So, regulation of these transposon movements is really not well understood. Scientists don't have a good grasp on how these are moving, what causes them to move, what prevents them from moving, but there has been some research into non-coding RNAs that can silence and stop the transposon movement. So, remember some examples of non-coding RNAs? Those are things like siRNAs, microRNAs, piRNAs. There are all these different types of non-coding RNAs, and some of them have been found by scientists to affect transposon movement.
The first example of this is actually the TC1 transposon in C. elegans. Remember, C. elegans are those worms, the C3 worms. And the TC transposon is found in the genome, meaning that it's going to be found in somatic cells, so the cells that make up the worm body and the worm neurons and all that, and also the worm germ cells, the worm, you know, eggs, essentially. But the transposon actually only jumps around in the somatic cells. In the germ cells, it doesn’t; it's completely stationary. And so scientists were like, well, it's present in the germ cell, so why isn't it moving? And so what they found is that in the germ cells, this TC1 transposon is actually transcribed. So, it's transcribed normally as part of another gene. So this gene is being transcribed and it's kind of found at the end of that gene, but that RNA polymerase, it keeps going, it keeps transcribing, and it eventually transcribes the TC1. Then you have TC1 RNA. And this TC1 RNA contains a repeated sequence, like most of these transposons have those repeated sequences at the end. And those repeated sequences, actually, because it's now transcribed, it's a single-strand RNA. Right? That causes that RNA to fold upon itself and bind those repeated sequences that are really similar. And when it folds upon itself, it becomes dsRNA. Now, does the cell like dsRNA? Does it just sort of allow it to sit there in the cell and just be like, oh, you’re fine. You know, you are a little abnormal, but we’re just going to allow you to sit here? No. Right? The cell is like, oh my gosh, there’s double-stranded RNA. I got to get rid of that immediately, and so it does. So, it activates the sort of pathway that we've talked about with microRNAs and siRNAs. So the cell recognizes double-stranded RNA and it brings in Dicer. Should you remember, we talked about that. We may have talked about that in the RNA interference, but if you're not familiar with it, your book may be a little bit out of order. But, essentially, there's this protein that comes in, it recognizes double-stranded RNA, and it's called Dicer. So, it processes it, and then a second protein comes in called RISC, and that binds to it. And when RISC binds to this processed TC1 transposon, it then targets it to degrade other TC1 transcripts. So what happens, the TC1 gets transcribed, the RNA folds on itself, the cell's like, whoa, there’s double-stranded RNA, brings in dicer, brings in RISC, and when TC1 is bound to RISC, it targets to degrade other TC1 transcripts. So that means that those transposons are never getting—they’re never jumping, because whenever they get transcribed, they’re immediately destroyed by this RISC-TC1 complex. So what happens is you have a gene and very close after you have this transposon. So when the protein comes on to bind to transcribe, what you get is you get the gene RNA and you also get the TC1 RNA. This TC1 RNA has inverted repeats that folds upon itself. When it folds upon itself, that's targeted by Dicer, and RISC, and RISC binds to it, after it's processed, and targets these transcripts for degradation. So, these and all the rest of them will be degraded. And so, this is an example of how non-coding RNAs work to degrade these transposons and suppress their movement.
Some examples of other elements that help regulate transposons are piRNAs, and this is an example in other animals. And this works very similarly to the method we talked about above, but I do just want to mention some of the differences. So, the first is that pi clusters exist, and pi clusters are huge regions of DNA that contain the transposons. And these transposons are just transcribed as these large pieces of DNA. So these, they have this long, long, long, long, long—huge transcript. Right? The RNA transcripts are processed, and when they are processed, they are complexed with a protein. This protein's name is Argonaute. You don’t necessarily need to know it, but I'm just putting it here in case you’re interested in what the protein's name is. But, essentially, you have this long RNA. It’s processed into little transposons. These come in. They bind to Argonaute. And when they are bound to Argonaute, it goes around and degrades all the other transcripts. Again, very similar to how this works above, just different names. The pi clusters and the Argonaute are the different names of how this works. There are ways that this works in bacteria through CRISPR-Cas systems, and, this is very similar. I’m not going through the process again, but essentially, this process of the mechanisms through which it works is called CRISPR, which you may have heard of. I think they’re maybe potentially making a show about CRISPR and gene editing, like, on a big network or something. But, anyways, you may have heard of CRISPR. It’s kind of this big new hit thing in science, for gene editing. But, essentially, it works by targeting different genes for silencing and degradation, and it does so by targeting transposons as well. So, like I said, scientists aren't sure if this is the only way that transposons are regulated. They can be regulated in a number of different ways that scientists don't know about yet. But, essentially, they think that the non-coding RNA is at least one major way that transposons can be silenced in cells in which they're not expressed. So, with that, let's now move on.
