Clarifying Mendelian vs non-Mendelian inheritance

Abstract

Gregor Mendel developed the principles of segregation and independent assortment in the mid-1800s based on his detailed analysis of several traits in pea plants. Those principles, now called Mendel's laws, in fact, explain the behavior of genes and alleles during meiosis and are now understood to underlie "Mendelian inheritance" of a wide range of traits and diseases across organisms. When asked to give examples of inheritance that do NOT follow Mendel's laws, in other words, examples of non-Mendelian inheritance, students sometimes list incomplete dominance, codominance, multiple alleles, sex-linked traits, and multigene traits and cite as their sources the Khan Academy, Wikipedia, and other online sites. Against this background, the goals of this Perspective are to (1) explain to students, healthcare workers, and other stakeholders why the examples above, in fact, display Mendelian inheritance, as they obey Mendel's laws of segregation and independent assortment, even though they do not produce classic Mendelian phenotypic ratios and (2) urge individuals with an intimate knowledge of genetic principles to monitor the accuracy of learning resources and work with us and those resources to correct information that is misleading.

Keywords: Mendel's laws; Mendelian inheritance; genetics; genotypic and phenotypic ratios.

Fig. 1.

Punnett squares illustrating Mendel's laws of segregation and independent assortment. These Punnett squares show the genotypes of gametes produced by each heterozygous parent during meiosis (on the sides of the squares) and the genotypes and phenotypes of the offspring that result from the various unions of gametes (in the center of the squares). a, b) According to Mendel's law of segregation, the 2 alleles of a gene are segregated to different gametes during meiosis and then united at random, 1 from each parent, at fertilization. b) According to Mendel's law of independent assortment, when 2 genes are on different chromosomes (i.e. unlinked), they segregate independently. Only offspring phenotypes are shown. In these examples, T is the dominant allele that causes pea plants to be tall and G is the dominant allele that causes pea pods to be green.

Fig. 2.

Examples of complete dominance, incomplete dominance, codominance, and variable dominance. From crosses of heterozygous parents, all display a Mendelian genotypic ratio of 1:2:1 among offspring and show Mendelian inheritance. a) Complete dominance results in a 3:1 phenotypic ratio, as illustrated in Fig. 1a. b) Incomplete dominance, c) codominance, and d) variable dominance cause altered phenotypic ratios as a result of the action of the gene products in offspring.

Fig. 3.

Examples of sex-linked traits and 2-gene traits. Both display Mendelian genotypic ratios and show Mendelian inheritance patterns. a) The sample pedigree shows the inheritance of hemophilia in humans (filled symbols). Because the mutant hemophilia allele h is recessive and resides on the X chromosome, the disease phenotype shows a sex bias. From the parents shown, sons (with only 1 X chromosome) have a 50:50 chance of being affected, while daughters (with 2 X chromosomes) will not be affected. b) Purple flower color in peas requires the synthesis of anthocyanin. In this example, the unlinked P gene and C gene function at different steps in the anthocyanin biosynthetic pathway. From crosses of heterozygous parents, the absence of either gene product (in p/p or c/c plants) results in white flowers in offspring and the unusual phenotypic ratio of 9 purple-flower : 7 white-flower plants. c) Labrador dog coat color is controlled by 2 unlinked genes: the E gene for the production of black pigment and the B gene for dense deposition of black pigment in dog hairs. From crosses of heterozygous parents, each gene displays a Mendelian genotypic ratio of 1:2:1 among offspring. However, the offspring display an unusual phenotypic ratio of 9 black : 3 chocolate : 4 yellow dogs as a result of the action of the E and B gene products and epistasis; among offspring, e/e is epistatic and masks the phenotype of the B gene.