function allele b/c it is complemented by the wild type allele. The wild type
allele complements the mutant allele & the phenotype expressed is wild type, it
is complementing the deficiency.
- Here is an important point. When mutant alleles are in the homozygous state,
they cannot complement each other. What does he mean by that? They’re said
to be allelic.
- Imagine that the coding sequence mutant allele & the promoter mutant allele
together in what would be a molecular heterozygote. This means they differ in
terms of their molecular structure so they look heterozygous. What we’re
going to see is that as far as the trait is concerned, they look homozygous b/c
what we end up with in the top allele is a non-functional protein & the bottom
allele is no protein at all so no function. Together, there is no function, there is
still going to be whatever the mutant is & what we’re seeing here again is that
the 2 mutant alleles cannot complement each other so the phenotype is mutant
& this is an indicator of what is known as allelism, that is the small acds allele is
allelic & allelism would be with apro allele.
- Here we have a bunch of different examples of different allelisms that would
not complement each other as shown in the square box in the slide.
- Mutant alleles 1 through 5, you can see that those mutant alleles give rise to
altered or non-functional protein can either reside in the coding sequence as we
see there at the top 2 alleles, could be giving rise to an altered stop codon as is
the case with the second or third allele, could give rise to a loss of an intron,
could also account for that. The loss of an intron could result in a mis-spliced
protein for example or a mis-spliced mRNA giving rise to a dysfunctional
protein. Then finally we will find just like the example we already seen before,
the mutation is occurring in the promoter region.
- All of these alleles in combination with each other in a diploid organism
would not complement, they do not give rise to function, you see the mutation
& therefore you would know that they are allelic. So the mutant alleles do not
complement each other so the phenotype is mutant & this is an indicator of
- Here is an important point, while the locus may appear heterozygous at the
molecular level and he touched upon this, the individual would appear
homozygous at the phenotypic level.
- For example, let us consider a heterozygote of those 2 alleles right here &
they were both dysfunctional or mutant alleles, alleles 1 & allele 2 while they
look heterozygous at the molecular level, they would appear as homozygotes
at the trait level.
- Does that make sense? Because it should make sense. So it all depends on
your level of resolution. At the molecular level, they look heterozygous but at
the trait level, they will produce a mutant so it will appear homozygous. Let us
consider some examples and actually make this a bit more tangible.
- We can see behind him a picture of tomatoes. They provide great examples
of application of Mendelian traits in giving rise to variation in populations.
- So a few words about tomatoes to begin with. They were domesticated in
south & central America roughly 5000 years ago though that is being revised,
possibly 6000 years ago. They were brought by European conquistadors, the
Spanish back to Europe some time b/w 1521 & 1544 where they were known
by various names. By 1622, there were already 4 varieties of tomatoes & we’re
going to see the importance of this very shortly. In fact we’ll see this in today’s
lecture, 4 varieties of red, yellow, orange & gold. By 1700, 7 varieties & things
increased from there. A very long history of breeding & this makes tomatoes a
very useful model for understanding genetic phenomena.
- Let’s give some consideration to tomatoes then with regards to our test for