Expressed another way, it is believed modern Alu elements emerged from a head to tail fusion of two distinct FAMs (fossil antique monomers) over 100 million years ago, hence its dimeric structure of two similar, but distinct monomers (left and right arms) joined by an A-rich linker.
[8] In 1988, Jerzy Jurka and Temple Smith discovered that Alu elements were split in two major subfamilies known as AluJ (named after Jurka) and AluS (named after Smith), and other Alu subfamilies were also independently discovered by several groups.
Dating back 65 million years, the AluJ lineage is the oldest and least active in the human genome.
[11] B1 elements in rats and mice are similar to Alus in that they also evolved from 7SL RNA, but they only have one left monomer arm.
The recognition sequence of the Alu I endonuclease is 5' ag/ct 3'; that is, the enzyme cuts the DNA segment between the guanine and cytosine residues (in lowercase above).
[17] Alu elements are retrotransposons and look like DNA copies made from RNA polymerase III-encoded RNAs.
[18] Alu element replication and mobilization begins by interactions with signal recognition particles (SRPs), which aid newly translated proteins to reach their final destinations.
[10] Alu elements in primates form a fossil record that is relatively easy to decipher because Alu element insertion events have a characteristic signature that is both easy to read and faithfully recorded in the genome from generation to generation.
This is because insertion of an Alu element occurs only 100 - 200 times per million years, and no known mechanism of deletion of one has been found.
In genetics, the presence or lack thereof of a recently inserted Alu element may be a good property to consider when studying human evolution.
[21] Alu elements have been proposed to affect gene expression and been found to contain functional promoter regions for steroid hormone receptors.
Thus due to their major heritable damage it is important to understand the causes that affect their transpositional activity.