Enomic transposition, and through horizontal transfer. TEs are able to replicate more rapidly than the genome, and so constitute a kind of genomic cancer. They are basically parasitic, i.e. selfish, and deleterious entities, conferring no benefits on the genomes they inhabit. For these reasons, they were long considered to be “junk DNA”, part of the genome that by definition it would be better to get rid of, because it has no role, no function, and is just a kind of genetic burden for the host genome. This simplistic view must now be tempered. First of all, TEs and the rest of the genome have lived side by PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/27107493 side for a very long time and such prolonged cohabitation almost inevitably leads to various kinds of interaction. Second, having no known role does not necessarily imply having no impact: day after day, portions of the genome that were previously thought to be useless have been shown to have important regulatory or structural roles. The same could be true for TEs. Hence, when considering genome evolution, TEs are far from being just parasitic sequences [39]. Starting from the simple assumption that DNA is separated into two compartments, the genome, and the TEs, we review below the relationships between them in all their diversity. We will focus first on how the genome deals with the sea of TEs that surrounds it, and then on how TEs deal with the host genome in which they are embedded.From mutations to polymorphism, genetic variants reflect the diversity within a population, and DNA alterations or changes constitute the basis of evolution. At the DNA level, two molecular mechanisms are responsible for generating diversity: mutation and recombination. Classically, mutations (changes in nucleotide sequences) arise either through uncorrected replication errors or after DNA lesions; whereas recombination is a normal process during the meiotic phase. However, both processes can also result from the activity or mere presence of a transposable element. Transposition does not result from fortuitous errors during replication or lesion repair, but can be considered to be an active mutagenic process, resulting in mutations that are different from SNPs (Single Nucleotide Polymorphisms). In contrast, TE-induced ectopic recombination can be viewed as an erroneous (albeit easy-to-produce) process in contrast to normal meiotic crossing-over. Such DNA alterations may affect the function (of genes) and the structure (of genomes), the worst outcome being the immediate death of the cell, or its inability to complete meiosis. However, mildly detrimental or neutral effects are also to be expected, and insertions that produce such effects may survive and contribute to the genetic variation of the host genome. There are many diverse ways in which TEs can alter the genome, ranging from small sequence modifications to gross rearrangements. Finally, the frequency of such events is not negligible, which means that TEs are major actors in diversity [40,41].1 – Genomes use TE sequences and TE-induced sequence changes to increase their functional variabilityEvolution of the genome in a sea of TEs Although Darwin had no idea about what constituted the support of heredity, he fully recognized the importance of variability as the raw material of natural selection. It was a long time before connections could be AZD4547 solubility established between continuous variation in a population, the discrete characters Mendel used to demonstrate the laws of heredity, and mutations (as defined by.
