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Describe, using an example for each, three ways in which genes can behave in a non-Mendelian manner?


Gregor Johann Mendel was a scientist and founder of the modern genetics concept. Inheritance is one of the most important and common area of study under modern genetics (Bardoe and Smith, 2006). The reception of genetic features from parents to children or offspring by transmission is known as inheritance (Kimura, 2008).  In genetics broadly two types of inheritance are well-known: Mendelian and non-Mendelian inheritance (Campbell, Reece and Simon, 2004). Segregation ratio of children considerably deviates from expected Mendelian ratio. Though in heritance pattern followed in bacteria, viruses and fungi is non-Mendelian, this term commonly applies to occurrences within eukaryotic reproduction where Mendelian inheritance is characteristically expected. Mendelian inheritance is said to be the inheritance of biological characteristics, which pursues the laws put forward by the renowned scientist Mendel in the year 1856 and 1866. Non-Memdelian inheritance is said to be a common term, which refers to any type of inheritance pattern where traits do not separate in relation to Mendel’s laws. The laws illustrate the traits inheritance related to particular genes on chromosomes inside the cell nucleus (Shontz and Cummings, 2011). According to the Mendelian laws, individual parent donates one out of two possible alleles for a single trait (Van den Veyver and Peng, 2009). Non-Mendelian inheritance takes part in various disease processes. Genes can behave in a non-Mendelian manner or can also be termed as the exceptions of Mendelian inheritance. Few are discussed here.

Incomplete dominance: incomplete dominance is said to be a type of intermediate inheritance where a single allele for a particular trait is partially dominant over the other allele. This gives rise to a completely new phenotype where the characteristic is a combination of recessive and dominant phenotypes (van Heyningen, 2004).  Crossing of two transitional phenotypes will give rise to the return of intermediate and parental phenotypes. Generally in this condition, the wild type allele produces functional protein and recessive allele either produces no functional protein or does not have correct function. Few examples of incomplete dominance are: a pink snapdragon flower, result of cross-pollination between a white and a red flower, where neither the red nor the white allele is dominant. Rabbit with brown coloured fur, result of one parent rabbit with red allele and one parent rabbit with white allele for fur colour, but no colour is dominating over each other (Phadnis, 2005). Mating of big size American Bulldog and small size American Bulldog and their pup is medium in size. Incomplete dominance is also termed as partial dominance. In this case the phenotype of heterozygous genotype is different and frequently intermediary to the phenotypes of homozygous genotypes (Pritchard and Korf, 2013). In terms of quantitative genetics, if the phenotype of a heterozygote is accurately between the two homozygotes then the phenotype is supposed to express “no dominance” at all.

Co-dominance: co-dominance is said to be an association between two genetic versions. Individuals obtain single version of an allele from each parent. If these alleles are different the dominant allele will get expressed usually and the effect of the recessive allele is masked. In this type of inheritance neither allele is recessive. In co-dominance phenotypes of both the alleles get expressed (Shontz and Cummings, 2011). Co-dominance is different from incomplete dominance where an additional phenotype is generated and both alleles get expressed completely. AB blood group is the example of co-dominance. In human ABO blood group system, the chemical modifications of H antigen on the red blood cell surfaces are controlled by three alleles (Cummings, 2014). IA and IB are co-dominant to each other and dominant over recessive i. The IA coded enzyme adds N-acetylgalactosamine to the H antigen that is membrane-bounded. The IB coded enzyme adds galactose to the H antigen and i allele produces no alteration. Thus IA and IB are dominant over i. Individuals with IAIA and IAi have A blood group, similarly, individuals with IBIB and IBi have B blood group. Individuals with IAIB have alterations on the blood cells and therefore have AB blood type. Hence IAIB alleles are co-dominant. A and B proteins are functional here and are expressed on the blood cells.

Epistasis: epistasis is said to be an interaction between two or more than two genes to manage a particular phenotype. It is an incident which includes single gene effect being reliant on the presence of single or more modifier genes (Zwick, 2010). In this type of gene interaction the epistatic gene can prohibit the manifestation of phonotypical characteristics of hypostatic gene. In case of dominant epistasis inhibitor allele (I) is the dominant allele. Therefore, the inhibition takes place within dominant homozygosity (II) or heterozygosity (Ii). In recessive epistasis inhibitor allele (i) is the recessive allele of epistatic gene. Hence, inhibition takes place just in recessive homozygosity (ii). The word epistasis is originated from a Greek word and the meaning of this word is standing over (VanderWeele and Laird, 2010). So, simply this term represents an interaction between two loci, where phenotypic effect of a single locus depends on the genotype of another locus (Oetting and King, 1999). It is important to note the basic differences between dominance and epistasis. Dominance involves gene interactions which are intra-allelic (Hartl, 2011). But epistasis involves gene interactions which are inter-allelic. In case of dominance single allele hides the result of another allele at same pair of a gene. But in case of epistasis individual gene covers the consequence of other gene at dissimilar gene loci (Ahluwalia, 2009). The gene responsible for albinism is an epistatic gene. Albinism means lack of pigmentation. Albinism gene has two variations: non-albino allele and albino allele. The albino allele cannot synthesize melanin pigment. Mice have other allele pairs involved in the placement of melanin. These are agouti allele that generates dark melanisation of hair, except yellow band at tip and black allele that generates melanisation of entire hair (Lewis, 2007). If melanin is not generated then neither black nor agouti can get expressed, in situations where mouse is homozygous for albino gene. Therefore, homozygosity for the gene responsible for albinism is epistatic to black or agouti alleles and stop their expression (Campbell, Reece and Simon, 2004). In case of incomplete dominance epistasis is present and in case of co-dominance, genes are self-governing and can exist together. This association can be illustrated by one more example: suppose, gene S directs the spine sharpness in cactus. Cactus with dominant allele (S) has sharp spines and homozygous recessive cactus (ss) has dull spines. Simultaneously, N, a second gene determines whether cacti have spines and homozygous recessive (nn) cacti have no spines. Therefore, in this condition, the association between the genes S and N is the example of epistasis (Pritchard and Korf, 2013). When epistatic alleles are aa, and hypostatic alleles are BB, Bb and bb, then the phenotypic expression will be a. When the epistatic alleles are AA and Aa, hypostatic alleles BB and Bb, then the phynotypic expression will be B and when the epistatic alleles are AA, and Aa and hypostatic alleles are bb, then the phenotypic expression will be b.

This paper thus describes how genes can behave in a non-Mendelian manner by focusing on the main three ways: incomplete dominance, co-dominance and epistasis.



Ahluwalia, K. (2009). Genetics. New Delhi: New Age International.

Bardoe, C. and Smith, J. (2006). Gregor Mendel. New York: Abrams Books for Young Readers.

Campbell, N., Reece, J. and Simon, E. (2004). Essential biology. San Francisco: Pearson/Benjamin Cummings.

Cummings, M. (2014). Human heredity. CA : USA: Yolanda Cossio.

Hartl, D. (2011). Essential genetics. Sudbury, Mass.: Jones and Bartlett Publishers.

Kimura, R. (2008). Genetic inheritance patterns. New York: Nova Biomedical Books.

Lewis, R. (2007). Human genetics. Boston: McGraw-Hill Higher Education.

Oetting, W. and King, R. (1999). Molecular basis of albinism: Mutations and polymorphisms of pigmentation genes associated with albinism. Hum. Mutat., 13(2), pp.99-115.

Phadnis, N. (2005). Widespread Correlations Between Dominance and Homozygous Effects of Mutations: Implications for Theories of Dominance. Genetics, 171(1), pp.385-392.

Pritchard, D. and Korf, B. (2013). Medical Genetics at a Glance. Hoboken: Wiley.

Shontz, N. and Cummings, M. (2011). Study guide [for Cumming's] human heredity principles and issues. Pacific Grove, CA: Brooks/Cole Thomson Learning.

Van den Veyver, I. and Peng, H. (2009). Mendelian Inheritance and Its Exceptions. GLOWM.

van Heyningen, V. (2004). Mechanisms of non-Mendelian inheritance in genetic disease. Human Molecular Genetics, 13(suppl_2), pp.R225-R233.

VanderWeele, T. and Laird, N. (2010). Tests for Compositional Epistasis under Single Interaction-Parameter Models. Annals of Human Genetics, 75(1), pp.146-156.

Zwick, M. (2010). Reconstructability Analysis of Epistasis. Annals of Human Genetics, 75(1), pp.157-171.


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