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Mendelian Genetics How Genes Work Who Are You? Phenotype – How you look; PHysical appearance Genotype – Your genetic makeup; GENEs Father of Genetics Modern genetics began with Gregor Mendel’s quantitative experiments with pea plants Stamen Carpel Figure 9.2A, B White Mendel crossed pea plants that differed in certain characteristics and traced the traits from generation to generation This illustration shows his technique for cross-fertilization Figure 9.2C 1 Removed stamens from purple flower Stamens Carpel PARENTS (P) 2 Transferred Purple pollen from stamens of white flower to carpel of purple flower 3 Pollinated carpel matured into pod 4 OFFSPRING (F1) Planted seeds from pod Genetics Basics Chromosomes occur in pairs, one from MOM, one from DAD (homologues) Genes are carried on chromosomes Genes code for a trait or characteristic (I.e. hair color) Alternate forms of that trait are called ALLELES (ie. Blond, brown, redhead, etc) Alleles… Alleles can be dominant or recessive Heterozygous vs. homozygous Only way to “see” a recessive trait? Mendel ‘s basic laws Law of Segregation Law of Independent Assortment The chromosomal basis of Mendel’s principles Figure 9.17 Walter Sutton’s Theory of Chromosomal Inheritance (Mendel’s proof) Gametes contribute to heredity via nuclear material (chromosomes) Homologues segregate during meiosis Homologues separate independently of other homologous pairs Probability Mathmatical model of how often specific events will happen # of occurances/# of attempts Punnett Square Visual representation or model of – what alleles can be present in gametes – how those alleles can recombine in offspring Used to determine the probability of offspring’s genetic makeup Monohybrid Cross One gene – 2 alleles considered (one from mom, one from dad Dihybrid Cross 2 genes – 4 alleles considered How can we determine Homovs. heterozygous individuals? Test Cross – Must use homo recessive to conduct cross in order to “see” the questionable allele What Mendel Didn’t See Multiple alleles Codominance Epistasis Polygenic traits or Continuous Variation Pleiotropy Incomplete Dominance or “blended inheritance” Environmental Effects Sex linked and sex influenced traits CoDominance – Both alleles expressed at the same time; both dominant Incomplete dominance: neither allele is fully dominant (blended inheritance) Figure 9.12Ax Epistasis Sequential action of genes – Product of one gene influences another (one gene gives “permission” for another allele to work – Gene action acts as a biochemical pathway & feedback inhibition Ex: Indian corn coloration Pleiotropy Where one allele may have multiple effects on phenotype – Normal and sickle red blood cells Figure 9.14x1 Individual homozygous for sickle-cell allele Sickle-cell (abnormal) hemoglobin Abnormal hemoglobin crystallizes, causing red blood cells to become sickle-shaped Sickle cells Clumping of cells and clogging of small blood vessels Breakdown of red blood cells Physical weakness Impaired mental function Anemia Heart failure Pneumonia and other infections Pain and fever Paralysis Brain damage Accumulation of sickled cells in spleen Spleen damage Damage to other organs Rheumatism Kidney failure Continuous Variation or Polygenic Traits Multiple genes acting to influence a characteristic – Produces gradual changes, not distinct “borders” Ie. Height, weight, nose length, skin pigment P GENERATION aabbcc (very light) AABBCC (very dark) F1 GENERATION AaBbCc Sperm Fraction of population AaBbCc Skin pigmentation F2 GENERATION Figure 9.16 Environmental Influence Example animals = color change of fur in arctic Same eyes, different lighting Multiple Alleles More than one allele per gene 3 alleles (ABO) – 4 phenotypes (A, B, AB, O) Uses concept of glycoproteins (sugar name tags or antigens) to mark cells Non-recognition of the correct “name tag” for blood type can cause agglutination Landsteiner Blood Groups – galactosamine – AA (homo) or AO (hetero) Type B – galactose – BB or BO Type AB – galactosamine + galactose (codominant) Type O – no sugar marker - OO Type A Blood Donor Facts Universal Donor Universal Recipient Rh factor Rh factor can be + or – + is like a “seen” name tag or antigen - is “invisible” Rh- moms that have Rh+ babies are subject to spontaneous abortions – Erythroblastosis fetalis – Controlled with an injectionof RhoGam to “hide” babies cells Sex Linked “Sex on the X” Specific trait/disorder is found on sex chromosome, usually the X Usually recessive traits Seen more often in males than females Ex: color blindness, hemophilia Barr Body inactivation In females, both X chromosomes are not metabolically active Random inactivation of one X chromosome may influence traits expressed