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Sickle cell

Genetics as it applies to evolution, molecular biology, and medical aspects.

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Sickle cell

Postby scottyiu » Sun May 14, 2006 1:35 am

How come when the normal cell gene is dominant and the sickle cell gene is recessive, if a person have a normal and a sickle cell gene, there will be still some sickle cell found in that person? (i thought dominant overides the recessive?)
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Postby victor » Sun May 14, 2006 12:40 pm

try to observe it by your own using Punnet square..
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Postby mith » Sun May 14, 2006 5:43 pm

if it's completely recessive that would be the case
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Postby scottyiu » Tue May 16, 2006 1:43 pm

Thank you for the response but i think you misunderstood me... :oops:

What i mean is that is there is one domiante plus one receesive gen in someone then that person is a carrier and symtoms are not meant to show. Why does many books says that the symtoms still shows if a person have a domiant and recessiv gene?
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Postby kiekyon » Wed May 17, 2006 3:07 am

they are not completely dominant..
in other word the gene for sickle cell is codominant to the normal gene
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Postby scottyiu » Wed May 17, 2006 11:19 am

Thanks for the reply.

Can you please give me more detail? do you mean that the domiant is not domiant and the recessive is not recessive?

Sorry as i don't fully understand... :oops:
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Postby mith » Wed May 17, 2006 2:23 pm

Remember there are different types of dominance such as codominance, incomplete dominance etc.

http://en.wikipedia.org/wiki/Codominant
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Postby daniel.kurz » Fri May 19, 2006 1:55 am

Don't use wikipedia I have found so many errors there. Try reading this article.

Sickle-cell anemia is a genetic disease that is of particular interest to geneticists because it occurs only among populations who have originated in regions where malaria is prevalent. The disease is produced by having a double "dose" of a recessive gene and heterozygotes (with one dominant and one recessive gene for the sickling trait) have an advantage in terms of resistance to malaria. The balance between beneficial and deleterious effects of the gene is referred to as a balanced polymorphism. Correspondence between geographic distribution of the sickle- cell gene and malaria provides a compelling example of evolution affecting human populations. It is also important in clarifying the significance of biological differences between human groups and is therefore relevant to ethical debates about race as well as about evolution.

People with sickle-cell anemia have abnormally shaped red blood cells due to an anomaly in the structure of the hemoglobin molecule within them. Hemoglobin plays a vital role in trapping oxygen and carrying it around to bodily tissues. Due to the molecular abnormality, hemoglobin molecules join together to form rods, which distort red blood cells into a sickle shape. Whereas normal blood cells are soft and pliable, allowing them to move easily through small blood vessels (capillaries), sickle cells are rigid and fragile. Their rigidity means that they tend to plug blood vessels from time to time, thereby obstructing the flow of blood and causing tissue and organ damage. Normal red blood cells last for 120 days but sickle cells survive for only 6 to 30 days. They are lost far faster than they can be produced in the bone marrow. The resulting chronic deficiency of red blood cells and hemoglobin constitutes anemia.

Prior to modern medicine most people affected by sickle-cell anemia would have died in childhood from infections and lung damage. It is a painful condition and pain-relieving medication is a common form of treatment. Infections are controlled using antibiotics. Blood transfusions are common. The disease can be cured using bone marrow transfusions but this is a high-risk procedure. Genetically engineered mice carry the human sickle-cell gene, which helps in understanding the biochemical basis of the disease and developing drug treatments. It is hoped that drug treatments can eventually modify the structure of the hemoglobin molecule and lead to a cure.

People who inherit a gene for sickle hemoglobin from both parents develop the disorder. People who inherit only one such gene are carriers. In their case, about half of their hemoglobin is of the sickle variety but this is not enough to produce rod formation and sickling of the red blood cells. Sickle-cell anemia is more common among African Americans than other ethnic groups living in the United States. The chances that an African American is a carrier are 1/12 and the chances of two carriers being married is 1/12 × 1/12, or 1/144. The chances that a child of two carriers will inherit both sickling genes is 1/4, which means that approximately one person in 576 contracts the disease.

There are many different human genes that vary as a function of geography and are therefore more likely to occur in people of one ancestry than another. Thus, the gene causing adult lactose intolerance is more common among Asians than Europeans and Asians are also more likely to have an adverse physiological reaction to small quantities of alcohol. Such group differences in gene frequencies have sometimes been used as an empirical justification for the view that different human populations constitute distinct races. That this is a mistake is well illustrated by the case of sickle-cell anemia.

Just because the sickle-cell gene crops up in African Americans but almost never in European Americans, there is a tendency to think of it as an African trait. Yet only around 8% of African Americans carry the sickle-cell gene. The vast majority do not. The geographical distribution of the sickle-cell gene, which clusters in warm, humid, regions of the African continent, has provided a fairly compelling clue to its evolutionary origins. For some equatorial tribes, as many as 40% of the people are carriers. Maps of the malarial parasite Plasmodium falciparum and of the human sickle-cell gene match each other quite closely both inside and outside Africa.

The sickle-cell trait is not distinctive of all Africans, and it also crops up at frequencies of up to 8% in the Middle East and in southern Asia. These regions are also infested with Plasmodium falciparum, the malarial bacterium. This indicates that far from being a racial characteristic, the sickle-cell trait, which occurs in very low frequencies for most of the world's population, is really a pan-human adaptation to living in malarial regions.

The advantages conferred by the sickle gene for populations in malarial regions means that its carriers survive and reproduce more successfully than others. Over many generations, the frequency of the gene increases at these sites. It seems probable that the gene can never entirely penetrate a population because the more frequent the gene is, the greater the probability of two carriers getting married and their children developing anemia. Apparently when the gene frequency rises to 40% the advantages conferred by malarial resistance are counteracted by the decline in reproductive success from producing children having the illness. Sickle-cell anemia thus shows natural selection at work in human populations.

Source: Barber, Nigel. "Sickle-Cell Anemia." Encyclopedia of Ethics in Science and Technology. Facts On File, Inc., 2002. Facts On File, Inc. Science Online. <www.fofweb.com>.
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