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If sickle cell trait is due to be heterozygous with respect to a single gene mutation on the haemoglobin β-globin chain, why is it the case that ~50% of RBCs are sickled rather than half of the haemoglobin in every RBC containing haemoglobin-S β-globin chains?

Is it due to some form of monoalleic expression that occurs by chance or are all the proteins in one RBC formed from one random allele during erythropoiesis?

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    $\begingroup$ Welcome to SE Biology. I am not sure that I understand what you say or that it is correct. What do you mean by the "trait is due to be heterozygous"? The heterozygotes are carriers and do not suffer sickling. Only the red cells of homozygotes sickle. Likewise your statement about only half the blood cells sickling. Presumably that is just statistical chance as the oxygen concentration decreases and nothing to do with expression. Could you please clarify and support your statements with links to references. Then we may be able to help sort it out for you. $\endgroup$
    – David
    Commented Oct 10, 2019 at 16:50
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    $\begingroup$ Sickle cell carriers (heterozygous) don't have sickle cells, but do have altered blood cells $\endgroup$
    – John
    Commented Oct 11, 2019 at 3:20

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"The sickle cell trait" affects people who are homozygous for the HbS allele. These individuals only have hemoglobin S (after all fetal and embryonic hemoglobin genes are switched off). Hemoglobin S forms large crystal aggregates under conditions of low oxygen tension, and cause red cells to sickling and then to lyse. Anemia is most often severe and lethal.

Heterozygous subjects (HbA/HbS) form both hemoglobin A (normal) and hemoglobin S in approximately equal quantities, and suffer only a mild form of anemia, that may be even unnoticed.

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