In an earlier post, I presented the viewpoint that organisms have the built-in ability to respond to the changes in their environment or to stress, which may lead to changes that are passed down through generations. To support this idea, I referenced a number of studies. A newly published paper that appeared online just three days ago further reinforces this concept.
Interesting study, @Midhun. I only glanced through the paper, but I find the possible correlation of transposable elements with possible environment-induced heritable changes to be interesting. Might this be the long sought-after role for junk DNA - namely, promoting evolutionary change? Wouldn’t it be something if one ID-friendly concept (functionality of junk DNA) refuted another ID theoretical notion (namely, that huge increases in information must accompany evolutionary change).
I wonder of this research group plans on following for more than 4 generations, or if they intend to do a whole bunch of genome sequencing (to identify the heritable changes at the sequence level).
Careful now. There’s no indication of genetic changes, just changes in gene expression. The mechanism of inheritance of those changes is not considered, and whether the inheritance is long-term enough on an evolutionary time scale is unknown. Nor is the means of induction known, or whether it’s at all adaptive. Nor do I see any clue that a significant fraction of junk DNA is functional.
Ya perhaps. This paper states the same in it’s Discussion section.
While I support Design, my views may diverge from those of other supporters. I don’t share the belief that the entire human genome is functional, nor do I adhere to the notion that “huge increases in information must accompany evolutionary change”
Yes. It would be very useful if they uncover what happened at the sequence level.
Yes, this study doesn’t offer details at the sequence level. It would be beneficial if future research addresses these aspects.
Let me know if you’re interested to read other studies demonstrating how environmental stress triggers transposon insertions, thereby facilitating adaptive evolution.
If I understand correctly, this is actually promoting change to the genotype, not just changing levels of expression for the phenotype (epigenetic change)?
No, every insert is a change at the genotype or sequence level, whether or not it’s junk. There are two questions here. Does environmental influence cause trasposon insertions to increase? And are such insertions random or are they in some way biased toward adaptation? So far, not much to go on.
And since most transposon loci are actively silenced, it is entirely plausible that various environmental stressors can disturb this repression, resulting in increased transpositional activity.
Even if they are biased to be more likely to be adaptive in some way or another, it’s still essentially a chance-based process where large numbers of random events are “tested” by selection for their fitness-effects. The whole thing is Darwinian to the core.
An important side-question also: how would you determine the baseline probability that transposon insertions produce beneficial outcomes? I mean what is the expected ratio of deleterious:neutral:beneficial transposon insertions without bias?