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Clemson BCHM 3050 - Case Study on Skin Color

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BCHM 3050 1st Edition Lecture 28 Outline of Last Lecture I. Mutationsa. Substitution b. FrameshifII. Chromosome-Level MutationsIII. Mechanisms for Point MutationsIV. Transition and Transversion MutationOutline of Current Lecture I. Eugenic MovementII. Historical CaseIII. History of Skin ColorIV. The Yin and Tang of RadiationsV. Melanocytes Make MelaninVI. Sub-Saharan Africans adapted to have darker skinVII. Adaptation permitting light skin colorVIII. Golden Fish versus Black Pigmented Fish StudyCurrent LectureI. Eugenic Movementa. Eugenics” movement in scienceb. 1883, coined in England, by Sir Francis Galton, a cousin of Charles Darwinc. Greek word meaning “well born” or “ of good origins or breeding”d. “Science” of improving qualities of racee. The Triangle of life – Environment, education, heritageII. Historical Casea. Woman was diagnosed with feeble mindedness (IQ of 56) and was sterilized so that she could not have any more kids and pass on the traits of feeble mindednessb. This is a failure in the field of scienceIII. History of Skin Colora. Close to the equator – skin color is darkerb. Far away from the equator – skin color is lighterc. Migration of our ancestors out of Africa – first establishment of civilizationi. Migrated out 100,000 years agoIV. The Yin and Tang of RadiationsThese notes represent a detailed interpretation of the professor’s lecture. GradeBuddy is best used as a supplement to your own notes, not as a substitute.a. Vitamin D production proportional to light penetrationb. Folic acid (Vitamin B9) destruction proportional to light penetrationi. Too much radiation  destroys folic acidii. Expecting mothers need folic acid to allow for development of spinal chord and maxillary features in child  without folic acid, child my dieiii. In order for the people of Africa to adapt and not lose too much folic acid, they had extremely dark skin because of the harsh sunlight  allows them to not absorb as much sunlight and maintain folic acid levels1. Dark skin caused by high levels of melaninc. Closer to the equator has more exposure to high amount of UV radiationd. UV radiation causes cross-links and damages in DNAe. The darker the skin, do not absorb as much UV radiationV. Melanocytes Make Melanina. More melanocytes = more melaninb. When people with dark skin moved away from harsh sunlight, they could not absorb the little bit of sunlight needed to aid them with melanini. Over time, the people adapted to have lighter skin color in order to be able to obtain melaninVI. Sub-Saharan Africans adapted to have darker skina. Mutation in MC1R, a gene responsible for melanin production, allowed positive selection for dark skin in early sub-Saharan Africans about 130,000 years agob. When we evolved from monkeys, lost hair and had light pink skin so we needed to adapted to obtained dark skin colorVII. Adaptation permitting light skin colora. Many genes control melanin levelsb. Vitamin D: UV light  makes Vitamin Dc. Folic Acid (Vitamin B9): UV light  destroys vitamin B9d. Lots of sunlight  Africa  increased melanine. Cold/less sunlight  N. Europe  less melaninVIII. Golden Fish versus Black Pigmented Fish Studya. How was the gene responsible for the golden phenotype identified?i. Positional cloning – identify where a particular gene is; cloning all genes until I locate the position of the gene of interestii. Slc24a5 is the gene responsible for golden colorb. Knock-down using morpholinos?i. Morpholinos prevent mRNA from being expressedii. Used in reverse genetics, morpholinos are synthetic oligonucleotides, which can bind RNA sequences thereby blocking translationiii. Synthetic RNA molecule which is designed to bind to RNA to prevent it from getting translatediv. Can make a morpholino target a specific position in cellv. Prevent mRNA from getting translatedvi. Knockdown of slc24a5 with morpholinos in wildtype larvae phenocopies the golden mutationvii. Wild type – fish without mutationsviii. Golden larvae – lack melanin pigmentsix. Wild type larvae injected with slc24a5 morpholinos – wild type larvae started looking like golden larvaex. Shows that this gene is responsible for pigment in zebrafish  also responsible for skin color in humans1. By removing one gene, fish lost its melaninc. RNA in-situ hydridization to detect RNA in zebrafish larvaei. Take cell and make an RNA glowii. Send a color that attached to the RNA of interestiii. Add digoxigenin- labeled probe into cell and it attached to mRNA  send another enzyme to make it glow  able to locate where the mRNA is now because it is colorediv. Wildtype fish could pick up the dye-color but the golden fish couldn’t because they lacked the gene needed for the color to bind tov. Sent probe to seek out a gene, but it was not present in the mutant  showed scientists to determine that that gene was responsible for melanin productiond. How is this study relevant to human populations?i. Homology studies indicated that the human slc24a5 gene also is an ion transporter1. Search human gene pool for a similar gene, and found that humans havethe same gene 2. African decent – Ala 111 on slc24a5 gene3. European – Thr 111 on slc24a5 gene4. That change of one amino acid is contributes to the difference in skin colorii. Within this gene only a single SNP exists where the nucleotide G is converted to Aiii. Allele of slc24a5 with the nucleotide G codes for Alanine at position 111iv. Allele of slc24a5 with nucleotide A codes for Threonine at position 111 v. Dark skin – a G from mom and dadvi. Intermediate skin color – G from one parent and A from anothervii. Light skin – A from mom and dadviii. Skin color does not make you a fast


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Clemson BCHM 3050 - Case Study on Skin Color

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