https://www.ualberta.ca/folio/2023/12/researchers-reveal-full-structure-of-ancient-genetic-parasite.html

Paywalled article:
https://www.nature.com/articles/s41586-023-06947-z

This research group is trying to determine the structure of the LINE-1
transposon proteins. They want to know how to inactivate this DNA
parasite because it is implicated in cancer and genetic diseases. LINE
elements are just long interspersed nuclear elements. There are 3 of
them LINE-1, 2 and 3 (not very imaginative, but easy to remember).
There are around 900,000 copies of LINE transposon sequences in our
genome and they make up 21% of the human genome. LINE-1 is the most
abundant and makes up over 14% of our genome, but it is responsible for
1.5 million SINE transposons (short interspersed nuclear elements) that
use the LINE-1 protein sequences to jump around the genome. The SINEs
lack the ability to move on their own, but the LINE-1 machinery
recognizes them and can replicate them and stuff them into somewhere
else in the genome. This family of SINEs account for 13% of our genome,
and are a big reason why we want to shut down the LINE-1 machinery. The
LINE-1 family of transposon sequences have their own protein genes, and
transcriptional regulatory sequences and ENCODE initially counted them
among functional sequences in our genome, but they are selfish DNA
parasites. Just these three LINEs and their related SINE account for
34% of our genome.

I usually put up the ALU transposon (A type of SINE transposon) because
it recently evolved and exists in the primate lineage, and already
accounts for 10% of our genome after starting from nothing less than 80
million years ago. The LINES are ancient. They were jumping around our
ancestor's genomes when terrestrial vertebrates were evolving before
amniotes evolved. They have been involved in what makes us human
because like any other mutation they might not do much at all when they
jump into a new location. They might rarely do something good, and
likely more bad than good would be expected. As I indicated they are
associated with inducing cancer (they are jumping around in your cells
right now) and have been associated with genetic inherited diseases.
Most of the ALU transposons haven't been functional for over 30 million
years, so they have been stuck in place since they were inactivated, and
you will see some crazy numbers like we share 95% of our ALU sequences
with chimps because we both inherited them from our common ancestor. We
share more ALU sequences with chimps than we do with orangutans and less
with monkeys than we do with the other apes.

Transposons don't just kill the IDiotic junk DNA argument, but they are
amazing evidence for descent with modification.

Ron Okimoto