NOVEMBER 7, 2008 *PROTEINS: Proteins are the end products of genes. A full length polypeptide: All peptides have an amino acid and carboxyl terminus: *RNA GROUPS: RNA groups are unique for each of the 20 amino acids. There are: 1) Non-polar groups- These are hydrophobic, repel water, and are on the inside of proteins. 2) Polar groups ? These are hydrophilic, attract water, and are on the outside of proteins. 3) Positively charged (+) groups 4) Negatively charged (-) groups All peptides carry an overall net charge depending on the R-groups of the amino acids (the number of + and the number of ? charged amino acids). For the charge of this amino acid above, 3 (+) charges + 2 (-) charges = 1 (+) charge Therefore this has an overall net positive charge. This charge allows for separation of proteins in an electric field. The process of separating by charge is called electrophoresis. *POST-TRANSLATIONAL MODIFICATION: This is taking strings of amino acids and converting them to proteins. 1) The N- and C- terminus amino acids are removed or modified (e.g. N-terminus methionine). 2) Methyl groups or phosphates are added to particular amino acids. 3) Carbohydrate side chains may be attached. 4) Chains may be shortened. 5) Signal sequences are removed. 6) Metals may be added. By doing these things, we alter shape, and shape correlated with function. You can also control whether it?s working by adding methyl or phosphate groups and ?turning them on? or ?turning them off.? *FUNCTIONS: Shape drives function. Functions of proteins include: 1) Cell shape and integrity 2) Hormones and receptors 3) Structural components of cells (lamin) 4) Enzymes (the majority of proteins are enzymes) 5) Everyday housekeeping functions (histones) ? Histones help perform regular cellular function. *PEPTIDES: Peptides take on higher order, giving rise to function. The orders (from simplest to most complex include): 1) Primary 2) Secondary 3) Tertiary 4) Quaternary Most polypeptides are not functional until you get to at least the tertiary state. These changes in structure cause changes in function. *PROTEIN STRUCTURE: The primary structure includes the sequence of amino acids in the peptide. Example: MLVGGRSNAAN? Secondary structure is the configuration in space from the interaction between amino acids. There are 2 common types including Alpha helix: This is a spiral chain of amino acids stabilized by hydrogen bonds. It is a right-handed helix with 3.6 amino acids per turn. An alpha helix: Beta-pleated sheet: This is a single polypeptide chain folded back on itself or several chains running parallel (or anti-parallel) to each other. A beta-pleated sheet: You can get spirals with the two structures combined: Tertiary structure is also known as conformation and has an overall shape. It has a three dimensional conformation. The 3D structure is specific for a given protein. The polar hydrophilic groups are on the surface, and the nonpolar hydrophobic groups are on the inside. Quaternary structure applies to proteins composed of more than one polypeptide chain. Proteins with quaternary structure are called oligomeric proteins (e.g. hemoglobin). Oligomeric proteins do not work until you have 2+ polypeptide chains together. It is the association of multiple peptides to form a functional protein. The protein globin is made of alpha and beta peptides, and functions to carry oxygen, therefore it is often called hemoglobin. Globin: *SUMMARY: Protein function is dependent upon shape. Shape is determined by constituent amino acids. Amino acid composition is determined by nucleotide sequences (DNA via mRNA). Mutation at the level of the nucleotide can alter amino acid composition which, in turn, can alter protein function. NOVEMBE 12, 2008 *MUTATION: There are certain requirements that genetic material must have: Genetic material ?must haves? include: 1) effective transfer between generations 2) effective replication/high fidelity 3) store vast amounts of information 4) information can be changed/mutable (Biological systems like variation. There is always change in systems therefore one must be able to change yourself. Through history, if organisms get fixed, they go extinct. Sexual reproduction is great for variation.) *HIV MUTATIONS: There are 2 different major types of HIV mutations. HIV even mutates within people. It can change inside an organism. Different types of HIV mutations can be shown in a mutation tree. *MUTATION RELATED TO PROTEIN: We have learned that structure or the configuration of a peptide bond confers its function. Therefore if you alter the structure you may possibly alter its function. Therefore if you change the sequence of DNA then you could possibly change the expressed phenotype. This would be a mutation. *GENERAL TYPES OF MUTANTS: Some general types include: 1) Transition mutant ? This is when you exchange a purine for a purine or a pyrimidine for a pyrimidine. (Purines include A and G, and pyrimidines include C and T) An example would be ATG ( GTG This is more likely to occur. 2) Transversion mutant: This is the exchange of nucleotides outside of the family, such as a purine for a pyrimidine. An example would be GAG ( GTG This is energetically more costly. This is also less likely to happen, therefore more significant when it does happen. *CATEGORIES OF MUTANTS: A single nucleotide change is called a point mutation. For the example THE CAT SAW THE DOG, say each 3 letters forms a codon. The following represent categories of mutants, and their effects. 1) Silent mutation- This nucleotide change causes no effect due to the degeneracy of the genetic code. UCU, UCC, UCA, and UCG: A change in the 3rd nucleotide position causes no change in phenotype. This is known as ?wobbling.? The example would be changed to THE Cat SAW THE DOG. 2) Missense Mutation: A change at the nucleotide level that results in an amino acid change. DNA- CTC ( CAC mRNA- GAG (GUG Amino Acid- glu (Q) ( val (V) The example would be changed to THE BAT SAW THE DOG. CAT and BAT are allelic forms of each other. A change in the amino acid could change eye color, hair color, etc. 3) Nonsense Mutation: This is a nucleotide change that results in a stop codon during translation. DNA- ACC ( ACT mRNA- UGG (UGA Amino Acid- trp (F) ( STOP (term codon) In this case, a protein stops forming because of the mutation. It can range from having hardly no effect to a big effect depending on if the stop is early on. If the protein is too short, it may be a lethal protein. The example would be changed to THE CAT SAW 4) Frameshift Mutation: This is the gain or loss of a nucleotide resulting in a change in the reading frame during translation. DNA- CATCATCATG ( CATATCATG mRNA- GUAGUAGUAC (GUAUAGUAC Amino Acid- Leu - Leu- Leu ( Leu ? Trp ? Tyr The example would be changed to THE CAT AWT HED OG This makes no sense to the cell. It sometimes may end up with an unnecessary term code too, so usually the proteins are shorter and do not make any sense at all. Frameshift mutations usually have the most dramatic effect on the system. *MECHANISMS OF MUTATION: Two major mechanisms include: 1) Spontaneous: This is when there are no artificial or external regulators that cause the mutations to occur. 2) Induced: This is when mutations are caused by external factors, usually chemically or environmentally, which causes a nucleotide change. *WHERE DO MUTATIONS OCCUR? They generally occur in either: 1) Somatic cells: These are non-sex cells. Any mutations that occur here are during the lifetime of the organism. Depending on the stage of development, it can have differential effects on the phenotype ranging from silent to severe. However, any effect is only felt by that organism, and the mutation is not passed down on to the next generation. 2) Germ cells: These are sex cells or gametes. Mutations occurring affect the DNA which is carried in the sperm cell or the ova, and this is passed on to the offspring depending on the mode of transmission. *WHAT CAUSES MUTATION: There are 2 major ways including: 1) Spontaneous: This is when the mutation is natural and caused for nothing. This is associated with loss of DNA pol fidelity. 2) Induced: These are caused by environmental factors. These could include: a) Chemicals that interact with DNA b) free radicals: nitrosamines (dark part of grilled meat) c) UV light ? DNA nicking ? This is from sunlight d) X-rays e) carcinogens: this is from cigarettes f) Cell phones NOVEMBER 14, 2008 *?RECESSIVE AND DELETERIOUS? MUTATIONS: Most mutations are bad and deleterious. In Aa, one allele (A) confers normal function. One allele (a) confers abnormal function. Under the dominant/recessive mode of inheritance, the ?normal? gene masks the effects of the mutant recessive alleles. Both alleles contribute. The change in amino acids may change shape, which changes function. This may have no effect or this may have a large effect. This is costly because the system has to translate both, but may not use one, or one may cause detrimental effects. There is molecular co-dominance, where both allelic phenotypes are equally produced at the allelic level. At the phenotypic level, there could be incomplete dominance, dominant/recessive, codominance, etc. *MENDEL?S WRINKLED PEAS: Peas were either smooth (R) or wrinkled (r). The wrinkled condition is due to the biochemical change of unbranched starch molecules. For the dominant allele R, For the recessive allele r, *EXAMPLES OF MUTATION: Sickle cell anemia is an example. This is an autosomal recessive disorder affecting the protein hemoglobin. (Hemoglobin requires quaternary structure) In normal situations, red blood cells flow through the circulatory system unhindered. However, affected individuals have blood cells having a sickle shaped phenotype. These cells can become clogged in the bloodways, causing severe distress, organ damage, and even death. Capillary systems can get clogged up. A pleitotropic effect is when one mutation yields multiple physiological outcomes. In this case, a single point mutation causes oxygen deprivation, anemia, joint problems, and organ crisis. This is an example of pleotropy, where one gene effects multiple outcomes. The beta-globin gene has approximately 60,000 base pairs. One change changes the whole gene. This occurs in codon 6. Norman Mutant DNA CTG ( CAC mRNA GAG ( GUG Amino acid Glu (D) ( Val (V) A single nucleotide change in the entire sequence of the gene is responsible for changing the structure of the protein and conferring the mutant phenotype. Norman hemoglobin structure allows for the efficient transport of oxygen in the bloodstream. A single mutant copy of the gene changes the structure thus changes the function of the protein. Molecular defect in the Beta-Globin gene Some humans are heterozygotes (carriers). The recessive s gene is not gone because in one environment it?s very advantageous to be Ss and bad to be SS. This is typically in tropical areas where malaria is present. People with Ss have a better chance of surviving malaria over SS. If two people with Ss mate, ¼ of the progeny is ss, which is lethal. Electrophoretic tests show differing mobility patterns for those affected with sickle cell. The conversion of Glu to Val removes a (-) charge from the protein, thus the band migrates a shorter distance in an electric field. NOVEMBER 17, 2008 *CURRENT FACTS ABOUT THE HUMAN GENOME: The human genome contains around 3 billion nucleotide bases. The lab mouse has ~2.6 billion, the fruit fly has ~137 million, yeast has ~12.1 million, and E.coli has ~4.6 million nucleotides. The average gene is 3000 bases long. The longest human gene is 2.4 million bases long (drytrophin). 2% of the genome encodes for proteins. Genes are concentrated in random, separated areas. Chromosome 1 has 2,968 genes, chromosome Y has 231 genes. The functions are known for <50% of known genes. All human genome sequences have over 99% similarity. Over 40% of predicted human proteins share similarity with fruit flies? or worms? proteins. *GENE EXPRESSION: Genes ( RNA ( Protein (Genes code for RNA which make proteins). Genes give tissues their differentiated properties. Differentiated means specialized. The non-dividing cells have left the cell cycle G and have no telomerase activity (D). (D = differentiated). Chart of how many genes are active in each of the following areas: Brain 3195 Eye 547 White Blood Cell 2164 Red Blood Cell 8 Muscle 127 The 127 genes found in muscle are not necessarily the same as the 547 in the eye. 20,000-25,000 genes are available in each cell. Regulation in gene expression is important to differentiated state of cell and tissue. You need to be able to turn the gene on when needed and off to conserve energy. *LEVELS OF REGULATION OF GENE EXPRESSION: DNA ( transcription ( message ( translation ( protein The central dogma can be regulated at every level. It gives us very fine-tuned control. It is also very expensive, so it?s an energy cost. transcriptional: these are the ?on/off? switches. It is subject to influence by external environment and is conducive or inducible. Post-transcriptional: this is for message stability and increases the number of times an mRNA can be used. It prevents message degradation by using a long cap and tail (i.e. oocyte DNA). Translational: this is how and when mRNA is used. Post-translational: modifications are made to the protein product (lipid, sugar, methyl, acetyl, phosphate) determines the localization and function of the protein in the cell. *TYPE OF GENE EXPRESSION: 1) Constituitive- ?always? This refers to the gene always being on or always being off. It is always made and present. It always participates in phenotype. Examples include tRNA, rRNA, and some mRNA. 2) Inducible- This is subject to an ?on/off? mechanism. It is influenced by the environment and the needs of the organism (ex. Lactose in muscles?causes muscle stiffness). This includes most mRNA. *TRANSCRIPTIONAL CONTROL IN EUKARYOTES: This is by a DNA and protein interactions. Proteins + DNA promote RNA pol binding. Examples include transcriptional factors. Factors or hormones diffuse across the membrane to intracellular receptor. Interactions depend on specific receptor molecules being present. No receptor means no response, and no factor means no response. Then for the nucleus, the H/R complex binds to DNA at a specific site called enhancers. The effect is a structural change allowing more efficient recognition and binding by RNA pol. Enhancer sequences are shared by different genes, so 1 hormone or H/R complex regulates different genes (so different enhancers = different effects). SEPTEMBER 19, 2007 *REGULATION OF GENE EXPRESSION: Hormones are external proteins and enter into the cell and combine with the receptor to form the H/R (Hormone-Receptor) complex. The H/R complex then goes to the DNA in the nucleus and links to some TATA box. With the enhancer, this can affect multiple genes. There also may be transcription factors on the promoter. *EXAMPLE: Glucocorticoid- This is a steroid hormone produced in the adrenal gland. It regulates glucose metabolism. The three elements of regulation include: Glucocorticoid hormone- This is a protein. Glucocorticoid receptor- This is also a protein. The receptor is a zinc-finger transcription protein. There are N and C terminus modification, promoter activation domain, and a zinc-finger domain (4 zinc atoms) ? DNA binding. There is a dimer formation domain that has to make a quaternary form out of a tertiary with another. Glucocorticoid response elements ? DNA 5? AGAACAnnnTGTTCT 3? *STEPS IN REGULATION: 1) Hormone enters and binds to the receptor 2) Receptor binds to a second copy 3) Complex moves into nucleus 4) Complex binds to response elements (DNA) 5) Transcription factors activated Cell or tissue must have receptor present to respond. This is why not all tissues respond to all factors. *EXAMPLE: Growth Hormone (GH)- In the absence of GH, no growth genes expressed. No growth would result in dwarfism (a phenotype). If you supply GH, you get growth (the growth genes are expressed and are ?on?). Therefore if you take GH or other steroids (a type of hormone), this promotes growth. GH Free Milk Story: The dairy industry gives GH to cattle. It makes them bigger and produces more milk, but the cow has GH. For lactation, whatever is in the system ends up in the milk. Therefore there may be GH in the milk. There was a worry over too much GH in the milk. Actually this is not too much of a problem though because humans do not have the proper receptors so the hormones? affects are not carried out. Human-based steroids will have an affect though (such as with body builders, athletes, etc.) *EXAMPLE: Estrogen- In menopause, there is a decrease in the supply of estrogen. The tissues that express estrogen receptors and need estrogen for phenotype no longer respond. Bone density is under control of estrogen. Genes that are required for bone growth require estrogen. Therefore a diminished supply of estrogen results in osteoporosis. Some people opt to use hormone replacement therapy to help. Hormone replacement therapy (HRT) supplies synthetic hormones to keep genes on. It can keep bone density up, decrease hot flashes, mood swings, etc. There?s a catch though. When you quit taking supplementary estrogen after taking it a long time, breast cancer rate increases greatly within 5 years after quitting. *EXAMPLE: Testosterone- This controls genes that regulate expression of male secondary sex characteristics, such as hair, voice, deposition of body fat, etc. This can be used as a treatment for Klinefelters, and will give males more male features and characteristics. This can also be given to transsexuals in females, where you can inject testosterone for those who want to be more male. *REGULATION OF TRANSCRIPTION: Additional elements include enhancers, silencers, and insulators. Enhancers: The hormone/receptor complex binds to TATA to amplify effects and affect multiple genes. Silencers: These are stretches of DNA usually between the enhancer and control region to silence genes. They can permanently lock down genes. Insulators: This is DNA with 42+ base pairs. It is located between enhancers and promoters. These have a CCCTC binding factor, and are ?all? vertebrate insulators. Insulators work in two ways: Say you want to turn on genes 1 and 3, but not gene 2. With the insulator, gene 2 interaction is prevented. It is found on almost all genes so can specifically control each one. It works by binding factors, so the first job is to stop a locus from being used. Imprinting: Example- Insulin-like growth factor 2 (IGF2)- In mammals, only alleles from the father are active. The mother?s allele is inactivated. The insulator on the homolog provided by the male is methylated (CCCTC factor can bind). Genetic imprinting is turning off one of the genes in a pair. Often 2 activated genes in a pair is lethal. *GENETIC IMPRINTING: This has loci where the expression of alleles is determined by the parents that contributed the allele. There are around 80 genes currently known in humans. Imprinting is the reason that parthenogenesis (?virgin birth?) does not occur in mammals. An example is that a father?s active lgf2 allele required for embryo. The XIST locus is an X chromosome inactivation locus. This is corresponded with Barr bodies and is random in fetuses (Lyon Hypothesis). There are extra-embryonic membranes produced from the female fetus. This includes the amnion, placenta, and umbilical cord. The X from the male is inactivated. This is a protection mechanism, and the tissue is much more likely to not be rejected. This involves ?anti-sense? RNA that shuts down all genes on the ?Barr? chromosomes. *TAKE HOME MESSAGE: Replication occurs at multiple levels. There are tissue-specific gene expression. Certain genes are expressed only in certain tissues. It provides tissue phenotypes and is a differentiated property. The hormone/receptor interactions are examples. SEPTEMBER 21, 2008 *POPULATION GENETICS: Remember Mendel?s Big 6. But in populations, mating is random and the final ratios will not be as simple as 3:1 or 1:1, etc. They will instead vary depending on mating. The Hardy-Weinberg equation predicts actual allele outcomes for mating populations: p = the frequency of A allele. q = frequency of a allele. p + q = 1 (p + q)² = 1² p² + 2pq + q² = 1 p² is the frequency of homozygotes (AA) 2pq is the frequency of heterozygotes (Aa) q² is the frequency of homozygotes (aa) *HARDY-WEINBURG PRINCIPLE (1908): Single locus genotypic frequencies, after one generation of random mating, can be represented by a binomial or multinominal function of the allele frequencies. Hardy Weinberg predicts (states) that a genetic equilibrium will be reached after one generation of random mating. This occurs with panmitic mating (another word for random mating), where every allele has to have the probability of mating around the same amount of its frequency. It is random based on frequency. *POPULATION: This is a group of interbreeding or potentially interbreeding individuals. *GENE POOL: This is the total of all alleles (genetic information) possessed by reproductive members of a population. *POPULATION GENETICS: This is a branch of genetics involved with the study of the mechanisms responsible for modifying gene pools. *POPULATION GENETICS: The basic starting points for any population genetics are: 1) Allele frequency 2) Hardy-Weinberg Principle- If you know the allele frequency, you can predict the genotype frequencies. *USES OF HARDY-WEINBURG: Uses include: 1) Test for changes in the gene pool 2) To estimate frequency and number of carriers in a dominant/recessive trait 3) It is a basis for modeling mechanisms of gene pool changes *GENETIC DEFECT: These are deletions of a section of a gene, or a mutation. For this study, 1 out of 100 humans sampled were homozygous for this mutation. They wanted to find the number of carriers (heterozygotes). We know was 1/100 = q². Therefore q² = 0.01 therefore q = 0.1 p = 1 ? q = 1 ? 0.1 = 0.9 therefore p = 0.9 2pq = (2)(0.9)(0.1) = 0.18 Therefore 18% of the human population should be carriers. This protein is a docking point for HIV in this example. *ASSUMPTIONS OF HARDY-WEINBURG: Assumptions include: 1) Large, random mating population 2) No genetic drift 3) No selection 4) No mutation 5) No migration For the large population size, it assumes an infinite population size. But in real populations, population size in finite. The major population genetics question is how does a finite population affect this? Effective population (Ne) size is a major concept: Effective population size is the number of independent genomic units successfully contributing to the gene pool of the next generation. Anything that divides a population will normally reduce Ne. Examples include separate sexes, age structure (differing ages of reproduction), and spatial substructure (things divided up in area). *SEPARATE SEXES: Elephant seals are an example. Say in a sample population: 10 males + 40 females ( 50 total animals When the number of males and the number of females are not equal, you use the equation: Ne = (4)(NF)(NM) / (NF) + (NM) Ne = (4)(40)(10) / (40) + (10) = 32 If you change the situation and say that only one male is involved in the population with 40 females, then 1 male + 40 females ( 41 total animals And Ne = (4)(40)(1) / (40) + (1) = 3.92 Now what about the situation of 10,000 females with 1 male: Ne = (4)(10,000)(1) / (10,000) + (1) = ~4 (turns out the number will always be around 4 with one male) This demonstrates the stud system. You take a male and introduce him to a lot of females, trying to overcome meiosis (trying to reproduce as much of the stud?s genotype as possible). The bad side- This occurs in zoos were males get shipped around, inbreeding occurs, etc. *AGE STRUCTURE: Effective population size is not going to be equal to the census structure because not all individuals will reproduce or be capable of reproducing because of age, etc. *SPATIAL STRUCTURE: The Linear Population Hypothesis- Scientists thought that a mice population was linearly distributed along a beach. They found out instead though that the mice form gamodemes. The Gamodeme Hypothesis is that the mice build there own neighborhoods with different genes in each pool. This is a way of protecting genetic information. DECEMBER 1, 2008 *RANDOM MATING: Hardy-Weinberg assumes random mating. This is also known as panmitic mating, which means that alleles are combined with other alleles based on the allele frequency. If we depart from random mating, we could have either Positive Assortative Mating ? This is like inbreeding, and ?like with like.? Organism chooses a mate that looks like itself. Negative Assortative Mating ? This is like outbreeding, where organisms mate with things that do not look like themselves. ?Unlike together.? An example would be the ?rare male effect? where a male comes into a population and all the females want to mate with him. Natural populations are constantly in flux between inbreeding and outbreeding. *RELATEDNESS: F is the inbreeding coefficient. F = ½^N The relatedness between 2 siblings is ¼ = 0.250. The relatedness between an uncle and a niece is 0.125. The relationship between first cousins is 0.0625. The relationship between first cousins once removed is 0.0312. The relationship between second cousins is 0.0156. *INBREEDING: Inbreeding is mating among genetically related individuals. This is also known as consanguineous mating. Legal unions start with first cousins once removed and second cousins. It is illegal to marry your first cousin, uncle, brother, etc. Inbreeding always increases the frequencies of homozygotes. Genetic diseases are carried in heterozygotes, and with inbreeding these individuals, you start to see more homozygote recessives, which are lethal. Lethal equivalents refer to the mathematical equivalents of lethals in different species. Some species can be inbred a lot and not have a lot of problems, and others have a lot of problems with just a little inbreeding. This depends on how many loci you have in your genome that are recessive lethals. The more you have, the more problems that will surface with inbreeding. Humans have 4 lethal alleles. We therefore have inbreeding avoidance, and this is done by most plants and animals. Some ways of inbreeding avoidance include dispersal (of seeds and young), self incompatibility (some plants cannot fertilize themselves, have different structures or sperm mechanisms, beach mice can detect second degree relatives), and incest taboos (humans have an incest taboo against marrying close relatives). *NO GENETIC DRIFT: Hardy-Weinberg assumes no genetic drift. Genetic drift is chance changes in allele frequencies. The smaller the effective population size (Ne), the greater the effect of drift. Genetic drift causes the loss of alleles. Drift causes the loss of alleles. Drift occurs in all finite population and results in the loss of alleles. *NO SELECTION: Hardy-Weinberg assumes no selection. Selection is the mechanism responsible for modifying the reproductive success of an individual. ?fitness? The necessary and sufficient conditions for selection include: Variation ? Variation among individuals in some trait. Fitness Differences ? A consistent relationship between the trait and mating ability, fertility, fecundity, and/or survivorship. Inheritance ? Variation among individuals must be under genetic control. *SELECTION EXAMPLES: 1) Stabilizing Selection: This works against the extremes and makes everything toward an average. An example is with human birth weight. 2) Directional Selection: This is the trend towards one end or another. This is what humans do with domestication, when they are selecting for fast horses, meatier animals, etc. 3) Disruptive selection: This is when you do not want to be average or in the middle. An example is with butterflies, where you want to be either big so you can fight, or small so you can sneak in and breed. You do not want to be in the middle. SEPTEMBER 3, 2008 *DARWIN: Darwin?s idea led to big outbreaks in 4 major areas: 1) Science 2) Religion 3) Social Darwinism 4) Eugenics- This is what we are going to discuss. *EUGENICS: Eugenics is the improvement of humans through selective breeding. Eugenics means ?good birth,? and was invented by Sir Frances Galton (1822-1911). This was all the material that we needed to know for this day. He said we did not need to write any further information down, but I took notes from the rest of the lecture anyway. Just know that he said none of this further information was needed to be written down. ?Eugenics is the study of agencies under social control that may improve or impair the racial qualities of future generations, whether physically or mentally.? ? Galton 1863 This idea goes all the way back to Plato and the Republic, which had the same idea talking about city states. Other leaders in this field included Alexander Bell, Theodore Roosevelt, and David Starr Jordan. Bell thought we could breed out deafness, and Roosevelt thought that there were superior classes of people. Davenport was also a leader and provided ways to ?improve the population? by suggesting restricting inferior people from having children. The Eugenics Family Studies were also known as the ?Joe Sixty Studies? and were attempts to identify ?bad? people (people with IQs below 60). They were linking low IQ with immoral habits. The ?worst? people were found to be sub-Appalachian, and were called ?white trash.? Davenport compiled data and came up with the ?Best? American. The highest ranked were people from Switzerland, Japan, natives of the country, African Americans, etc. The really ?bad? people included Mexicans, Irish, and people from Serbia. He concluded that the absolute ?best? American was a native born at least 3rd generation white Anglo-Saxon protestant from ?The Hill? (wealthy area) in Boston. It turns out that was where Davenport was from. Madison Grant put forth another view and wanted to eliminate inferior people. He wanted to sterilize those people, and get rid of criminals, bad races, insane people, etc. Davenport and Laughlin pushed sterilization. Thomas Hunt Morgan and Theodosius Dobzhansky were geneticists and said that in Mendelian Genetics there were ?no normals,? but rather just different phenotypes that existed. In Buck vs. Bell (1927), Supreme Court Justice Oliver Wendell Holmes Jr. ruled for the sterilization of people. This stood for the next 40 years. This movement started out with positive eugenics, then became negative eugenics. Some effects from negative eugenics included: sterilization immigration laws anti-miscegenation laws (who can marry whom) caste systems DECEMBER 5, 2008 *LECTURE FINAL: This lecture started out with a discussion of the final exam which will be on Wednesday, December 10th at 8am in the lecture room. The lab practical will be on Monday December 8th in the lecture room as well (not in the lab room). There will be no more notes given for the class, only the review that was done today. Dr. Wooten said the exam would be comprehensive and all multiple choice. He said to review all past material, and the new material would be 25-35% of the final. The whole final will be around 100 multiple choice questions. Be sure to bring a calculator. He listed some examples of things to be sure to review including phenograms, pedigrees, sequencing, epigenesist, and meiosis and mitosis with pictures. He said he would go back to chapters 3 and 4 and work problems from the book on Mendelian genetics. He also said there would be probably one linkage problem. *REVIEW: We did a jeopardy review where he gave us a phrase and we had to say the term associated with it. The phrases were: - Alternate forms of genes ( alleles - All offspring of the F1 generations are heterozygous ( classic parental cross - More than one gene interacts to influence a single trait ( epistasis (pleiotropy is the opposite) - Mode of inheritance that produces intermediate phenotypes ( codominance (also incomplete heritance can do this) - Traits affected by the environment ( conditional - adenine, guanine, cytosine, thymine ( bases (be able to recognize these in a picture) - a right-handed double helix with 10 base pairs per turn ( B form of DNA (the Watson and Crick form) - they hold bases in pairs ( hydrogen bonding - a 9-membered ring ( purine - oh, POO ( phosphodiester bond, which is the backbone of DNA and has 3? ? 5? linkage - More Peas, Please ( Mendel - The double helix ( Watson, Crick, Franklin, and Wilkins (Franklin did not get a Nobel Prize) - He described the ratio of bases in DNA ( Chargaff (know his rules) - Albert, put down that candy bar and help me with these bacteriophages ( Hershey and Chase - He could never select genes for his pan ( Darwin (developed idea of pangenesis as proposal) - Color blindness mode ( recessive sex linked (more specifically X-linked) - Linkage, I feel violated ( Independent Assortment, Mendel?s 2nd Principle - Dihybrid Backcross Ratio ( 1:1:1:1 ratio - We?re the two loci that would never cross the line ( complete linkage (can be found near centromeres, telomeres, and in male fruit flies there is no crossover) - That double crossing locus. I?ll put him in his place ( 3-point mapping and determining what goes in the middle - the reason x-linked recessive traits show up most often in males ( males are hemizygous (in humans) - gender means everything to these autosomes ( sex-limited - the homogametic sex in birds ( males (including chickens, penguins, etc.) - butterflies and moth?s mode ( Lygaeus Mode (ZZ and ZW); this is also revered from humans - expression of trait depends on the gender of the person having it ( sex influenced - Thanks Dad, just don?t tell mom that you gave it to me ( holandric (passed father to son) - Non-coding regions within a gene ( introns - where the enhancer, CCAAT box, and TATA box are found ( upstream - RNA is copied off of this DNA strand ( sense strand - the whole thing is copied into mRNA ( transcriptional unit - what?s that RNA doing in my DNA strand? I put it there?( during replication, primase puts down an RNA primer - It defines function ( shape - these groups give polypeptides their polarity ( markers, also the ends - I?m small, but when I enter a cell, enhancers come to life ( hormones - A centromere finds itself in the middle of an inversion ( pericentric inversion - Translations? work bench ( ribosome - The reason ?sisters? always share something old and something new ( semi- conservative replication - Inbreeding always increases these ( homozygotes - Barr bodies are an example of ( faculatative heterochromatin - Mother of 2N = 46 Down?s child ( translocation carrier
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