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Mutation in a regulatory element increases resistance to malaria (a) Duffy normal (b) Duffy mutant Duffy, protein -Malarial -Parasites cannot bind parasite Blood Blood Purkinje Endothelial cells Purkinje Endothelial cells GATA Duffy GACA Duffy FIGURE 20-17 A regulatory mutation in a human Duffy gene enhancer is associated with resistance to malaria. (a) The Duffy protein (dark blue) is typically expressed on blood cells as well as on Purkinje cells in the brain and endothelial cells. (b) A high proportion of West Africans lack Duffy expression on their red blood cells due to a mutation in a is the second most prevalent form of malarial parasite in most tropical and sub- tropical regions of the world but at present is absent from sub-Saharan Africa. The parasite gains entry to red blood cells and red-blood-cell precursors by bind- ing to the Duffy glycoprotein (see Figure 20-17). The very high frequency of Fymull homozygotes in Africa prevents P. vivax from being common there. Moreover, if we suppose that P. vivax was common in Africa in the past, then the Fyull allele would have been selected for. blood-cell enhancer (the GATA sequence is mutated to GACA). Since the Duffy protein is part of the receptor for the P. vivax malarial parasite (orange), individuals with the regulatory mutation are resistant to infection but have normal Duffy expression elsewhere in the body. The complete absence of Duffy protein on the red blood cells of a large sub- population raises the question of whether the Duffy protein has any necessary function, because it is apparently dispensable. But it is not the case that these individuals lack Duffy protein expression altogether. The protein is expressed on endothelial cells of the vascular system and the Purkinje cells of the cerebellum. As with the evolution of Yellow expression in wing-spotted fruit flies and of Pitx expression in stickleback fish, the regulatory mutation at the Fy locus allows one aspect of gene expression (in red blood cells) to change without disrupting others (onn lüguro 20 17)

Mutation in a regulatory element increases resistance to malaria (a) Duffy normal (b) Duffy mutant Duffy, protein -Malarial -Parasites cannot bind parasite Blood Blood Purkinje Endothelial cells Purkinje Endothelial cells GATA Duffy GACA Duffy FIGURE 20-17 A regulatory mutation in a human Duffy gene enhancer is associated with resistance to malaria. (a) The Duffy protein (dark blue) is typically expressed on blood cells as well as on Purkinje cells in the brain and endothelial cells. (b) A high proportion of West Africans lack Duffy expression on their red blood cells due to a mutation in a is the second most prevalent form of malarial parasite in most tropical and sub- tropical regions of the world but at present is absent from sub-Saharan Africa. The parasite gains entry to red blood cells and red-blood-cell precursors by bind- ing to the Duffy glycoprotein (see Figure 20-17). The very high frequency of Fymull homozygotes in Africa prevents P. vivax from being common there. Moreover, if we suppose that P. vivax was common in Africa in the past, then the Fyull allele would have been selected for. blood-cell enhancer (the GATA sequence is mutated to GACA). Since the Duffy protein is part of the receptor for the P. vivax malarial parasite (orange), individuals with the regulatory mutation are resistant to infection but have normal Duffy expression elsewhere in the body. The complete absence of Duffy protein on the red blood cells of a large sub- population raises the question of whether the Duffy protein has any necessary function, because it is apparently dispensable. But it is not the case that these individuals lack Duffy protein expression altogether. The protein is expressed on endothelial cells of the vascular system and the Purkinje cells of the cerebellum. As with the evolution of Yellow expression in wing-spotted fruit flies and of Pitx expression in stickleback fish, the regulatory mutation at the Fy locus allows one aspect of gene expression (in red blood cells) to change without disrupting others (onn lüguro 20 17)

Human Anatomy & Physiology (11th Edition)
Human Anatomy & Physiology (11th Edition)
11th Edition
ISBN:9780134580999
Author:Elaine N. Marieb, Katja N. Hoehn
Publisher:Elaine N. Marieb, Katja N. Hoehn
Chapter1: The Human Body: An Orientation
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Using Figure 20-17, explain how the mutation in the
GATA sequence of the Duffy gene imparts resistance to
P. vivax infection.

Mutation in a regulatory element increases resistance to malaria (a) Duffy normal (b) Duffy mutant Duffy, protein -Malarial -Parasites cannot bind parasite Blood Blood Purkinje Endothelial cells Purkinje Endothelial cells GATA Duffy GACA Duffy FIGURE 20-17 A regulatory mutation in a human Duffy gene enhancer is associated with resistance to malaria. (a) The Duffy protein (dark blue) is typically expressed on blood cells as well as on Purkinje cells in the brain and endothelial cells. (b) A high proportion of West Africans lack Duffy expression on their red blood cells due to a mutation in a is the second most prevalent form of malarial parasite in most tropical and sub- tropical regions of the world but at present is absent from sub-Saharan Africa. The parasite gains entry to red blood cells and red-blood-cell precursors by bind- ing to the Duffy glycoprotein (see Figure 20-17). The very high frequency of Fymull homozygotes in Africa prevents P. vivax from being common there. Moreover, if we suppose that P. vivax was common in Africa in the past, then the Fyull allele would have been selected for. blood-cell enhancer (the GATA sequence is mutated to GACA). Since the Duffy protein is part of the receptor for the P. vivax malarial parasite (orange), individuals with the regulatory mutation are resistant to infection but have normal Duffy expression elsewhere in the body. The complete absence of Duffy protein on the red blood cells of a large sub- population raises the question of whether the Duffy protein has any necessary function, because it is apparently dispensable. But it is not the case that these individuals lack Duffy protein expression altogether. The protein is expressed on endothelial cells of the vascular system and the Purkinje cells of the cerebellum. As with the evolution of Yellow expression in wing-spotted fruit flies and of Pitx expression in stickleback fish, the regulatory mutation at the Fy locus allows one aspect of gene expression (in red blood cells) to change without disrupting others (onn lüguro 20 17)
Transcribed Image Text:Mutation in a regulatory element increases resistance to malaria (a) Duffy normal (b) Duffy mutant Duffy, protein -Malarial -Parasites cannot bind parasite Blood Blood Purkinje Endothelial cells Purkinje Endothelial cells GATA Duffy GACA Duffy FIGURE 20-17 A regulatory mutation in a human Duffy gene enhancer is associated with resistance to malaria. (a) The Duffy protein (dark blue) is typically expressed on blood cells as well as on Purkinje cells in the brain and endothelial cells. (b) A high proportion of West Africans lack Duffy expression on their red blood cells due to a mutation in a is the second most prevalent form of malarial parasite in most tropical and sub- tropical regions of the world but at present is absent from sub-Saharan Africa. The parasite gains entry to red blood cells and red-blood-cell precursors by bind- ing to the Duffy glycoprotein (see Figure 20-17). The very high frequency of Fymull homozygotes in Africa prevents P. vivax from being common there. Moreover, if we suppose that P. vivax was common in Africa in the past, then the Fyull allele would have been selected for. blood-cell enhancer (the GATA sequence is mutated to GACA). Since the Duffy protein is part of the receptor for the P. vivax malarial parasite (orange), individuals with the regulatory mutation are resistant to infection but have normal Duffy expression elsewhere in the body. The complete absence of Duffy protein on the red blood cells of a large sub- population raises the question of whether the Duffy protein has any necessary function, because it is apparently dispensable. But it is not the case that these individuals lack Duffy protein expression altogether. The protein is expressed on endothelial cells of the vascular system and the Purkinje cells of the cerebellum. As with the evolution of Yellow expression in wing-spotted fruit flies and of Pitx expression in stickleback fish, the regulatory mutation at the Fy locus allows one aspect of gene expression (in red blood cells) to change without disrupting others (onn lüguro 20 17)
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