Mendelian epigenetics

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A paper in Nature Genetics describes a mutation in a tomato gene that leads to fruits that don’t ripen. This would be an important discovery in itself–the ripening of fruits is certainly an economically interesting trait–but a further twist makes it even more interesting. The twist: the mutation is actually an epimutation. That is, the two alleles–the non-ripening allele and the wild type allele–have no difference is sequence, but rather a difference in the methylation status of the promoter. The methylated allele is expressed at a lower level, leading to an inhibition of ripening.

Also interesting is that the methylation status of the allele seems to be fairly stable– they claim to have seen a tomato revert from the non-ripening phenotype to wild type three times in 3000 plants grown since 1993. So this epimutation acts essentially in a Mendelian fashion. Whether this will be a common occurrence in plants (or other taxa) remains to be seen.

Related: epigenetics in humans


  1. i don’t remember all the details, but this reminds me of the Arabidopsis superman/kryptonite story 

  2. Given that my green tomato pickle recipe is one of my leading search engine hit generators, I would say that there is commercial value in a tomato that does not ripen. If the effect had been discovered in another plant, I would guess we are not far from being able to apply this understanding to develop a GM green tomato. Kind of silly that it wil be much easier to market a “naturally occuring” one.

  3. So identical DNA sequences might actually be different genes, especially in the case of quantitative traits. 
    Should we be more excited about this?

  4. So identical DNA sequences might actually be different genes, especially in the case of quantitative traits. 
    you mean different alleles? but yeah, it’s intriguing stuff. if epigenetic inheritance is widespread, it would be pretty revolutionary, though if epimutations are stable and thus inherited in a mendelian fashion, it wouldn’t change a whole lot in terms of theory– evolution is substrate-neutral, after all.  
    but in practice, when looking for genes involved in complex traits, epigenetics adds another layer of complexity.  
    I think linkage studies should be robust to causal mutations being stable epimutations, but I’m not so sure about association studies. a reason for irreprodicible association results? (thinking out loud here, but I’m not so sure. I imagine there’s some correlation between genetic variation and epigenetic variation) 
    but there are only a few examples of epigenetic inheritance now. no one knows how big a role it’s going to play.

  5. a whole-genome look at methylation would give us a better picture of how important this is in humans. i expect this kind of data before too long.

  6. i expect this kind of data before too long 
    no doubt