Alu elements , Arthrobacter luteus repeat

* https://journals.aai.org/jimmunol/article/206/8/1691/234400/Cutting-Edge-Reduced-Adenosine-to-Inosine-Editing

Alu elementti, mistä tulee tuo nimi? Löysin suomalaisesta keskustelupalstasta selityksen:  "An Alu element is a short stretch of DNA originally characterized by the action of the Arthrobacter luteus (Alu) restriction endonuclease." englantilaisen sitaatin nimittäin. Jokin keltainen artrobakteeri on kyseessä mistä se kai sitten on löytynyt. Katson vielä  Pub; Med lähteestä tuosta bakteerista. https://pubmed.ncbi.nlm.nih.gov/35251637/

https://en.wikipedia.org/wiki/Palindromic_sequence 

* SINE elements, https://en.wikipedia.or/wiki/Short_interspersed_nuclear_element#Classification_and_structure

* Published: 28 December 2011 Alu elements: know the SINEs Prescott Deininger Genome Biology volume 12, Article number: 236 (2011) Cite this articleAbstrac

Alu elements are primate-specific repeats and comprise 11% of the human genome. They have wide-ranging influences on gene expression. Their contribution to genome evolution, gene regulation and disease is reviewed.

Alu elements represent one of the most successful of all mobile elements, having a copy number well in excess of 1 million copies in the human genome [1] (contributing almost 11% of the human genome). They belong to a class of retroelements termed SINEs (short interspersed elements) and are primate specific. These elements are non-autonomous, in that they acquire trans-acting factors for their amplification from the only active family of autonomous human retroelements: LINE-1 [2].

Although active at higher levels earlier in primate evolution, Alu elements continue to insert in modern humans, including somatic insertion events, creating genetic diversity and contributing to disease through insertional mutagenesis. They are also a major factor contributing to non-allelic homologous recombination events causing copy number variation and disease. Alu elements code for low levels of RNA polymerase III transcribed RNAs that contribute to retrotransposition. However, the ubiquitous presence of Alu elements throughout the human genome has led to their presence in a large number of genes and their transcripts. Many individual Alu elements have wide-ranging influences on gene expression, including influences on polyadenylation [3, 4], splicing [5–7] and ADAR (adenosine deaminase that acts on RNA) editing [8–10].

This review focuses heavily on studies generated as a result of the advent of high-throughput genomics providing huge datasets of genome sequences, and data on gene expression and epigenetics. These data provide tremendous insight into the role of Alu elements in genetic instability and genome evolution, as well as their many impacts on expression of the genes in their vicinity. These roles then influence normal cellular health and function, as well as having a broad array of impacts on human health.

*  https://genomebiology.biomedcentral.com/articles/10.1186/gb-2011-12-12-236#Abs1

Alu elements have also been found to host a number of transcription-factor-binding sites. Some of these binding sites are specific to certain Alu subfamilies, and some are also enhanced by changes that occur in Alu elements post-insertion. Dozens of different transcription-factor-binding sites have been predicted within subsets of Alu elements [72]. Although most of these are not validated, it does illustrate the opportunity for such sites to evolve at specific loci into regulatory elements. Sites that have used transcription-factor binding to demonstrate the association with Alu include several families of nuclear receptors [73–75], NF-kappaB [76] and p53 [77]. Thus, Alu elements have, at the least, a tremendous capacity to serve as a sink of bound transcription factors, and in limited specific cases have been found to influence expression of nearby genes.

 https://genomebiology.biomedcentral.com/articles/10.1186/gb-2011-12-12-236/figures/5

 Alu elements and post-transcriptional processing of transcripts. (a) The majority of primary transcripts from genes contain Alu elements, both sense and antisense, within their introns. These Alu elements gradually accumulate mutations that can activate cryptic splice sites, or polyadenylation sites, within the Alu. This can lead to alternative splicing of RNAs that can either include a portion of an Alu in the coding region or result in premature termination of translation. Similarly, Alu elements may cause premature termination and polyadenylation resulting in truncated genes. (b) Alu elements in introns located in opposite orientations can fold into secondary structures that are then a major substrate for ADAR (adenosine deaminase that acts on RNA) activity. The edited RNAs may then have cryptic splice sites activated or may also result in retention of the RNA in the nucleus.