Lecture Week 3
Genetics and Heredity
- Gregor Mendel (1822-1884) & the discovery of the laws of heredity
- Background
- Mendel's pea plants 1857-1865
- Controlled breeding & extensive records
- Tracked simple traits
- First bred pure plants
- Next cross-bred different varieties
- Traits disappeared in first generation
- Cross-bred those & traits reappeared
- 3:1 ratio in traits
- The laws of heredity
- Particulate inheritance
- Law of Segregation
- Law of Independent Assortment
- Dominant & Recessive
- Forgotten and rediscovered
- Paper published in 1866
- No-one understood it; was ignored
- Re-discovered in 1900 by 3 separate botanists; de Vries, Correns, & Tschermark
- Chromosomes, Genes and mutations
- First came discovery of cell, nucleus (1820's) & cell division (mitosis)
- Chromosomes found in 1870's
- Duplicate & divide to create new cells
- Each species has set number- 46 for humans
- Come in pairs; one of each pair from each parent- Homologous Chromosomes
- Sex cell division produces gametes with 1/2 number (meiosis)
- First homologous pair off then divide
- Then duplicate & divide to produce gametes
- Mutations
- Hugo deVries- 1890's
- Studied primroses looking for source of variation
- Discovered "new" traits- mutations
- Closing in on Mendel's Laws when discovered Mendel's work
- Called units of inheritance "pangens" later contracted to "genes"
- Genes- term coined in 1909
- By 1880's, people suspect that chromosomes made up of smaller bits that controlled for certain structures
T. E. Morgan
- Professor at Columbia, fascinated by thought of mutations
- Decided to work with fruit flies
- First mutation discovered in 1910- White eyes
- Further work (& more mutations) proved that genes existed
- Important concepts
- Alleles- different types of the same gene
- Genotype- genetic constitution
- Phenotype- physical expression
- Homozygous- Homologous Pair with same allele
- Heterozygous- Homologous Pair with different alleles
- DNA - Deoxyribonucleic acid
- Studies during 1930's proved that chromosomes made up of DNA
- What it does is make proteins- strings of amino acids (20 different kinds of a.a.)
- Watson and Crick and the discovery of the shape of DNA- double helix 1950's
- Two backbones twisted around each other
- Base pairs connect as "steps" in center
- Four bases; A, G, C, & T
- A connects to T and G connects to C
- How DNA works
- Double helix allows "unzipping" of DNA
- During replication, new bases connect to each side of old; result 2 strands
- During protein synthesis, only part unzips
- messenger RNA copies gene
- goes out of nucleus where it connects with transfer RNA
- tRNA carries amino acids which connect to make a protein
- sequence of 3 bases equals a codon- codes for a particular amino acid
- 64 possible combos of base pairs; allows redundancy & 3 stop codes
- Mutation occurs when a base is changed (point mutation)
- Different base changes codon
- Since redundant, may not change amino acid
- If does, changes protein
- Population genetics and speciation
- Interbreeding populations of a species
- Where evolution occurs- changes in allele frequencies
- Total all genes in a population called the "gene pool"
- Changes in gene frequencies
- Mutations- introduces new traits into a population
- Gene flow- transfer of alleles between populations
- Genetic Drift- random events that change frequencies (including "founder effect")
- Speciation- when enough change has occurred that different populations are no longer the same species- often through reproductive isolation
- Gradualism
- When a slow accumulation of changes leads to speciation
- Adapting to conditions of particular enviro or to conditions that change slowly
- Punctuated Equilibrium
- Sudden changes giving rise to new species
- Mutations with large effects or rapidly changing environment
- Most of time Natural Selection "fine-tunes" to particular environment
- Example putting it all together- Sickle-Cell Trait
- Hemoglobin (in Red Blood Cells) has two pairs of proteins (2 alfa & 2 beta chains)
- Since genes are paired, one chain of each pair inherited from each parent
- Normal HbA (BetaABetaA)
- Beta chain 146 amino acids long
- Position 6- Glutamic Acid; codon CTC
- Mutation T>A; codon CAC, Valine
- Hemoglobin's job is to take up and release oxygen
- When both Beta chains have mutation (called HbS; BetaSBetaS)
- When oxygen released, cells "sickle"; become oddly shaped
- Valine causes Hb to stack up and make Red Blood Cells rigid
- Sickle cells then clog capillaries, get destroyed
- Many health effects from anemia; too few RBC's; die at an early age
- Yet Sickle-Cell trait very prevalent in certain populations
- More than mutation alone could account for
Something must be selecting it- but not homozygous, heterozygous (BetaABetaS)
- Distribution HbS coincides with distribution of malarial parasite Plasmodium falciparum, a very nasty form of malaria
- Heterozygous, having one Beta chain mutated and one normal
- Survive malaria better than homozygous
- Malaria carried in RBC
- Reproduce till fill cell, then burst out and infect other RBC's
- If one Beta chain HbS,
- Sickles easier when parasite grows because parasite uses up oxygen
- Sickled cells get destroyed, removing parasite from system quicker
- In malarial areas, homozygous people either die from malaria or from anemia, heterozygous survive
- This is called a Balanced Polymorphism
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