So-called 'junk' DNA plays a key role in speciation

Now, in the latest installment of their work, published online July 24 in the journal Molecular Biology and Evolution , Yamashita and former postdoctoral fellow Madhav Jagannathan, currently an assistant professor at ETH Zurich, Switzerland, take these studies a step further, proposing that the system of chromosomal organization made possible by satellite DNA is one reason that organisms from different species cannot produce viable offspring.


So much wrong with that brief excerpt. Calling Larry Moran.

  1. “do not code for proteins” used as synonym for “junk”.
  2. “organisms from different species cannot produce viable offspring”
  3. “key role in speciation”

Some of this is probably not the fault of Yamashita and Jagannathan but of whoever wrote that article/press release.


From their actual paper:

Little or no sequence conservation is not a criterion for a genome segment to be regarded as junk. This is probably what contributed to the misunderstanding of popular press article writer.

“Well, these are junk sequences, who cares if your junk is different from mine?'” said Jagannathan.

You mean other than Susumu Ohno in the paper that coined the term?

Link to source paper:

Defective Satellite DNA Clustering into Chromocenters Underlies Hybrid Incompatibility in Drosophila

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Lack of conversation is definitely a significant indication of whether some given stretch of DNA is likely to be actual junk or not. If something is not functional, it’s going to be under relaxed selection (probably only weak purifying selection will be affecting the locus), and hence it won’t be conserved as mutations can almost indiscriminately accumulate. That means generally expect junk to be show lack of conservation, and hence lack of conservation is evidence favoring the junk hypothesis.


The rise of inarticulate DNA – what is the world coming to. :wink:


I’m surprised more people don’t talk about this.


Not even gonna edit that.


So if I have this right (and I’m not sure I do), just because increasing divergence of junk DNA might play a role in genetic isolation of descendent species, does not mean that the DNA is any less “junky”; in fact the opposite, its non-essential character may allow the accumulation of hybrid incompatibility while passing without notice within each isolated population.

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I frequently run into the misapprehension that lack of conservation is meant to conclusively prove junk, and the reverse that conservation is meant to conclusively prove function. But we do of course know of examples of both genes that were relatively well conserved, only to no longer become necessary and turn into junk, and where a useful gene with a significant effect on fitness recently evolved from junk DNA that had, up to that point, been accumulating mutations under almost no purifying selection.

Conservation is nevertheless evidence. A very good indicator of whether you are dealing with junk or not. But exceptions, minor(though important) deviations from that main pattern are of course known.


Thoughtful response, but…


I’d have to disagree. It’s one of the main diagnostic criteria. That doesn’t mean it always works, though. Further, junk DNA could easily cause reproductive incompatibility and remain junk. Reproductive incompatibility is not a function.


Oops! I forgot to insert “sure” before “criterion”. Don’t blame me, blame my exam-study-fatigued brain at the time when that comment was written (is my brain me?).

To me, the authors seemed to saying that if there is poor sequence conservation then biologists would definitely proclaim junk DNA. I was kicking against the seeming absoluteness in that excerpt.

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Surely reproductive compatibility is a function and incompatibility is hence a lack of function?

(I’m imagining junk DNA preventing chromosomes lining up properly or some such).

P.S. Serious question for a change, in case it’s not obvious.

Function is in the eye of the beholder.

Yes. Though there is such a thing as reinforcement. If there is strong selection against hybrid individuals, selection may favor increased prezygotic isolation.

Careful. That way lies ENCODE. Words do have meanings.

Yes reproductive compatibility is a function, and of course critical to the continued existence of the species, so any locus that is strictly required for reproduction I would say isn’t actually junk, even if the sequence in question is evolving under very little sequence constraint. We could imagine that despite the locus evolving near to the neutral rate, this is nevertheless still so slowly that any two members of the population are unlikely to be so different from each other that they are incompatible.

But reproductive compatibility between members of ostensibly different species is not a function that is critical to the continued existence of either of two such populations, so the inability of sufficiently diverged members of two populations to reproduce with each other doesn’t mean the locus has become nonfunctional, it just means they’ve diverged too much from each other. Within each population(which we could define due to their reproductive compatibility) they might very well still be similar enough that they can reproduce.

The question is, has anyone ever pinpointed the specific DNA analyzed in the OP paper and declared this to be junk, or is that just a more general inference about most fast-evolving microsattelite repeats? I’ve seen too many papers declaring that they’ve found a new function for “something previously thought to be junk”, only to not actually cite anyone declaring the DNA being studied junk. For the most part I think these geneticists don’t understand the rationale behind the junk inference, nor it’s non-absolutism.

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This was interesting to me. Interested also in comments from the forum.

Furthermore, the researchers could create a healthy hybrid fly by mutating certain genes in the parent flies called “hybrid incompatibility genes,” which have been shown to localize to satellite DNA in the cells of pure species. Via these experiments, the researchers were able to demonstrate how these genes affect chromosomal packaging in hybrids, and pinpoint the cellular phenotypes associated with them for the first time. “I think for me, that is probably the most critical part of this paper,” Jagannathan said.

Taken together, these findings suggest that because satellite DNA mutates relatively frequently, the proteins that bind the satellite DNA and keep chromosomes together must evolve to keep up, leading each species to develop their own “strategy” for working with the satellite DNA. When two organisms with different strategies interbreed, a clash occurs, leading the chromosomes to scatter outside of the nucleus.

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