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E. The Power of Independent Assortment

E. The Power of Independent Assortment 1. If you can assume that the genes assort independently, then you can calculate ‘single gene’ outcomes and multiply results together… 2. You can easily address more difficult multigene problems: (female) AaBbCcdd x AABbccDD (male)

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E. The Power of Independent Assortment

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  1. E. The Power of Independent Assortment 1. If you can assume that the genes assort independently, then you can calculate ‘single gene’ outcomes and multiply results together… 2. You can easily address more difficult multigene problems: (female) AaBbCcdd x AABbccDD (male) - how many types of gametes can each parent produce? - What is the probability of an offspring expressing ABCD? - How many genotypes are possible in the offspring? 2 x 3 x 2 x 1= 12 - how many phenotypes are possible in the offspring? 1 x 2 x 2 x 1 = 4 At A: At B: At C: At D:

  2. E. The Power of Independent Assortment 1. If you can assume that the genes assort independently, then you can calculate ‘single gene’ outcomes and multiply results together… 2. You can easily address more difficult multigene problems. As you can see, IA produces lots of variation, because of the multiplicative effect of combining genes from different loci together in gametes, and then combining them together during fertilization… we’ll look at this again; especially with respect to Darwin’s 3rd dilemma.

  3. F. WHY do these patterns occur? Meiosis: Gamete Formation a. Overview: In sexually reproducing species, gametes carry exactly ½ the genetic information as the parent; so that the fusion of gametes reconstitutes the correct genetic complement. 1n = 2 2n = 4 Fertilization (fusion)

  4. F. WHY do these patterns occur? Meiosis: Gamete Formation a. Overview: In sexually reproducing species, gametes carry exactly ½ the genetic information as the parent; so that the fusion of gametes reconstitutes the correct genetic complement. The divisional process that produces these special cells is called meiosis. Thus, meiosis ONLY occurs in reproductive tissue (ovary, testis), and only produces gametes. All other cells in multicellular organisms are produced by mitosis. Diploid Haploid MEIOSIS 1n = 2 2n = 4 Fertilization (fusion)

  5. F. WHY do these patterns occur? Meiosis: Gamete Formation a. Overview: In sexually reproducing species, gametes carry exactly ½ the genetic information as the parent; so that the fusion of gametes reconstitutes the correct genetic complement. The divisional process that produces these special cells is called meiosis. Thus, meiosis ONLY occurs in reproductive tissue (ovary, testis), and only produces gametes. All other cells in multicellular organisms are produced by mitosis. MEIOSIS has two divisional cycles, “reduction” and “division” Diploid Haploid MEIOSIS 1n = 2 2n = 4 Fertilization (fusion)

  6. F. WHY do these patterns occur? Meiosis: Gamete Formation a. Overview: b. Meiosis I: “The Reduction Cycle” - Prophase I: condensation in pairs possible crossing over

  7. F. WHY do these patterns occur? Meiosis: Gamete Formation a. Overview: b. Meiosis I: “The Reduction Cycle” - Prophase I: condensation in pairs possible crossing over - Metaphase I: Homologs align In PAIRS

  8. F. WHY do these patterns occur? Meiosis: Gamete Formation a. Overview: b. Meiosis I: “The Reduction Cycle” - Prophase I: condensation in pairs possible crossing over - Metaphase I: Homologs align In PAIRS - Anaphase I: Replicated chromosomes move to opposite poles

  9. F. WHY do these patterns occur? Meiosis: Gamete Formation a. Overview: b. Meiosis I: “The Reduction Cycle” - Prophase I: condensation in pairs possible crossing over - Metaphase I: Homologs align In PAIRS - Anaphase I: Replicated chromosomes move to opposite poles - Telophase – Prophase II transition

  10. F. WHY do these patterns occur? Meiosis: Gamete Formation a. Overview: b. Meiosis I: “The Reduction Cycle” - Prophase I: condensation in pairs possible crossing over - Metaphase I: Homologs align In PAIRS - Anaphase I: Replicated chromosomes move to opposite poles - Telophase – Prophase II transition PLOIDY REDUCED 2n parent cell 1n daughter cells

  11. F. WHY do these patterns occur? Meiosis: Gamete Formation a. Overview: b. Meiosis I: “The Reduction Cycle” c. Meiosis II: “The Division Cycle” Like mitosis, but a haploid cell… chromsomes line up in single file in Metaphase II, and sister chromatids (of replicated chromosomes) separate and move to opposite poles.

  12. F. WHY do these patterns occur? Meiosis: Gamete Formation a. Overview: b. Meiosis I: “The Reduction Cycle” c. Meiosis II: “The Division Cycle” d. Variations in the Process: In spermatogenesis: Karyokinesis is equal and cytokinesis is equal, resulting in 4 equal-sized sperm.

  13. WHY do these pattern occur? • Meiosis: Gamete Formation • a. Overview: • b. Meiosis I: “The Reduction Cycle” • c. Meiosis II: “The Division Cycle” • d. Variations in the Process: • In oogenesis, karyokinesis is equal (dividing the genetic information exactly in half), but cytokinesis is unequal, with one daughter cell getting the majority of the cytoplasm and organelles. The smaller may/may not be able to divide. These are ‘polar bodies’

  14. III. Uniting Genetics and Cell Biology A. The Chromosomal Theory – Sutton and Boveri Theodor Boveri Walter Sutton

  15. III. Uniting Genetics and Cell Biology A. The Chromosomal Theory – Sutton and Boveri Saw homologous chromosomes separating (segregating). If they carried genes, this would explain Mendel’s first law. A a Theodor Boveri Walter Sutton

  16. III. Uniting Genetics and Cell Biology A. The Chromosomal Theory – Sutton and Boveri And if the way one pair of homologs separated had no effect on how others separated, then the mvmnt of chromosomes would explain Mendel’s second law, also! A A b B a a B b Theodor Boveri AB ab Ab aB Walter Sutton

  17. III. Uniting Genetics and Cell Biology A. The Chromosomal Theory – Sutton and Boveri This was a major achievement in science. The patterns of heredity had been associated with physical entities in biological cells. The movement of chromosomes correlated with Mendel’s patterns. Scientist now went about testing if this relationship was causal – and they found it was. Theodor Boveri Walter Sutton

  18. III. Uniting Genetics and Cell Biology A. The Chromosomal Theory – Sutton and Boveri B. Solving Darwin’s Dilemma – The Source of Variation

  19. III. Uniting Genetics and Cell Biology A. The Chromosomal Theory – Sutton and Boveri B. Solving Darwin’s Dilemma – The Source of Variation Independent Assortment produces an amazing amount of genetic variation. Consider an organism, 2n = 4, with two pairs of homologs. They can make 4 different gametes (long Blue, Short Red) (Long Blue, Short Blue), (Long Red, Short Red), (Long Red, Short blue). Gametes carry thousands of genes, so homologous chromosomes will not be identical over their entire length, even though they may be homozygous at particular loci. Well, the number of gametes can be calculated as 2n or

  20. III. Uniting Genetics and Cell Biology A. The Chromosomal Theory – Sutton and Boveri B. Solving Darwin’s Dilemma – The Source of Variation Independent Assortment produces an amazing amount of genetic variation. Consider an organism with 2n = 6 (AaBbCc) …. There are 2n = 8 different gamete types. ABC abc Abc abC aBC Abc AbC aBc

  21. III. Uniting Genetics and Cell Biology A. The Chromosomal Theory – Sutton and Boveri B. Solving Darwin’s Dilemma – The Source of Variation Independent Assortment produces an amazing amount of genetic variation. Consider an organism with 2n = 6 (AaBbCc) …. There are 2n = 8 different gamete types. And humans, with 2n = 46? ABC abc Abc abC aBC Abc AbC aBc

  22. III. Uniting Genetics and Cell Biology A. The Chromosomal Theory – Sutton and Boveri B. Solving Darwin’s Dilemma – The Source of Variation Independent Assortment produces an amazing amount of genetic variation. Consider an organism with 2n = 6 (AaBbCc) …. There are 2n = 8 different gamete types. And humans, with 2n = 46? 223 = ~ 8 million different types of gametes. And each can fertilize ONE of the ~ 8 million types of gametes of the mate… for a total 246 = ~70 trillion different chromosomal combinations possible in the offspring. ABC abc Abc abC aBC Abc AbC aBc

  23. III. Uniting Genetics and Cell Biology A. The Chromosomal Theory – Sutton and Boveri B. Solving Darwin’s Dilemma – The Source of Variation Independent Assortment produces an amazing amount of genetic variation. And each can fertilize ONE of the ~ 8 million types of gametes of the mate… for a total 246 = 70 trillion different chromosomal combinations possible in the offspring. YOU are 1 of the 70 trillion combinations your own parents could have made. IA creates a huge amount of genetic variation, and that doesn’t include crossing over!!!!

  24. III. Uniting Genetics and Cell Biology A. The Chromosomal Theory – Sutton and Boveri B. Solving Darwin’s Dilemma – The Source of Variation C. Modification to Evolutionary Theory Darwin’s Model Sources of VariationCauses of Change ????????????????  VARIATION  NATURAL SELECTION (use and disuse??)

  25. III. Uniting Genetics and Cell Biology A. Early Studies B. Divisional Processes C. The Chromosomal Theory – Sutton and Boveri D. Solving Darwin’s Dilemma – The Source of Variation E. Modification to Evolutionary Theory Darwin’s Model Sources of VariationCauses of Change Independent Assortment  VARIATION  NATURAL SELECTION

  26. IV. Modifications to Mendelian Patterns

  27. IV. Modifications to Mendelian Patterns - Overview: Mendels conclusions regarding dominance, equal segregation, independent assortment, and independent effects hold for many genes and traits. But they are not true of ALL traits.

  28. IV. Modifications to Mendelian Patterns - Overview: Mendels conclusions regarding dominance, equal segregation, independent assortment, and independent effects hold for many genes and traits. But they are not true of ALL traits. Here, we will consider how the effect of a gene is influenced at three levels:

  29. IV. Modifications to Mendelian Patterns - Overview: Mendels conclusions regarding dominance, equal segregation, independent assortment, and independent effects hold for many genes and traits. But they are not true of ALL traits. Here, we will consider how the effect of a gene is influenced at three levels: - Intralocular (effects of other alleles at this locus)

  30. IV. Modifications to Mendelian Patterns - Overview: Mendels conclusions regarding dominance, equal segregation, independent assortment, and independent effects hold for many genes and traits. But they are not true of ALL traits. Here, we will consider how the effect of a gene is influenced at three levels: - Intralocular (effects of other alleles at this locus) - Interlocular (effects of other genes at other loci)

  31. IV. Modifications to Mendelian Patterns - Overview: Mendels conclusions regarding dominance, equal segregation, independent assortment, and independent effects hold for many genes and traits. But they are not true of ALL traits. Here, we will consider how the effect of a gene is influenced at three levels: - Intralocular (effects of other alleles at this locus) - Interlocular (effects of other genes at other loci) - Environmental (the effect of the environment on determining the effect of a gene on the phenotype)

  32. IV. Modifications to Mendelian Patterns - Overview: Mendels conclusions regarding dominance, equal segregation, independent assortment, and independent effects hold for many genes and traits. But they are not true of ALL traits. Here, we will consider how the effect of a gene is influenced at three levels: - Intralocular (effects of other alleles at this locus) - Interlocular (effects of other genes at other loci) - Environmental (the effect of the environment on determining the effect of a gene on the phenotype) And finally, we will examine the VALUE of an allele – are there “good genes” and “bad genes”?

  33. IV. Modifications to Mendelian Patterns A. Intralocular Interactions A a

  34. IV. Modifications to Mendelian Patterns A. Intralocular Interactions 1. Complete Dominance: - The presence of one allele is enough to cause the complete expression of a given phenotype.

  35. IV. Modifications to Mendelian Patterns A. Intralocular Interactions 1. Complete Dominance: 2. Incomplete Dominance: - The heterozygote expresses a phenotype between or intermediate to the phenotypes of the homozygotes.

  36. IV. Modifications to Mendelian Patterns A. Intralocular Interactions 1. Complete Dominance: 2. Incomplete Dominance: 3. Codominance: - Both alleles are expressed completely; the heterozygote does not have an intermediate phenotype, it has BOTH phenotypes. ABO Blood Type: A = ‘A’ surface antigens Genotypic and phenotypic ratios of F1 x F1 crosses are both 1:2:1

  37. IV. Modifications to Mendelian Patterns A. Intralocular Interactions 1. Complete Dominance: 2. Incomplete Dominance: 3. Codominance: - Both alleles are expressed completely; the heterozygote does not have an intermediate phenotype, it has BOTH phenotypes. ABO Blood Type: A = ‘A’ surface antigens B = ‘B’ surface antigens Genotypic and phenotypic ratios of F1 x F1 crosses are both 1:2:1

  38. IV. Modifications to Mendelian Patterns A. Intralocular Interactions 1. Complete Dominance: 2. Incomplete Dominance: 3. Codominance: - Both alleles are expressed completely; the heterozygote does not have an intermediate phenotype, it has BOTH phenotypes. ABO Blood Type: A = ‘A’ surface antigens B = ‘B’ surface antigens O = no surface antigen from this locus

  39. IV. Modifications to Mendelian Patterns A. Intralocular Interactions 1. Complete Dominance: 2. Incomplete Dominance: 3. Codominance: - Both alleles are expressed completely; the heterozygote does not have an intermediate phenotype, it has BOTH phenotypes. ABO Blood Type: A = ‘A’ surface antigens B = ‘B’ surface antigens O = no surface antigen from this locus Phenotype Genotypes A AA, AO B BB, BO O O AB AB codominance AB Phenotype

  40. IV. Modifications to Mendelian Patterns A. Intralocular Interactions 1. Complete Dominance: 2. Incomplete Dominance: 3. Codominance: 4. Multiple Alleles: - While not really specifying an ‘interaction’, it does raise a complication of looking at a single trait.

  41. IV. Modifications to Mendelian Patterns A. Intralocular Interactions 1. Complete Dominance: 2. Incomplete Dominance: 3. Codominance: 4. Multiple Alleles: - While not really specifying an ‘interaction’, it does raise a complication of looking at a single trait. - You might presume that a ‘single-gene’ trait could only have a maximum of three phenotypes (AA, Aa, aa). But with many alleles possible for a gene (as for A,B,O), there are many diploid combinations and effects that are possible (as in the 4 phenotypes for the A,B,O system).

  42. IV. Modifications to Mendelian Patterns A. Intralocular Interactions 1. Complete Dominance: 2. Incomplete Dominance: 3. Codominance: 4. Overdominance – the heterozygote expresses a phenotype MORE extreme than either homozygote – see class notes.

  43. IV. Modifications to Mendelian Patterns A. Intralocular Interactions - Summary and Implications: populations can harbor extraordinary genetic variation at each locus, and these alleles can interact in myriad ways to produce complex and variable phenotypes.

  44. IV. Modifications to Mendelian Patterns • A. Intralocular Interactions • - Summary and Implications: • populations can harbor extraordinary genetic variation at each locus, and these alleles can interact in myriad ways to produce complex and variable phenotypes. • Consider this cross: AaBbCcDd x AABbCcDD • Assume: • The genes assort independently A and a are codominant • B is incompletely dominant to b • C is incompletely dominant to c • D is completely dominant to d • How many phenotypes are possible in the offspring?

  45. IV. Modifications to Mendelian Patterns • A. Intralocular Interactions • - Summary and Implications: • populations can harbor extraordinary genetic variation at each locus, and these alleles can interact in myriad ways to produce complex and variable phenotypes. • Consider this cross: AaBbCcDd x AABbCcDD • Assume: • The genes assort independently A and a are codominant • B is incompletely dominant to b • C is incompletely dominant to c • D is completely dominant to d • How many phenotypes are possible in the offspring? • A B C D • x 3 x 3 x 1 = 18 • If they had all exhibited complete dominance, there would have been only: • x 2 x 2 x 1 = 4 • So the variety of allelic interactions that are possible increases phenotypic variation multiplicatively. In a population with many alleles at each locus, there is an nearly limitless amount of phenotypic variability.

  46. IV. Modifications to Mendelian Patterns A. Intralocular Interactions B. Interlocular Interactions: The genotype at one locus can influence how the genes at other loci are expressed.

  47. IV. Modifications to Mendelian Patterns A. Intralocular Interactions B. Interlocular Interactions: The genotype at one locus can influence how the genes at other loci are expressed. 1. Epistasis: one gene curtails the expression at another locus; the phenotype in the A,B,O blood group system can be affected by the genotype at the fucosyl transferase locus.

  48. IV. Modifications to Mendelian Patterns A. Intralocular Interactions B. Interlocular Interactions: The genotype at one locus can influence how the genes at other loci are expressed. 1. Epistasis: one gene curtails the expression at another locus; the phenotype in the A,B,O blood group system can be affected by the genotype at the fucosyl transferase locus. This locus makes the ‘H substance’ to which the sugar groups are added to make the A and B surface antigens.

  49. IV. Modifications to Mendelian Patterns A. Intralocular Interactions B. Interlocular Interactions: The genotype at one locus can influence how the genes at other loci are expressed. 1. Epistasis: one gene curtails the expression at another locus; the phenotype in the A,B,O blood group system can be affected by the genotype at the fucosyl transferase locus. This locus makes the ‘H substance’ to which the sugar groups are added to make the A and B surface antigens. A non-function ‘h’ gene makes a non-functional foundation and sugar groups can’t be added – resulting in O blood regardless of the genotype at the A,B,O locus

  50. IV. Modifications to Mendelian Patterns A. Intralocular Interactions B. Interlocular Interactions: The genotype at one locus can influence how the genes at other loci are expressed. 1. Epistasis: one gene curtails the expression at another locus; the phenotype in the A,B,O blood group system can be affected by the genotype at the fucosyl transferase locus. This locus makes the ‘H substance’ to which the sugar groups are added to make the A and B surface antigens. A non-function ‘h’ gene makes a non-functional foundation and sugar groups can’t be added – resulting in O blood regardless of the genotype at the A,B,O locus So, what are the phenotypic ratios from this cross: HhAO x HhBO?

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