Non-Mendelian inheritance
Non-Mendelian inheritance is any pattern in which traits do not segregate in accordance with Mendel's laws. These laws describe the inheritance of traits linked to single genes on chromosomes in the nucleus. In Mendelian inheritance, each parent contributes one of two possible alleles for a trait. If the genotypes of both parents in a genetic cross are known, Mendel's laws can be used to determine the distribution of phenotypes expected for the population of offspring. There are several situations in which the proportions of phenotypes observed in the progeny do not match the predicted values.
Non-Mendelian inheritance plays a role in several disease which affected the processes.[clarification needed][1]
Types
Incomplete dominants, codominance, multiple alleles, and polygenic traits follow Mendel's laws, display Mendelian inheritance, and are explained as extensions of Mendel's laws.[2]
Incomplete dominance
In cases of intermediate inheritance due to incomplete dominance, the principle of dominance discovered by Mendel does not apply. Nevertheless, the principle of uniformity works, as all offspring in the F1-generation have the same genotype and same phenotype. Mendel's principle of segregation of genes applies too, as in the F2-generation homozygous individuals with the phenotypes of the P-generation appear. Intermediate inheritance was first examined by Carl Correns in Mirabilis jalapa used for further genetic experiments.[3] Antirrhinum majus also shows intermediate inheritance of the pigmentation of the blossoms.[4]
Co-dominance
In cases of co-dominance, the genetic traits of both different alleles of the same gene-locus are clearly expressed in the phenotype. For example, in certain varieties of chicken, the allele for black feathers is co-dominant with the allele for white feathers. Heterozygous chickens have a colour described as "erminette", speckled with black and white feathers appearing separately. Many human genes, including one for a protein that controls cholesterol levels in the blood, show co-dominance too. People with the heterozygous form of this gene produce two different forms of the protein, each with a different effect on cholesterol levels.[citation needed]
Genetic linkage
When genes are located on the same chromosome and no
Multiple alleles
In Mendelian inheritance, genes have only two alleles, such as a and A. Mendel consciously chose pairs of genetic traits, represented by two alleles for his inheritance experiments. In nature, such genes often exist in several different forms and are therefore said to have
Many other genes have multiple alleles, including the human genes for
Epistasis
If one or more genes cannot be expressed because of another genetic factor hindering their expression, this epistasis can make it impossible even for dominant alleles on certain other gene-loci to have an effect on the phenotype. An example in dog coat genetics is the homozygosity with the allele "e e" on the Extension-locus making it impossible to produce any other pigment than pheomelanin. Although the allele "e" is a recessive allele on the extension-locus itself, the presence of two copies leverages the dominance of other coat colour genes. Domestic cats have a gene with a similar effect on the X-chromosome.[citation needed]
Sex-linked inheritance
Genetic traits located on
Extranuclear inheritance
Extranuclear inheritance (also known as cytoplasmic inheritance) is a form of non-Mendelian inheritance also first discovered by Carl Correns in 1908.[9] While working with Mirabilis jalapa, Correns observed that leaf colour was dependent only on the genotype of the maternal parent. Based on these data, he determined that the trait was transmitted through a character present in the cytoplasm of the ovule. Later research by Ruth Sager and others identified DNA present in chloroplasts as being responsible for the unusual inheritance pattern observed. Work on the poky strain of the mould Neurospora crassa begun by Mary and Hershel Mitchell[10] ultimately led to the discovery of genetic material in the mitochondria, the mitochondrial DNA.[citation needed]
According to the
It is the transmission of this
In humans, mitochondrial diseases are a class of diseases, many of which affect the muscles and the eye.[citation needed]
Polygenic traits
Many traits are produced by the interaction of several genes. Traits controlled by two or more genes are said to be polygenic traits. Polygenic means "many genes" are necessary for the organism to develop the trait. For example, at least three genes are involved in making the reddish-brown pigment in the eyes of fruit flies. Polygenic traits often show a wide range of phenotypes. The broad variety of skin colour in humans comes about partly because at least four different genes probably control this trait.[citation needed]
Non-random segregation
Non-random segregation of chromosomes is a deviation from the usual distribution of chromosomes during meiosis and in some cases of mitosis.
Gene conversion
Infectious heredity
Another form of non-Mendelian inheritance is known as infectious heredity. Infectious particles such as viruses may infect host cells and continue to reside in the cytoplasm of these cells. If the presence of these particles results in an altered phenotype, then this phenotype may be subsequently transmitted to progeny.[13] Because this phenotype is dependent only on the presence of the invader in the host cell's cytoplasm, inheritance will be determined only by the infected status of the maternal parent. This will result in a uniparental transmission of the trait, just as in extranuclear inheritance.[citation needed]
One of the most well-studied examples of infectious heredity is the killer phenomenon exhibited in yeast. Two double-stranded RNA viruses, designated L and M, are responsible for this phenotype.[14] The L virus codes for the capsid proteins of both viruses, as well as an RNA polymerase. Thus the M virus can only infect cells already harbouring L virus particles. The M viral RNA encodes a toxin that is secreted from the host cell. It kills susceptible cells growing in close proximity to the host. The M viral RNA also renders the host cell immune to the lethal effects of the toxin. For a cell to be susceptible it must therefore be either uninfected or harbour only the L virus.[citation needed]
The L and M viruses are not capable of exiting their host cell through conventional means. They can only transfer from cell to cell when their host undergoes mating. All progeny of a mating involving a doubly infected yeast cell will also be infected with the L and M viruses. Therefore, the killer phenotype will be passed down to all progeny.[citation needed]
Heritable traits that result from infection with foreign particles have also been identified in
Although this process is usually associated with viruses, recent research has shown that the Wolbachia bacterium is also capable of inserting its genome into that of its host.[16][17]
Genomic imprinting
Genomic imprinting represents yet another example of non-Mendelian inheritance. Just as in conventional inheritance, genes for a given trait are passed down to progeny from both parents. However, these genes are
Genes are imprinted differently depending on the parental origin of the chromosome that contains them. In mice, the insulin-like growth factor 2 gene undergoes imprinting. The protein encoded by this gene helps to regulate body size. Mice that possess two functional copies of this gene are larger than those with two mutant copies. The size of mice that are heterozygous at this locus depends on the parent from which the wild-type allele came. If the functional allele originated from the mother, the offspring will exhibit dwarfism, whereas a paternal allele will generate a normal-sized mouse. This is because the maternal Igf2 gene is imprinted. Imprinting results in the inactivation of the Igf2 gene on the chromosome passed down by the mother.[18]
Imprints are formed due to the differential methylation of paternal and maternal alleles. This results in differing expression between alleles from the two parents. Sites with significant methylation are associated with low levels of gene expression. Higher gene expression is found at unmethylated sites.[19] In this mode of inheritance, phenotype is determined not only by the specific allele transmitted to the offspring, but also by the sex of the parent that transmitted it.
Mosaicism
Individuals who possess cells with genetic differences from the other cells in their body are termed mosaics. These differences can result from mutations that occur in different tissues and at different periods of development. If a mutation happens in the non-gamete forming tissues, it is characterized as somatic. Germline mutations occur in the egg or sperm cells and can be passed on to offspring.[20] Mutations that occur early on in development will affect a greater number of cells and can result in an individual that can be identified as a mosaic strictly based on phenotype.
Trinucleotide repeat disorders
Trinucleotide repeat disorders also follow a non-Mendelian pattern of inheritance. These diseases are all caused by the expansion of
See also
- Meiotic drive
- CoRR Hypothesis
- Epigenetic inheritance
- Gene drive
- Intragenomic conflict
References
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- ^ Hartwell, L. (2000). *Genetics: From Genes to Genomes*. United Kingdom: McGraw-Hill. Page 39.
- ^ Biology University of Hamburg: Mendelian Genetics
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- ^ Schmidt-Küntzel, Nelson G. David et al.: A domestic cat X chromosome linkage map and the sex-linked orange locus: mapping of orange, multiple origins and epistasis over nonagouti.
- ^ Le gène Orange chez le chat : génotype et phénotype
- ^ Joseph Schacherer: Beyond the simplicity of Mendelian inheritance Science Direct 2016
- ^ Khan Academy: Variations on Mendel's laws (overview)
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- ^ Stacey K. A. (1994). Recombination. In: Kendrew John, Lawrence Eleanor (eds.
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- ^ Russell, Peter J. (2006). iGenetics: A Mendelian Approach. San Francisco: Pearson Education, Inc. pp. 649–650.
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- ^ "University of Rochester Press Releases". Retrieved 2007-10-16.
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- ^ Lewin, Benjamin (2004). Genes VIII. Upper Saddle River, NJ: Pearson Education Inc. pp. 680–684.
- ^ "Lesson 3: Mosaicism". Retrieved 2007-10-16.
- ^ "Genetics of Calico Color".
- ^ "Genetic Mosaicism". Retrieved 2007-10-28.
- ^ "Lesson 1: Triplet Repeat Expansion". Retrieved 2007-10-16.
- ^ "FMR1-Related Disorders". Retrieved 2007-10-29.