#transposons

Keeping Order

A teacher roams the classroom, keeping groups of children focussed on their separate projects. When she steps outside, desks start creeping, groups fuse, and chaos ensues. Such is the regulatory role of Copia – a sliver of genetic material in fruit flies that new research shows can form a protective shell around itself and shuffle between brain cells. It crosses synapses, where brain cells meet, and then restricts the formation of new connections to keep things in order. The researchers stimulated synapse formation in the junction between cells (pictured, new synapse formation in red) and found that reducing Copia’s activity (middle) or movement (bottom) increased synapse growth compared to normal conditions (top). This suggests Copia keeps this dynamic growth in check until it is needed, showing that the brain has built-in regulators of flexibility. Understanding these elements in humans might help explain brain disease, or even unveil new tools for intervening.

Written by Anthony Lewis

Image from work by P. Githure M’Angale, Adrienne Lemieux and Yumeng Liu, and colleagues

Department of Neurobiology and Department of Biochemistry and Molecular Biotechnology, University of Massachusetts Chan Medical School, Worcester, MA, USA

Image originally published with a Creative Commons Attribution 4.0 International (CC BY 4.0)

Published in PLOS Biology, February 2025

Recent studies show that the emergence of Eusociality in these shrimp seems to have been rapidly driven in a short window of time by a mysterious flurry of motherfuckin Transposon activity!? Fuck me if I don't even think I can begin to grasp the full implications of transposons being able to drive evolution on short time scales, let alone change the entire social/reproductive strategy for a whole species complex in like a handful of generations.

Seriously, typein: 'Synalpheus regalis "Transposons"' into Google Scholar if you need further convincing that the fundamental stuff of reality is information and not the matter it underlies. Its wack as all hell I tell you. Theres like 6 people studying these out of Columbia and I have a strange research crush them and their weird Jesuit friends in Seattle.

One of the simplest ways a transposon can ruin a perfectly good day for a cell is by moving into the middle of a gene. Because transposons move seemingly randomly, there’s no reason one couldn’t move into the middle of a gene. The odds of this are fairly small so don’t sweat it too much, most of your genome isn’t functional anyway. And even on the off chance, a vital gene is disrupted with a transposon, that one cell dying won’t really be of much concern to the other trillion cells in your body. But every once in a blue moon a transposon can move into a really important gene, like a tumor suppressor, and that has the potential to cause cancer. According to research from Johns Hopkins we aren’t sure how common kind of event this is, but new research is slowly narrowing down the connection between cancer and transposons.

Thankfully it’s not all bad news, as over the (millions) of years transposons have been co-opted to help us evolve. While making a gene inoperable is a very probable cause, it’s also possible that the gene can be given a new function, after all over 50% of your genome is or once was a transposon and only 2% of your genome codes for proteins.

A transposon in a normal cell, like a skin, bone or liver cell, won’t be passed on and once that cell dies it will be forgotten entirely. But a transposon that has moved in an egg or sperm cell will be remembered, and be part of that organism for as long as it lives. It even has a chance of being passed on. If the transposon moves into a functional gene it can harm the cell, but it can also add a function that gene previously didn’t have. This transposition, if it winds up in a sperm or egg, and if it causes a change in the organism for good or for bad, will continue to be spread as its descendants breed.

Humans are a good example of this. As our brains have evolved more rapidly than any other organism we know of. One study shows that transposon activity almost perfectly coincides with this rapid evolution, implying that transposons may have had an effect on human intelligence. And this transposition must have started in an egg or a sperm cell to be passed on.

Exit for Two

We all begin as one cell which divides into two – but for an embryo to advance further in development, a so-called jumping gene MERVL needs to be rapidly switched off. MERVL is known to be controlled by a factor called Dux, but how Dux is regulated and affects exit from the two-cell stage was unclear. Now, researchers have discovered that the cell’s nucleolus plays a role in regulating Dux. The nucleolus (pictured; DNA in cyan, nucleolus compartments in various colours) is part of our cell’s headquarters – the nucleus – and responsible for making our protein-making factories called ribosomes, and not commonly associated with gene regulation. By disrupting the nucleolus, Dux quickly re-activated, leading to increased levels of MERVL keeping the embryo stuck at the two-cell stage. Not only does embryonic exit from the two-cell stage require genes, like MERVL, to be switched off, the embryo also requires a functioning nucleolus to advance.

Written by Sophie Arthur

Image from work by Sheila Q. Xie and colleagues

Chromatin and Development Group, MRC London Institute of Medical Sciences, Imperial College London, London, UK

Image copyright held by the original authors

Research published in Genes & Development, March 2022

Hot and Bothered

Nematode worms (C. elegans) are able to fertilise themselves, so it might seem odd to probe them for clues to human fertility. Yet both C.elegans and humans need to protect their precious germline cells – sex cells like the early spermatocytes, which mature along the transparent body of a wriggling worm, shown here stained under a fluorescence microscope. The DNA inside the cells (coloured green-blue) has been exposed to a blast of heat, leaving some damaged areas (purple). Researchers found that ‘heat shock’ harms this DNA by causing genes to ‘jump’, while the worm’s early egg cells or oocytes shield themselves from these damaging alterations. As heat may also damage DNA inside human sperm leading to infertility – perhaps studying the different responses in nematode sex cells might suggest treatments to bolster fertility in response to heat stress from lifestyle, illness and even climate change.

Written by John Ankers

Image by Nicole Kurhanewicz

Institute of Molecular Biology, Department of Biology, University of Oregon, Eugene, OR, USA

Image copyright held by the original authors

Research published in Current Biology, October 2020

I’ve talked before the research done in my lab here, but I haven’t talked about my personal research interests. My of interest is, yes you read the title, transposons. What are transposons though? Transposons, or transposable elements, are bits of genetic code that is transposable (hence the name). In essence, I, you, and nearly every organism that has ever existed has bits of DNA in them that will jump around at random. One minute you could have DNA in spot A in chromosome 1, and the next day it will be in spot Q in chromosome 12. This is the nature of a transposable element.

Transposons were discovered in the late 40s by Barbara Mcclintock while experimenting with maize with broken chromosomes who had noticed that some leaves had unusual color patterns. She hypothesized that these were due to certain parts of the gene breaking in some cells and being added to other cells during cell division. This turned out to be false after she had observed that parts of chromosomes had switched places. The fact that DNA could move was so groundbreaking that she was largely ignored for 20 years. However, her work was fortunately rediscovered when transposable elements were discovered in bacteria in the late 70s. And in 1983 she won a Nobel prize for Physiology or Medicine, so the waiting game did pay off eventually.

Today we know transposable elements are in nearly every organism, from the lowly starfish to the mighty echidna, and everything else with DNA. Why and how they came to exist is anyone’s guess. It’s possible that one transposon developed in the first organism and spread, or it occurs multiple times separately. We don’t have DNA samples from the dawn of life, which makes answering this question very hard. Another curiosity of the transposon is how similar it operates to a retrovirus. A retrovirus inserts its own DNA to a host cell’s DNA (like a transposon) to trick the host into producing more viruses (also like a transposon).

There are two classes of transposons, aptly named Class I and Class II, and both of these classes has to do with how they ‘jump’. Class I transposons (aka retrotransposons) move by being copied into DNA’s sister molecule, RNA. The RNA, now free from the chromosome, moves around until it is copied back into DNA. Like a bad neighbor, this DNA then takes the liberties of reinserting itself back into the DNA.

Class II transposons (aka DNA transposons) are much more direct. Instead of going through the messy process of being copied and converted multiple times, it just up and leaves the spot in the chromosome it’s located in and then enters a new area. What’s good (for the transposons anyway) is that most of the information needed to move is located within the transposon, meaning that as long as it doesn’t mutate it can keep up this seemingly random nomadic lifestyle.

The Scientific Research Notes Of S. Sunkavally (years: 2002-2011).