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How did you get to be you? In other words, what selfish genes made humans have...

How did you get to be you? In other words, what selfish genes made humans have some of their unique features. Be succinct.

The Selfish Gene by Richard Dawkins:

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The existence of stretches of DNA that can promote their own transmission at the expense of other genes in the genome, but have no or a negative effect on organismal fitness known as selfish genetic elements,later on it is known parasitic DNA, selfish DNA, ultra selfish genes, genomic outlaws, and self-promoting elements.  

Genes as “selfish replicators” encoding phenotypes that increase their transmission to future generations and organisms fundamentally as “vehicles” for the transmission of genes.

Rapid advances in molecular biology began to reveal that many eukaryotic genomes contain large amounts of repetitive DNA without any clear function, although their potential role within the genome was the subject of much speculation A group (or a species) can survive only if individuals behave in their genetic self-interest and form alliances, and make sure that their genes are passed on. And that the genes have the conditions and opportunities to become hardier and replicate themselves more fluently. Human whole genome act as selfish where repeating element act protector for the genome. The modification in these repeat play a crucial role in the gene expression and function. there is well establish linkage between them and accumulation of these repeats have been majorly derived by transposable element(TE).Transposable element (TE) have been a part of human evolution. In eukaryote genomes, the abundance of TEs can vary widely.  For example, ∼40% of the human genome is composed of TEs, whereas only 3% of the pufferfish genome As a result, TEs and other repetitive DNA can be major determinants of genome size within taxa . Majority of TEs that insert near or in protein-coding regions are deleterious, mounting evidence indicates that fragments of inserted TE DNA have also evolved cis-regulatory or posttranscriptional regulatory functions. Evidence for this includes conservation of TE-derived fragments in ∼25% of human promoters and deeply conserved fragments in cis-regulatory modules of mammals, as well as evidence of a regulatory role.These regulatory elements have evolved from ancient insertions of TEs that are no longer active in the mammalian lineage. A basic interpretation is that TE insertions provide abundant sequence variation in regulatory regions on which selection can act.


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