Chapter 3: Extensions to Mendel's Laws Flashcards
What about God’s Sovereignty and advances in science/beauty & complexity?
- He decides when discoveries occur
- Beauty and complexity are for His glory
What causes phenotypic variations that challenge Mendelian analysis?
- No definitively dominant or recessive allele (incomplete dominance or codominance)
- More than two alleles exist
- Multiple genes involved
- Gene-environment interactions
What are the options of dominance?
- Complete dominance: hybrid resembles on of the two parents
- Incomplete dominance: hybrid resembles neither parent (mix) 1:2:1 geno & phenotypic ratio
- Codominance: hybrid shows traits from both parents: both together 1:2:1 geno & phenotypic ratio
(2 normal alleles (enzyme), 1 normal alleles (less enzyme), 0 normal alleles, (no enzyme)
What determines dominance? What does this mean for Mendel’s laws?
- type and function of protein
- does not negate Mendel’s laws of segregation
- interpretation of pheno/genotype relations is more complex
What about when a gene has more than two alleles?
- Multiple alleles in population but individuals only have two
- Dominance is relative to second allele and is unique to allele pair
ie blood type: I^A, I^B, i –> A, B, AB, O
A has antibodies for B, B for A, AB for neither, and O for both
Pleiotropy:
one gene–> many traits,
- ie Maori men, gene controlling cilia and flagella causes respiratory and sterility issues
- heterozygous have visible phenotype
- homozygous could be lethal (not all genes equally viable)
What is the seed pattern example for multiple alleles? What about histocompatibility?
Seed Pattern: There are 5 alleles: Marbled 1 > marbled 2 > spotted = dotted > clear
Histocompatibility: 100s alleles, (protein on surface of all cells but RBS and sperm for proper immune response)
- gene has 400-1200 alleles each, each codominant, each genotypes produces a distinct phenotype, producing enormous variation
What about mutations and alleles?
Mutations (spontaneous chance variations) produce new alleles
- occurring in gamete-producing cells potential to transfer to offspring (10-4 -10-6 occurrence)
- resulting in phenotype variation useful for following gen transmission
What is the nomenclature of alleles?
- allele frequency: percent of total number of gene copies of one allele in a population
- wild type (+): most common
- mutant: rare allele
- monomorphic: 1 common wild-types
- polymorphic: more than 1 common wild-type
–high frequency alleles of polymorphic genes are common variants
What happens when two or more genes influence a single trait?
- novel phenotypes: result from gene interactions
Vary from F2 9:3:3:1 phenotypic ratio - fewer phenotypes than expected due to complementary gene action
- epistasis: gene masks phenotype of another gene
- Redundant: gene performs same function
What about complementary gene action?
Two genes are at work: 9:7 dihybrid cross
- need both enzymes to work so need at least one of each dominant allele
What are the terms of epistasis?
epistatic: allele that does masking (active)
hypostatic: allele that is masked (acted upon)
- dominant (homo/hetero for function) or recessive (homo for function)
What is an example of redundant genes?
- leaf size in corn - A & B necessary
- “normal” : “skinny” 15:1
(skinny only if both: aabb)
What are the different dihybrid F2 phenotypic ratio?
No gene interactions:
- 9:3:3:1
Complementary interaction: 1 D allele of each gene necessary
- 9:7
Recessive epistasis: Homo r of one gene masks both alleles of other
- 9:3:4
Dominant epistasis I: D allele one gene hides affects both other gene alleles
- 12:3:1
Dominant epistasis II: D allele hides effect of dominant allele of other gene
- 13:3
Redundancy: only one D allele either genes necessary
- 15:1
Why does the same genotype not always produce the same phenotype?
- modifier genes
- environment
- pure chance
