Single genes do not always work as simply as indicated by a dominance and recessive relationship

Single genes do not always work as simply as indicated by a dominance and recessive relationship

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Single genes do not always work as simply as indicated by a dominance and recessive relationship. Other genes can affect the phenotypic expression of a given gene. One example is epistasis ("standing on") where one locus can mask the expression of another. Classic example is a synthetic pathway of a pigment. Mutations at loci controlling the early steps in the pathway (gene 1) can be epistatic on the expression of genes later in the pathway (gene 3) by failing to produce pigment precursors (e.g. albinos) A-> gene 1 -> B -> gene 2 -> C gene 3 -> Pigment Genes can also be pleitropic when they affect more than one trait. The single base pair mutation that lead to sickle cell anemia is a classic example. The altered hemoglobin sequence is not the only effect: lower oxygen affinity=anemia; clogged capillaries=circulatory problems; in heterozygote state=malarial resistance.
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Unformatted text preview: Mutations in cartilage are another example since cartilage makes up many different structures the effects of the mutation are evident in many different phenotypic characters. Polygenic inheritance can be explained by additive effects of many loci: if each "capital" allele contributes one increment to the phenotype. With one locus and additive effects we have three phenotypic classes: AA, Aa and aa. With two loci and two alleles in a strictly additive model (i.e., no epistasis or other modifying effects) we can have five phenotypic classes aabb<Aabb=aaBb<AaBb=AAbb=aaBB<AABb=AaBB<AABB and the intermediate phenotypic values can be produced in more ways, so should be more frequent. The more loci affecting the trait, the greater number of phenotypic classes....
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