Genes and Inheritance [8]: Huntingdons (High band Biology)
Articles Blog

Genes and Inheritance [8]: Huntingdons (High band Biology)

A Level Biology: Genes and Inheritance 8 – Huntingdon’s Hi! Welcome to my eight video on the series
about Genes. Today, we are looking at Huntingdon’s disease. Huntingdon’s disease affects thousands
of people in the UK and it is caused by a dominant allele, which unfortunately means
that you only need one of those alleles for the disease to be expressed. Technically,
there is no such thing as a carrier with Huntingdon’s disease. You either are a sufferer or you’re
healthy. Some of the symptoms of Huntingdon’s disease,
because it is a disease that affects the brain, it’s related to things like loss of muscle
control, forgetfulness, loss of understanding. Something else with Huntingdon’s disease,
it is usually later onset. You don’t start to notice the symptoms of the disease until
you reach roughly around 30 years old; in some cases, sooner and in some cases, later.
But generally speaking, Huntingdon’s disease tends to be late onset. We have here a family tree diagram and the
family tree diagram shows whether the individuals have the disease or do not have the disease.
If we look at the top line first, the parents there. Karl is a man with Huntingdon’s and
Sarah is a woman without. I would just give you a second to think about what you think
the genotype of Karl and Sarah might be. Sarah should be quite straightforward because
Sarah is non-sufferer and because the disease is caused by a dominant allele, then the only
possible permutation that she could be is hh. Karl is a bit trickier to establish. Karl
could be either heterozygous or homozygous. He must obviously have the Huntingdon’s
disorder, so he must have at least one allele. But deciding whether he is HH or Hh, then
you need to look at their offspring. If you look at the three offspring with Liam, Kate
and Susan, then Kate is the one that gives away what Karl’s genotype is. Because they
can give birth to an offspring that doesn’t have the disease, it therefore means that
Karl must at least have one healthy allele. Therefore, Karl must be Hh and that’s his
genotype. So we can probably establish all of the other
offspring. We can actually look at what their genotypes are and their partner’s genotypes
as well. So we can see that Lisa, because she’s healthy, that means she must have
both healthy alleles. Liam, because he is a sufferer and because Sarah is his mother,
he must have at least one healthy allele. Kate is healthy. Susan must be a sufferer,
but also must heterozygous and Sean, obviously is healthy has both recessive alleles. On
the bottom row, you have John, Alex, Jo and Paul, who are all healthy and who do not have
the disease and you have Emma who is one sufferer and again her genotype, because her parents
are Susan and Sean, she must have received the recessive h from Sean and because she
actually has the disease, she must have received the dominant Huntingdon’s allele from Susan. In summary, Huntingdon’s affects the brain
so it affects things like memory and it can affect things like movement, as well. Why there are no such things as carrier with
Huntingdon’s? Because it is caused by a dominant allele,
it means that you either have it or you do not. You do not carry the allele because you
either have the disease or you won’t. So if a heterozygous father with Huntingdon’s
breeds with a healthy mother, what is the probability that the child is a sufferer?
Draw a diagram to help. So heterozygous father, heterozygous means
he’s got two different alleles in his genotype so Hh. Half of the sperm, he has H which is
causing Huntingdon’s and h allele which means that it is healthy. The mother has this
genotype so hh. All of her eggs, she carries h. So you can see there, that the offspring,
these two here would be completely healthy and these two would be sufferers. So it is
2/4 and therefore it is 50% [end of audio – 04:43]
A Level Biology: Genes and Inheritance 8 – Huntingdon’s Page…1

Leave a Reply

Your email address will not be published. Required fields are marked *

Back To Top