supercoiled Proteins are positively charged the DNA has a lot of interaction with the backbone Eukaryotic chromosomes Eukaryotes have multiple chromosomes organized into chromatin Chromatin the mess of DNA RNA and proteins that associate in the nucleus Chromosomes are always there just more visible during mitosis Most compacting is based on the action of histone proteins Histones are basic which in solution makes them positively charged Diameter of DNA is 2 nm Histones and nucleosomes Barrel shape structure with long tails Histone H1 acts like a clamp to hold histones and DNA There is a second coiling level beyond coiling about nucleosomes Fitting to a scaffold Non histone scaffold proteins are left behind Includes chromosome skeleton and unspooled DNA in long strands Levels of DNA packaging 2 nm double stranded DNA Protein scaffold is not present during interphase All chromatin is not equal Euchromatin associated with most gene expression is more relaxed Heterochromatin associated with less gene expression is more condensed Structures Within the chromosome centromeres telomeres microsatellite regions Centromeres Just DNA sequences Regions of attachment of microtubules to the chromosome In most eukaryotes there are multiple microtubules Kinetochores connect the centromere and microtubules At mitosis a chromosome two separate DNA strands chromatids tethered together by cohesin proteins Centromere region is heterochromatic Telomeres Structure is of highly repeated DNA Tloop prevent cell from trying to fix telomeres Cell will not try to fix telomeres but Will fix DNA Satellite DNA Long stretches of repetitive DNA GC content 9 denser DNA here 80 Can be visualized by density centrifugation Techniques In situ on site in the location FISH Fluorescent InSitu Hybridization Probe is labeled with uorescent DNA marker Multiple things can be visualized at once Bonding patterns and karyotypes Cytogenetics staining multiple different regions used to differentiate chromosomes Bonding patterns homologous chromosomes Karyotyping cells are treated with drug to knock out mitotic spindle and lock cells in mitosis Karyotype chromosome and ploidy Variants of in situ hybridization Chromosome painting SKY technique special karyotype specific probe to label Whole chromosomes a color Allows for identification of translocation events Centromeres can be at the ends of the chromosome Remember that homologous chromosomes can have multiple alleles Whereas sister chromatids are assuming no error in replication exactly identical Jan 31 Mitosis and Meiosis Homologues vs sister chromatids Homologous chromosomes are slightly different copies of the same type of chromosome same genes different alleles Each homologue has its own centromere Sister chromatids on the other hand are recently replicated copies of the same chromosome same homologue same alleles Funny analogy We look at chromosomes as cookbooks we get a complete set from each parent with little alterations in the margins guys get more like a pamphlet from dad What we observe phenotype comes from trying to make both recipes at the same time A dividing cell needs protein machinery to make copies of all the important parts and segregate them in an ordered way so to ensure no damage Cell division Prokaryotic cell division binary fission pretty simple There is some regulation to make sure the new chromosomes move to opposite sides We think it has to do with attachment to membrane most of the rest of the cell just oats around randomly distributes Eukaryotes have a complex cytoplasm full of stuff How do you split the nucleus with all its linear chromosomes evenly lnterphase is usually the majority of the cell s life except in early embryonic growth S phase very important it s important to regulate that each chromosome is only replicated once Most of our focus will be on M phase Most of this is regulated by checkpoints There must be growth for cell division to continue MTOC microtubule organizing center That is where cytoskeleton is presumably organized structure in animal cell is called centrosome and has centrioles made of organized microtubules Centrioles purpose is unclear cells can sometimes do without them Centrosomes duplicate during interphase and separate during M phase just like chromosomes There are weird mutations that cause overreplication of centrosomes and they are a disaster you end up with multipolar spindles Yeast cells just break the nucleus in half but most cells just break it down Chromosomes condense into thick sobanoodle like things Sister chromatids made by replication remain stuck together due to cohesin proteins process termed cohesion During prophase kinetochores are assembled on the centromere protein to DNA linkage Microtubules will attach to kinetochore and that s how chromosomes are attached to the spindle Each centrosome sends out aster of microtubules star shaped protrusion away from the chromosomes not as many as in the spindle Remember that microtubules are dynamically unstable unless they attach to something like a kinetochore There will be a force combined of motor proteins and dynamic instability of microtubules that moves the chromosome toward the centrosome Eventually the microtubule will fall apart When a chromosome gets attached to opposite centrosomes we get a well matched tug of war and chromosome ends up in the middle By metaphase the nuclear envelop is gone and the chromosomes are in the tugofwar state Anaphase is triggered by an enzyme called separase enzyme which is a protease that cleaves cohesin Then the chromatids are pulled to opposite ends and the centrosomes polarize further There is a checkpoint that tells separase when to act ensures everything is distributed Telophase is basically prophase in reverse Cytokinesis is a separable process in terms of regulation Cytokinesis is the mechanical division of the cell Actin and associated motors act like drawstrings in a purse in animals there s a cell plate in plants There are specialized cell divisions where lots of rounds of mitosis occur without cytokinesis Mitosis know the phases where the chromosomes are when and not get it confused with me1os1s Meiosis Cells produced are called gametes and are haploid Mathematicians have questioned whether genetic variation benefits the population as a whole or not Meiosis somewhat cruelly eliminates mutations that are deleterious Eliminating mutational load may be more of a big deal than introducing beneficial mutations this is just Professor Thomton s thinking Cell division splits the genetic content in half There is a great slide in the lecture slides titled Meiosis vs Mitosis that goes through the c values or number of sets of chromatids at each phase Heterologous chromosomes chromosomes that are not paired with each other Prophase I of meiosis is divided into different phases don t memorize them look them up if you need Leptonema phase chromosomes condense nuclear envelope begins breaking down homology search may be underway but pairing is not yet visible Unique trait of meiosis is that homologous chromosomes must find each other Zygonema synaptonemal complex forms between homologues This is almost like a zipper central element of proteins has ladders of transcerse fibers connecting it to lateral elements This aids in recombination but is not found in all species In diplomena we begin to see chiasmata Diakinesis spindle forms nuclear envelop breaks down spindle fiber attachments cause the chromosome pairs to move to the middle Now we are in metaphase homologous pairs are aligned on metaphase plate This is where chiasmata are resolved What s holding everything together We don t have cohesin for this so what holds them together are in fact the recombination events the cohesins holding the sister chromatids together are now a tangled mess Kinetochores assemble only as one structure on each homologue so only one chromatid has a kinetochore on it per chromosome Anaphase homologous chromosomes separate sister chromatids still the same Chromosome number has been cut in half because chromosome number is defined as number of discrete chromosomes Telophase chromosomes decondense ready for a round of cytokinesis Meiosis II is mechanistically exactly like mitosis we just start with half the number of chromosomes This is how we get four gametes for each round W ze v i g 439r 39 H 5 33 quotAw fe 55quotquot 39z 3939 rWz ltltv2 A 39 cquotquot rquot Wquot 39 lt quot392 No Datza R F I p sO 391 I I r 9 391J7rEjE3Lm 19 ifs Huh EMy f 39quot 5fquot quot2 quotmm w quot quot v glt z I p H rf1rf Z 3r 0 9amp9 b ar a53rw amg ig 2 k V Lq si vrg I 39 M f i 39 i fi I E zE39xr239quot 0 0 39179a739 j 7 kzt 2Mquot39Iquotf3 f WlbquotJE6 f quotH at 3339mgrH 339 quot quot1 u p W i 39 39 P Jiwiri 3 l39If39K quot3w39 Fg 57 1 L 0 1 xua tKLJL iL W9 j i 3t2 ZP 5 uh ea 3 w 3 L 393 1E g quotquotquot39 f Pm V gTga9SS r J Vg W p PG pOd ampf wLrlt M aj n 5339 L 1 2 h 3 39w3 quot5 J 39 z lt9 4 IV aw amp c quot amp 39 e quot x ampquot A yxM s C 3 r ax 3939J 1 quot i5L pjl r f f 39j I 39 39 f 39 I I JmH uLm 39HLuh Feb 5 Mendelian Genetics Announcements 0 Week 3 Lab exercise is posted so download and review for next week 0 Make sure you plan how you get your crosses done next week 0 Lab protocols will be less intense over the next couple weeks since our crosses are in progress but this is temporary Mendelian Genetics 0 This is a topic that refuses to go away no matter how much we study genetics 0 This will come up again and again throughout this class and later Evolution 0 Punnett squares are one tool for thinking about transmission 0 Principles were set in place regarding transmission 0 Principle of Dominance for any set of alleles one may mask the other 0 Principle of Segregation alleles separate during a cross so gametes at random get one or the other from each parent not both 0 Dihybrid cross 0 He crossed a yellow round and green wrinkled 0 F1 was always yellow round and when he selfed it he got four gametes with the four possible combinations of those two traits and he got a 933l ratio 0 To assess if this fits with his observations we use same nomenclature G g with color and Ww for shape 0 Always use one letter per gene with capital letter for dominant allele 0 Recessive phenotype determines the letter by tradition 0 That has to do with how geneticists observe things 0 Say you have 500 brown bunny rabbits and one that s white the white phenotype is what brought that gene to your attention even though it s the product of a 1oss of function mutation most likely 0 If we have truebreeding parents we can assume they are homozygous so the truebreeding yellow round parent was GGWW and the green wrinkled was ggww 0 The fact that they re homozygous means each can only produce one kind of gamete GW from one parent and gw from the other 0 That means F1 is heterozygous for both traits and 100 yellow round 0 So the F1 being GgWw means it can produce four possible gametes GW Gw gW gw 0 If we let the F1 self we can produce a Punnett square that s 4x4 for each type of gametes 0 That makes 16 possible genotypes we then add up the offspring with equivalent phenotypes 0 We get 9 yellow round 3 yellow wrinkled 3 green round 1 green wrinkled 0 Note from note taker I recommend drawing this Punnett square out 0 The fact that the traits are inherited independently of each other led to the principle of independent assortment 0 That means that genes separate independently of each other the four gametes from the F1 parent are equally viable 0 It s the way they combine that creates the genotypic ratio 0 However this does not hold completely true if there s linkage 0 Mendel s data seems statistically unlikely as to how exact it is 0 He also wrote his paper on 7 traits that all happen to be unlinked 0 Did he have some results that showed linkage and conveniently fail to communicate it 0 Very different scientific environment at the time Punnett Squares 0 Great for mono and dihybrid crosses become problematic when you go larger cumbersome 0 For use with bigger problems the forkline method is useful 0 This takes advantage of independent assortment 0 For a trihybrid cross of heterozygotes you need to break it down one trait at a time 0 Then list out three genotypestwo phenotypes 0 Of the three tall plants we get 3 yellow one green same with the dwarf plants 0 Then for each combination of height and color we get three round and 1 wrinkled 0 Then just multiply across the line 0 ie 3 tall X 3 yellow X 3 round 27 tall yellow round 0 do that for all the other lines and you get a total of 64 offspring and their ratio Testcross 0 that is a cross against a homozygous recessive 0 if you cross a heterozygote to a homozygous recessive what you get is a 5050 or 11 ratio 0 if you do a testcross for three traits you get a 11111111 of offspring 0 forkline takes up space but it s still useful Probability 0 probabilities are always between 0 and 1 0 the expectation for ipping a quarter is even numbers of heads and tails even if the results are different that s the result of random chance 0 sample space collection of all possible outcomes 0 individual probabilities should be between 0 and 1 and all the probabilities of all possible outcomes should add up to 1 0 some events can happen at the same time 9 overlap 0 if there is no overlap the events are called mutually exclusive Rules 0 Multiplicative rule If events A and B are independent the probability that they will occur together denoted PA and B PA x PB 0 For example in the deck of cards the probability of drawing the ace of hearts 0 PA 452 0 PH 11 0 Multiply the two together and you get 152 which is the case because the deck contains 52 cards and there is only one ace of hearts 0 The additive rule or rule If events A and B are independent the probability that at least one of them occurs is given by PA PB PA x PB 0 For example if you add the probability of a heart 1352 and the probability of drawing an ace 452 we have double counted the ace of hearts and that s why we need to subtract 1 52 0 Corollary for mutually exclusive events 0 If they are mutually exclusive we don t have a double count 0 So the probability of drawing either an ace of a king from a deck you just add the two together 452 452 852 0 Example Say we cross Aa x Aa 0 Probability that the sperm is A 12 0 Probability that egg is A 12 0 Probability that zygote is AA 12 x 12 11 0 Heterozygote there are two possibilities each with a probability of 11 A egg a sperm and a egg A sperm 0 Those are mutually exclusive so we add them together and get 12 0 So you can see that the Punnett Square though less cumbersome for this case is just another way of looking at probability 0 A means that the zygote is Aa or AA unknown 0 Probability of this is the odds of AA and Aa added together 31 0 Also remember that prior events have no in uence on future events note from the note taker for some related humor read Stoppard s Rosencrantz and Guildenstern are Dead 0 Say we have a tetrahybrid cross either thing we ve learned would be cumbersome 0 How do we shortcircuit this to answer a specific question 0 Say the question is what s the probability for being homozygous recessive at all alleles 0 The probability of being homozygous for one loci is 11 0 Here the multiplicative rule applies 11 x 11 x 11 x 11 1256 0 What fraction will be tall round yellow and terminal 0 So we need the fraction that will be D W G and tt 0 Weget31x31x31x1127256 0 What fraction will be homozygous for all four alleles either dominant or recessive 0 Probability that you re homozygous at one locus 12 0 So we get 12 X 12 X 12 X 12 116 for the probability that all are homozygous 0 Let s say we re crossing AaBb and AaBb and we want the probability of being aa or bb 0 We would thing that it s 11 11 but we re double counting something 0 We need to subtract 14 X 11 16 for a total of 716 Summary 0 The probability of an event happening is eXpressed as a value between 0 and 1 0 The probability of two independent events occurring together is equal to PA X PB 0 If two events A and B are mutually exclusive then the probability the either A or B occurs is equal to PA PB 0 The probability that at least one of two independent events occurring is equal to PA PB PAPB Feb 7 Extensions of Mendel Mendelian genetics memorize the principles We intuitively understand the difference between and and or those are ways of expressing probability Hugo de Vries Worked with Mendel s principles to explain his cross with campion owers Did a dihybrid cross with redwhite and hairysmooth got the 933l ratio To calculate your expected results take the expected ratio and multiply by the number of events After the experiment you have to ask if observed results look like expected results Nature is random it will not be exact Question then is how close to the numbers have to be Chisquare x2 test for a set of experimental results take the summation of observedexpected2 expected The chi squared numbers give you a good indication of how close the results are to the theoretical results A value of 0 means your results are exactly what you predicted The bigger the number the farther your results are from what you predicted Still have to decide how big of a chisquare number is reasonable Use degrees of freedom n l where n is the number of result categories What that tells us is how many categories can vary in relation to each other Once you know how many heads you have you immediately know how many tails you have in a coin ip that s why degrees of freedom l for a coin ip not 2 5 critical value the chisquare value or higher is observed 5 of the time The critical value you use depends on the size of the data set for our purposes we will use a 5 critical value we will believe our results if they fall in the 95 range Proof is restricted to mathematicians we cannot say we proved our hypothesis we can say results do not reject the hypothesis That s because multiple hypotheses may be consistent with your results All science works as us trying really hard to disprove our theories Example Mendel s Dihybrid Cross Remember for expected values multiply expected ratio ie 916 by the TOTAL number of plants observed Degrees of freedom 4 1 3 How about Hugo de Vries Chisquared value is larger than critical value hypothesis is rejected What possibilities are there He s wrong or really unlikely The usual thing to do is repeat the experiment then if your results continue to be inconsistent you investigate Remember whole master s theses have been put forward about whether Mendel s data was fudged a little Coin ip experiment continued Results can be considered a binomial distribution two mutually exclusive independent outcomes So let s say we have 32 ppl ip the coin five times Odds of five tails 132 Four tails and five heads can happen five different ways each with a 132 chance so you have to add them up or rule Further there are ten different ways you can get two heads and three tails is 1032 same for two tails and three heads The normal distribution graph is a bell curve Normal distribution equal number of events on either side of the mean evenly spaced These are the AVERAGE values predicted set of results By the way expected results mathematically are allowed to be fractions The chisquared test can tell you if your results are what should only happen 5 of the time If those 32 different people are 32 different labs all over the world a certain number of labs will get inconsistent results this is the mechanism of dissent and consensus in the scientific community Let s say we have sets of parents that are heterozygous for the recessive disorder cystic fibrosis We can ask what the probabilities are of a certain number of kids being affected Say they have 4 kids we can calculate the probability of 4 unaffected 3 1 22 13 etc Just like the bell curve there are multiple ways these ratios can occur that must be added Binomial probabilities of a set of events can be calculated whenever there are two mutually expected outcomes that are independent Binomial probability nx ypXqy First part is the number of different events p and q are the probabilities X and y are the numbers of events with outcomes p and q N number of events Example odds of ipping two tails in a row if P and Q are heads and tails N 2 for two ips 2O2 1 P and Q are 05 so the result is 025 What are the odds of having five girls and 1 boy Where P girl and Q boy Number of events n is 6 for six kids X 5 and y 1 615051O55 To make this easier 6 1X2X3X4x5X6 5 1x2X3X4X5 so they cancel out and 1 1 so the term is 6 For a monohybrid cross What if We have Dd X Dd What is the probability that 25 will be dwarfs P tall D and Q dwarf dd N 5 X number with outcome P 3 y number with outcome 2 We end up with 026 Inverse If parents with allele for sicklecell anemia Ss and Ss have 3 kids What are the odds that at least one is affected lt s easier to calculate the odds that none are affected The chances of each child being affected is 34 so multiple that by 3 and you get 2764 Subtract that from 1 since all probabilities must add up to 1 and you get a 3764 chance that at least one kid will have the disease This is the kind of information you share with someone in genetic counseling It is Very important to understand the theory behind chi square analysis and how to carry it out
Are you sure you want to buy this material for
You're already Subscribed!
Looks like you've already subscribed to StudySoup, you won't need to purchase another subscription to get this material. To access this material simply click 'View Full Document'