This is a guest post by JoeCoder.
It’s often argued that when two or more organisms share viral genes in the same place, it is evidence those organisms evolved from a common ancestor. Wikipedia’s Evidence for Common Descent page frames it as follows:
Endogenous retroviruses (or ERVs) are remnant sequences in the genome left from ancient viral infections in an organism. The retroviruses (or virogenes) are always passed on to the next generation of that organism that received the infection. This leaves the virogene left in the genome. Because this event is rare and random, finding identical chromosomal positions of a virogene in two different species suggests common ancestry.
This argument presupposes that the viruses inserted themselves into genomes randomly and stick around as junk DNA baggage, rather than genomes originally being designed with viral-like genes that perform useful functions. However this argument has unraveled as we’ve discovered useful functions for many viral-like genes, including functions that specifically require a viral-like sequence. Some examples among many:
- ERV sequences protect against viral infection through interference–a matching-but-opposite strand of RNA is created to bind to and disable RNA from a virus.
- Likewise, ERV’s seem to function “during embryo implantation to help prevent immune recognition by the mother’s immune system”
- In worms, an ERV has been observed to create actual viruses that transfer DNA from somatic cells (skin/brain/heart/etc.) to germline (sperm/egg) cells whenever the worm is exposed to too much heat, allowing them to rewrite their own DNA for future generations.
- Viral envelopes from ERV transcripts attach to cell membranes in the placenta and causes them to fuse as a normal part of development: “The HERV-W [a human ERV] envelope glycoprotein named syncytin 1 is expressed in all trophoblastic [part of the placenta] cells and directly involved in human trophoblast fusion and differentiation [cells taking on specialized roles]”
These aren’t isolated cases of function. Phys.org interviewed one researcher: “When we investigated public data from embryonic cells, we found that many RNAs originated from regions in the human genome that are ERVs. We did not only observe isolated events, but systematic activation of these ERVs. Every cell type showed transcription of specific classes, something that is very unlikely to occur by chance”.
Those cases all involve RNA viruses and that’s old news. But two weeks ago, a single-celled eukaryote called Cafeteria roenbergensis was found to harbor maviruses within its own DNA that remain dormant until it is attacked by a large virus known as CroV. When this happens the maviruses activate to form an attack fleet, as NewScientist reports:
A voracious marine predator plagued by a giant virus has a defence system we’ve never seen before – it fights back by making its very own virus… Rather than waiting for maviruses to arrive by chance when CroVs attack, it actually carries the genes that code for mavirus inside its own genome. These genes are usually dormant, but they get turned on when Cafeteria is invaded by CroV. “It acts as an inducible antiviral defence system,” write Fischer and his colleague Thomas Hackl in a new preprint paper.
This process kills the Cafeteria roenbergensis cell, but is useful in defending other members of its own species. In this experiment maviruses were deliberately inserted into the Cafeteria roenbergensis genome (see the original paper), but more interestingly, sequences similar to the Cafeteria roenbergensis viral genes have been found in a wide range of animals:
A wide range of animals, from sea anemones to crocodiles, harbour genetic elements called Maverick transposons that closely resemble the mavirus genes. It’s possible that some of these organisms can also unleash viruses that attack giant viruses.
In spite of this, New Scientist still argues “our genomes are littered with the mutant remains of viruses and genetic parasites.” But these discoveries reveal this as a rapidly-shrinking argument of the gaps.
Save this for the next time someone insists that viral genes are useless junk DNA and therefore evidence of common descent.