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Lecture 11; 2007
Biology 207; Section B2; Good
Lecture#11 - Alleles, Dominance, and Morphs
Readings: Griffiths et al (2000)
8th Edition: pp. 27-36, 192-199 + 535-537
7th Edition: Ch. 2 pp 28-34 & Ch. 4 pp 109-111
Assigned Problems:
8th: Ch.2: 1-5, 7-13 ; Ch.6: 7-18, 22-24, 51-52
7th: Ch.2: 1-3, 7, 9-13 ; Ch.4: 1-2, 4-7, 9
Concepts:
How do genes behave in diploids?
1. Offspring from heterozygous parents may have a recessive phenotype, because of
the segregation of alleles in meiosis.
2. Dominance/recessiveness is not always complete.
3. Genetic tests can identify mutations that have elevated, reduced, eliminated, or
changed functions (Muller's Morphs)
Alleles of genes do not always exhibit simple Dominance/Recessive relationship:
Incomplete dominance (semi-dominance) Fig. 6-9
Sometimes there is an intermediate (or blended) phenotype in the heterozygote
Example in "Four-o'clock" plants or Snapdragons
Strains have flowers with either:
Red petals CRed / CRed - homozygotes
White petals CWhite / CWhite - homozygotes
Heterozygote CRed / CWhite = has a pink colour (intermediate between the two
homozygotes)
Co-dominance
In certain circumstances both alleles can be seen in the phenotype.
Example: Human Blood types HbS and HbA; Figure 4-6
Can see both alleles and thus distinguish the homozygotes from the heterozygote. Note:
It is interesting that the heterozygote has enhanced resistance to malaria and there this
trait is a classic example of heterozygote advantage.
Note: sickle-cell anemia is recessive phenotype of HbS/HbS individuals
"Muller's morphs" classification - (1932)
H.J. Muller (1946) was awarded Nobel prize for his contributions to radiation genetics.
He designated five classes of mutant as "amorph, hypomorph, hypermorph, neomorph
and antimorph. - "morph" meaning "form" Fig. 16-22 (8th) 15-12(7th) Figure 16.22
below distinquishes various functional classes of mutants.
Amorph - A- absence
- mutation with complete absence of wild type function
- also called "null" mutation - no function - no expression of wild type gene at any level
- eg. gene deleted - deletion
- loss-of-function - loss of enzymatic function
Hypomorph - hypo -> less than
-> less than wild type level of expression of the wild type gene - same quality
- range from slightly less than wild type to almost complete loss (amorph) - reduction-of
function - also referred to as "leaky" - reduced activity of enzyme
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Lecture 11; 2007
Biology 207; Section B2; Good
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Lecture 11; 2007
Biology 207; Section B2; Good
Hypermorph - hyper -> more than
-> more than wild type level of gene expression
- same quality more quantity
- gene duplication - 2 genes -> more product
- gain-of-function - more of the same
- more enzyme activity than wild type
Neomorph - neo -> new
- mutations which create a new and different from the wild type function for the gene
- gain-of-function - novel function
Antimorph - anti -> against
- mutant gene product results in a reduction or loss in the function and interferes with
normal gene product from any wild type gene that may be present
See: Supplement on "Muller's Morphs" below
Summary - last two lectures
The several schemes for classifying mutations are not mutually exclusive.
They describe mutations at different levels
- DNA, chemical level - e.g. frameshift,
- gene product level - e.g. functional/non-functional
- phenotypic level, mutant vs wild type
"Muller's Morphs" classify all types of mutations
Allelic interactions give us: dominant/recessive
Co-dominance; Incomplete dominance
Forward versus Reverse Genetics:
The description of mutants using a classical approach is often now referred to as
“Forward Genetics”. The gene is first identified by a mutant allele, and then the gene is
later cloned and analysed at a molecular level to understand (a) what the mutation is
and (b) how mutations allow us to dissect gene function.
Reverse genetics is a much more recent phenomena, in which you first identify a
mutation in your gene of interest and then you attempt to look at gene function. There
are a number of approaches to identifying genotypes with mutations in your gene of
interest, some of which will cover at later points in the course.
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