To non-sciencey types, there's a technology that's become very powerful in the last 6 years or so called RNA interference or RNAi. Basically, this technology involves the formation of small duplexes of RNA (called small interfering RNA or siRNA) that match the sequence of a transcript, and using machinery conserved across many species, are then able to destroy or disable that transcript thereby preventing expression of the protein the transcript encodes. Here's an image I whipped up a few years ago.



There are some funny things going on here. For one, usually people only think of DNA has forming a binary structure, but RNA, the "messenger" of the cell also forms very complex secondary structures and can form duplexes when a complementary strand is present, just like DNA. Second, RNA is getting many more roles ascribed to it than the dogma of molecular biology (the idea that DNA is transcribed into RNA which is then translated into a protein) originally allowed. We're finding out that RNA can act as an enzyme, that it forms complex structures in combination with proteins to carry out unique functions in a cell, and now that it might be regulating transcription itself through this conserved mechanism of RNAi. This has been a big deal in biology in the last few years even though people outside of biological science have heard little about it. Slowly, especially as the technology is being adapted for the treatment of disease (think about it, it allows you to destroy the gene product of a specific target - a virus, an oncogene, a genetic defect etc.) more people are finding out about it. Think of it this way, it's a little bit like a sniper rifle scientists can use to target a gene, it's pretty damned accurate (it does miss sometimes - not always 100% specific) and allows the specific destruction of a target gene product.

Further, there is evidence that RNAi, at least in lower organims like the flatworm C. elegans, is somewhat hereditary. Think about it, hereditary RNAi! Take that Mendel!

It has been shown that phenotypes induced in C. elegans by RNAi can last for two or three generations2. Because the generation time of a worm is only three days, however, it is not clear whether this effect can be explained simply by a slow dilution of the silencing factors. We have therefore investigated the heritability of gene silencing by RNAi over many generations in C. elegans and used an RNAi screen to identify genes that may influence this inheritance.

We injected wild-type Bristol N2 worms with a double-stranded RNA that targets the C. elegans gene ceh-13 for one generation. The Ceh-13 phenotype, in which the worm is small and dumpy, persisted in some animals indefinitely. Inheritance was not fully penetrant: only about 30% of the progeny of Ceh-13 worms inherited the phenotype. Wild-type siblings never had progeny with the Ceh-13 phenotype, and crossing worms that had a Ceh-13 phenotype with unaffected males showed that the trait is dominant. A single episode of RNAi can therefore induce heritable silencing that is not fully penetrant and behaves in a dominant fashion.

To show that this is a general phenomenon, we targeted 171 other genes by using a single treatment of RNAi and found 13 that could be inheritably silenced.
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We also showed that a single transgenic copy of a gene (gfp) expressing green fluorescent protein (GFP) could be silenced, and the silencing inherited. We used animals expressing GFP under the control of a germline-specific promoter and created interference by feeding them bacteria that express double-stranded RNA homologous to gfp; progeny that did not express GFP were then transferred to new plates. In all siblings, GFP expression was reduced relative to wild-type expression (Fig. 1). We detected animals that had reduced GFP expression over 80 generations.

80 generations! This is inheritance without DNA, over many generations, without a clear mechanism of transmission from generation to generation. It will be interesting to find out how these things propagate this effect, whether the siRNAs are somehow duplicating themselves, or whether they are generating a heritable DNA modification like methylation of the DNA or chromatin modification (they have data suggesting the latter). Makes you think we have to be careful not to generate germline RNAi in human experimentation (although it would be very unlikely to occur unless the reproductive tract were a target). Also, some astute readers will note that a related result was shown previously in Nature in mice in which RNA was creating a hereditary trait. However, despite being very interesting the study had major flaws in controls and explanation of some rather bizarre data. This flatworm one is much more clear cut.

I also like siRNA/RNAi because it really shoots the irreducible complexity arguments of the IDers all to shit. Scientists knock down gene products in cells all the time, and you know what? Most the time, very little happens (we'd graduate faster if more things happened). The cell is not a mouse-trap, and many cells can tolerate the loss of many functions without any adverse effect at all.