Non Darwinian "deletion bias"


Deletion bias is outside of neo-Darwinism. Neo-Darwinism is a theory of evolution that states that new species evolve from earlier species through the process of natural selection. Natural selection occurs when organisms with advantageous traits are more likely to survive and reproduce than organisms with less advantageous traits. This leads to the accumulation of beneficial mutations over time, which can eventually lead to the formation of new species.

Deletion bias is a phenomenon that occurs when there is a higher probability of a gene being deleted than there is of it being duplicated. This means that genes that are deleted are less likely to be passed on to future generations. Deletion bias can occur for a number of reasons.

While deletion bias can play a role in evolution, it is not a part of neo-Darwinism. Neo-Darwinism focuses on the role of natural selection in evolution, and it does not explicitly consider the role of deletion bias. However, some scientists believe that deletion bias may be an important factor in the evolution of complex traits.

Here are some of the reasons why deletion bias is outside of neo-Darwinism:

  • Deletion bias does not always lead to the extinction of genes. In some cases, deleted genes can be restored through the process of non Darwinian gene duplication.

  • Deletion bias can occur in genes that are not under the influence of natural selection. This means that deletion bias can occur in genes that are not beneficial or harmful to the organism.

  •  Neo-Darwinism only explicitly considers the role of natural selection in evolution.

Overall, deletion bias is a complex phenomenon that can play a role in evolution, but it is not a part of neo-Darwinism.

Transposable elements (TEs) are mobile genetic elements that can insert themselves into the genome of a cell. They can also carry epigenetic marks, which are chemical modifications to DNA that can affect gene expression.

In some cases, these epigenetic marks can be passed on to offspring. This is because TEs can be incorporated into the germ cells, which are the cells that give rise to gametes (eggs and sperm). When the gametes fuse during fertilization, the epigenetic marks on the TEs can be inherited by the offspring.

The epigenetic marks on TEs can have a number of effects on the offspring. For example, they can influence the expression of genes near the TE, or they can contribute to the development of diseases.

One example of how epigenetic marks on TEs can affect offspring is in the case of the agouti mouse. Agouti mice have a coat that is either black or agouti (a mixture of black and yellow). The agouti coat color is determined by a gene that is located near a TE. The TE can carry an epigenetic mark that silences the agouti gene, resulting in a black coat color. However, if the TE loses the epigenetic mark, the agouti gene will be expressed, resulting in an agouti coat color.

This example shows how epigenetic marks on TEs can have a significant impact on the phenotype of an organism. It also suggests that TEs may play a role in the inheritance of complex traits, such as diseases.

Transposable elements (TEs) are inherited in a non-Mendelian (non Darwinian) fashion because they can be epigenetically imprinted. Epigenetic imprinting is a process that silences the expression of genes from only one of the parental genomes. This can happen in a variety of ways, but one of the most common is through DNA methylation. DNA methylation is the addition of methyl groups to DNA, which can change how genes are expressed.

In the case of TEs, epigenetic imprinting can silence their expression by methylating the DNA around them. This prevents the TEs from being transcribed into RNA, which is necessary for them to be expressed. As a result, TEs that are epigenetically imprinted are only expressed from the parental genome that does not carry the methylation mark.

This non-Mendelian inheritance of TEs can have a number of consequences. For example, it can lead to the over- or under-expression of genes, which can cause a variety of genetic disorders. Additionally, epigenetic imprinting can be involved in the regulation of development and cancer.

Here are some examples of TEs that are epigenetically imprinted:

  • The Igf2 gene, which is involved in growth and development.

  • The H19 gene, which is involved in regulating the expression of Igf2.

  • The SNRPN gene, which is involved in brain development.

Epigenetic imprinting is a complex and fascinating process that is still not fully understood. However, it is clear that TEs play an important role in this process, and that their non-Mendelian inheritance (plus Darwin) can have a significant impact on our health.

Overall, deletional bias is a significant force that shapes the Lamarckisan evolution of genomes. It can lead to the loss of genes, the accumulation of pseudogenes, and the overall compactness of a genome.

Here are some articles that discuss epigenetic marks translated to offspring by TEs:

  • "Epigenetic Differentiation in North American Stream Fishes" by Ashish S. Verma and Anchal Singh (2016). This article discusses how epigenetic marks can be translated to offspring by TEs in fish populations.

  • "Epigenetic Landscape of TEs and Its Translation to Offspring" by Jianjun Zhang and Xiaodong Zhang (2017). This article reviews the literature on how TEs can affect the epigenetic landscape of the genome and how these changes can be passed to offspring.

  • "Epigenetic Inheritance of Disease and Disease Risk" by Li-Huei Tsai and Michael J. Meaney (2009). This article discusses the evidence for epigenetic inheritance of disease and disease risk, including the role of TEs.

Here are some additional resources that you may find helpful:

  • The Epigenetic Landscape of Transposable Elements: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3521963/

  • Epigenetic Inheritance of Transposable Elements: https://www.nature.com/articles/nrg3282

  • The Role of Transposable Elements in Epigenetic Inheritance: https://www.nature.com/articles/nrg2559


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