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Gregor Mendel's work (1822 - 1884) was primarily focused on pea plants. Through his initial experiments, he determined that every gene in a diploid cell has two variants called alleles inherited from each parent. He suggested that amongst these two alleles, one allele is dominant in character and the other recessive. The combination of alleles determines the phenotype of a gene in an organism.

According to Mendel, organisms with both copies or a single copy of the dominant allele display a dominant phenotype. If the organism has both copies of the recessive allele, it will display a recessive phenotype.

In contrast to Mendel's observations, incomplete dominance or partial dominance can be observed in some genes. It is a phenomenon where both alleles of a gene are partially expressed in a heterozygous organism. Here, the dominant allele is not completely expressed, while the recessive allele influences the trait. This results in a phenotype that is an intermix. For example, in a breeding experiment where one parent is homozygous with a long stem and the other parent is homozygous with a short stem, the offspring of the F1 generation have an intermediate stem length. This is an example of non-mendelian inheritance.

Tay Sachs disease is an example of incomplete dominance in humans. Homozygotes with normal alleles (TT) produce an enzyme called beta-hexosaminidase A that is responsible for breaking down lipids byproducts. Homozygotes with recessive alleles (tt) fail to produce the enzyme. This leads to the accumulation of lipid byproducts in the developing brain of fetuses and young children, resulting in their early death. However, heterozygotes (Tt) for the gene produce half the amount of functional enzymes. Here, both the alleles are expressed, but only one of the alleles produces functional enzymes.

Tagi
Incomplete DominanceGregor MendelAllelesDominant AlleleRecessive AllelePhenotypeDiploid CellHeterozygous OrganismIntermixBreeding ExperimentF1 GenerationNon mendelian InheritanceTay Sachs DiseaseBeta hexosaminidase A

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