Normally, the 6th position of the beta chain of hemoglobin is a Glutamic acid, encoded on the DNA as GAG. The sickle cell mutation has the sequence GTG, resulting in a Valine in the 6th position instead.
There is one main difference between sickle cells and normal cells, sickle cells, created in a sickle or crescent shape, while normal cells are shaped like doughnuts. As a result of the shape of the sickle cells, they can only carry a fractional amount of oxygen and nutrients. So people effected by sickle cell anemia, suffer from shortness of breath and weakness.
See related link for picture of sickle cell and normal cell
it has less, DNA, and, the sickle-cell is half the size of a regular cell
21
codominant
*An allele is basically the different forms a particular gene can take (describes the various genotypes/phenotypes a gene can take).* For example there is an allele of a gene which codes for haemoglobin in red blood cells, which gives them their characteristic concave shape. But there can also be a mutation in that gene, which causes a different allele to be produced which gives it a sickle-cell shape, which leads to sickle-cell anaemia.
If both parents are trait carriers the chances of them having a child WITH sickle cell is 4 to 1. Probability says, 1 will not carry the trait OR have sickle cell, 2 will be trait carriers and 1 will have it. But Keep in mind that every time you have a child its like rolling dice. I have heard of people where all four kids have the disease. and i have 2 children with the disease and 1 that's normal.
Gene therapy
None. =]
codominant
codominant
codominant
The pro of sickle cell hemoglobin is that if you have only one allele for sickle cell hemoglobin and the other allele is normal, then you are immune to malaria.
Malaria
Overdominance is when the heterozygote has an advantage over both the recessive and dominant homozygotes. Sickle cell disease is an example of this. When the individual is homozygous for the sickle cell allele, sickle cell disease is shown. When the the individual is homozygous for the wildtype allele, they appear normal. However, when the individual is heterozygous, he or she appears normal and will also be resistent to malaria.
Since people with the sickle cell allele trait are resistent to malaria, if malaria were eliminated there would be no change in the frequncy of sickle cell allele. This is because the presense of malaria does not have an affect on patients with the sickle cell allele trait.
The amino acid sequence of the sickle cell allele for hemoglobin varies from the normal allele for hemoglobin by one amino acid. The sickle cell allele for hemoglobin has valine instead of glutamic acid. When the oxygen level of the blood decreases, the hemoglobin molecules come out of solution, stick together, and form long chains that cause the red blood cells to become sickle shaped.
*An allele is basically the different forms a particular gene can take (describes the various genotypes/phenotypes a gene can take).* For example there is an allele of a gene which codes for haemoglobin in red blood cells, which gives them their characteristic concave shape. But there can also be a mutation in that gene, which causes a different allele to be produced which gives it a sickle-cell shape, which leads to sickle-cell anaemia.
SS,Ss
The sickle cell allele can be maintained in the central African population, above the frequency of gene mutation (balancing selection), because the heterozygous sickle cell individuals have an advantage in lifespan, in this malaria stricken region, over the homozygous alternatives. Homozygous sickle-sickle individuals die early from the sickle cell disease. Homozygous nonsickle-nonsickle die early from malaria. The heterozygous sickle-nonsickle have a higher survival against malaria and therefore the sickle cell allele is balanced selected.
Sickle cell disease is an autosomal reccessive sexlinked trait so, a female msut have 2 recessive alleles to have the trait and a male needs only one allele (this is because there is no corresponding site for this allele on the Y chromosome. The female can be a carrier of the disorder with the defective allele on one X chromosome and a normal allele on the other X chromosome. Female carrriers can have a mixture of normal and abnormal redblood cells.