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Published byBertina Hodges Modified over 8 years ago
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Genome evolution and the genotype-phenotype map
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Mendelian inheritance
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Epistasis and Pleiotropy http://www.biomedcentral.com/1741-7007/11/14
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Pleiotropy- one gene, many phenotypes http://mumtazticloft.com/PigeonGenetics1.asp
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Pleiotropy- Marfan syndrome http://www.marfan.net.au/showcontent.toy?cid=1515 FBN1- glycoprotein that serve as a structural component of 10-12 nm calcium- binding microfibrils. These microfibrils provide force bearing structural support in elastic and nonelastic connective tissue throughout the body.
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Epistasis- several genotypes one phenotype http://beacon-center.org/blog/2012/09/17/evolution-101-epistasis/
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http://www.hinsdale86.org/staff/kgabric/Disease10/Alpha%20Thalassemia/Index.html ɑ-thalassemia
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http://www.syncytiabeta.org/~syncyt5/syncytiabeta/index.php?title=Alpha-thalassemia ɑ-thalassemia
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http://www.biologyexams4u.com/2012/11/lethal-genes.html Sickle cell anemia
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Malaria is a parasitic infection caused by the protozoan parasites, Plasmodium. Each year, it causes disease in approximately 650 million people and kills between one and three million, most of them young children in Sub-Saharan Africa. Malarial parasites are transmitted by female Anopheles mosquitoes. The parasites themselves infect and multiply within the red blood cells Malaria disease
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Sickle cell anemia and Malaria
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Heterozygote advantage http://www.mjhid.org/article/view/10928/html
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Negative epistasis between the malaria- protective effects of ɑ + -thalassemia and the sickle cell trait
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Negative epistatic interaction between the effect of HbAS and ɑ+-thalassemia
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Negative epistasis between the malaria- protective effects of ɑ + -thalassemia and the sickle cell trait These genes may be acting epistatically with regard to their malaria-protective effects
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Negative epistasis between the malaria- protective effects of ɑ + -thalassemia and the sickle cell trait Epistasis could result a range of outcomes depending on the selective forces involved
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Do the “strongest” survive?
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