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Epigenetics and the “Drift-Barrier Hypothesis"

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The principle that "selection on gene-level mutation rates cannot overcome genetic drift" underscores the role of random chance in shaping evolutionary trajectories, particularly within smaller populations. This principle largely rests on the premise that genetic mutations occur randomly and at relatively stable rates, making them susceptible to the whims of genetic drift.  The "drift-barrier hypothesis" suggests that there's a limit to how much natural selection can reduce mutation rates. This limit is set by the genetic drift. In essence, when the selective advantage of further reducing the mutation rate becomes smaller than the random fluctuations caused by genetic drift, selection becomes ineffective. Therefore, genetic drift can constrain the ability of selection to fine-tune mutation rates. However, the burgeoning field of epigenetics introduces a nuanced perspective, suggesting that this dynamic might be more malleable than previou...
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Mutation Bias Not Random Mutations

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The article "Mutation bias alters the distribution of fitness effects of mutations" delves into a crucial aspect of evolutionary biology: how the inherent biases in the mutation process itself shape the landscape of evolutionary change. Rather than mutations occurring randomly with equal probability across all possible changes, the authors highlight that some mutations are inherently more likely than others, and this bias profoundly influences the distribution of fitness effects (DFE). The DFE is a fundamental concept in evolutionary genetics, representing the spectrum of selective consequences that mutations have on an organism's fitness. Traditionally, it's often assumed that the DFE is primarily shaped by natural selection , with beneficial mutations being rare and deleterious mutations being common. However, this article emphasizes that mutation bias, an often-overlooked factor, plays a significant dominant role. The central argument of the paper re...
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The Epigenetic cause of Multiple Sclerosis challenges Evolutionary Theory

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The role of DNA methylation in the development of multiple sclerosis (MS) brings to light the complexities of epigenetic mechanisms and how they interact with genetic and environmental factors. This area of research also raises intriguing questions that challenge the core tenets of neo-Darwinism. Here's a breakdown of the subject: DNA Methylation and Multiple Sclerosis: Epigenetics and MS: MS is a chronic autoimmune disease affecting the central nervous system. Research has increasingly highlighted the role of epigenetics , particularly DNA methylation, in its development. DNA methylation involves the addition of a methyl group to DNA, typically at cytosine-guanine dinucleotides (CpG sites). This process can alter gene expression without changing the underlying DNA sequence. Studies have revealed that MS is associated with altered DNA methylation patterns, particularly in immune cells. These changes can influence the expression of genes involved in immune regulation a...
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Epigenetics small RNA a challenge to Francis Crick's Central Dogma

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The central dogma of molecular biology, initially proposed by Francis Crick, outlines the flow of genetic information: DNA to RNA to protein. This linear model has been foundational, but the fields of epigenetics and small RNA biology have revealed complexities that challenge its strict unidirectional nature. Here's how these fields contribute to a more nuanced understanding of information flow: 1. Epigenetics: Beyond the DNA Sequence Definition: Epigenetics refers to heritable changes in gene expression that occur without alterations to the underlying DNA sequence. These changes influence how genes are turned on or off, affecting phenotype. Mechanisms: Key epigenetic mechanisms include: DNA methylation: The addition of methyl groups to DNA, often silencing gene expression. Histone modifications: Chemical modifications to histone proteins, which package DNA, influencing chromatin structure and accessibility. Chromatin remodeling: Changes in the structure...
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