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Mendelian inheritance (also known as Mendelism) is a type of biological inheritance following the principles originally proposed by Gregor Mendel in 1865 and 1866, re-discovered in 1900 by Hugo de Vries and Carl Correns, and later popularized by William Bateson. [1]
Later authors have suggested Fisher's analysis was flawed, proposing various statistical and botanical explanations for Mendel's numbers. [4] It is also possible that Mendel's results are "too good" merely because he reported the best subset of his data—Mendel mentioned in his paper that the data were from a subset of his experiments.
Autosomal dominant A 50/50 chance of inheritance. Sickle-cell disease is inherited in the autosomal recessive pattern. When both parents have sickle-cell trait (carrier), a child has a 25% chance of sickle-cell disease (red icon), 25% do not carry any sickle-cell alleles (blue icon), and 50% have the heterozygous (carrier) condition. [1]
Between 1856 and 1865, Gregor Mendel conducted breeding experiments using the pea plant Pisum sativum and traced the inheritance patterns of certain traits. Through these experiments, Mendel saw that the genotypes and phenotypes of the progeny were predictable and that some traits were dominant over others. [ 11 ]
The two schools were the Mendelians, such as Bateson and de Vries, who favoured mutationism, evolution driven by mutation, based on genes whose alleles segregated discretely like Mendel's peas; [21] [22] and the biometric school, led by Karl Pearson and Walter Weldon. The biometricians argued vigorously against mutationism, saying that ...
Mendel's results were quickly replicated, and genetic linkage quickly worked out. Biologists flocked to the theory; even though it was not yet applicable to many phenomena, it sought to give a genotypic understanding of heredity, which they felt was lacking in previous studies of heredity, which had focused on phenotypic approaches. [ 44 ]
[10] [11] Mendel's work was rediscovered in 1900 by the geneticist Hugo de Vries and others, soon confirmed that same year by experiments by William Bateson. [12] Mendelian inheritance with segregating, particulate alleles came to be understood as the explanation for both discrete and continuously varying characteristics.
Mendelian traits behave according to the model of monogenic or simple gene inheritance in which one gene corresponds to one trait. Discrete traits (as opposed to continuously varying traits such as height) with simple Mendelian inheritance patterns are relatively rare in nature, and many of the clearest examples in humans cause disorders.