Epigenic Inheritance
To kick off the 31 Days of Weird Science I wanted to start with a magnificent post. But there are so many interesting things going on in the world of science now, I had a hard time deciding what the quintessential weird thing is that they’re all talking about. The faster than light neutrino story would be a good one, but that’s already covered all over the place. What to do? What to do?
Last Friday I read Charles Tan’s interview with Athena Andreadis over at sfsignal.com. Athena stated she was surprised that science fiction writers don’t write about some of the more interesting stories from current science. Even though she was talking about science fiction, it gave me an idea for this non-fiction-about-science blog. She brought up several topics that piqued my interest. I picked one of them: epigenetics. It’s weird and appropriate.
In a nutshell epigenetic traits are changes in gene expression (what something looks like for instance) that have not occurred through changes in the DNA. It’s easy to see how environment affects our bodies after we’re born. We break legs, contract diseases. These things change the way our bodies look and function. What’s weird is that sometimes these changes due to environment can be passed on to offspring. Doesn’t that just fly in the face of everything you learned in Genetics 101?
As self-respecting denizens of the 21st Century, we pooh-pooh Lamarck. The Lamarckian model of evolution has the giraffe coming into being after generations of horses slowly stretched their necks through lifetimes of eating leaves higher and higher on the trees. One individual’s neck grew slightly longer in its lifetime and that slightly longer neck was passed on to the offspring whose neck also elongated slightly in their lifetime. After several lifetimes of slight neck stretches, voila! we have a long-necked horse.
How silly. Us self-respectors subscribe to Darwin and Mendel nowadays. Inherited change occurs in the genes rather than in the bodies of the gene expressors: the people. Or the animals.
But hold that thought. There is evidence afoot that we CAN inherit changes that come about due to environment acting on the phenotype rather than mutation in the DNA acting on the germ cells. We call that process Epigenetic Inheritance, and to this biology-major, college-graduate, that’s just weird.
Here’s a quick rundown of the classic example for epigenetic inheritance posted by the Institute of Science in Society:
“In the nest, the mother rat licks and grooms her pups, and while nursing, arches her back to groom and lick her pups. Some mothers (high performers) tend to do these more frequently than others (low performers). As adults, the offspring of high performers are less fearful and show more modest responses to stress in the hypothalamus-pituitary-adrenal (HPA) neuro-endocrine pathway.
Cross-fostering studies showed that the biological offspring of low-performers reared by high-performers, resemble the offspring of high performers, and vice versa. …
Amazingly, the pups of both high and low-performing mothers start out life genetically the same.”
There are other examples out and about. Children of holocaust survivors develop diseases they would not have developed had their parents not been malnourished during part of their lives. Fruit flies exposed to harsh chemicals grow bristly eyelashes (obviously these scientists are working with bodacious microscopes to be able see that) and then their younguns grow bristly eyelashes too.
When details of the methods for inheritance are explained, often I have a hard time deciding if this is something different than regular inheritance via genes. It seems to involve the DNA somehow. The difference between the two mechanisms is too subtle for me to happily accept a Lamarckian model. It begs further investigation.
Regardless, whatever is going on is certainly weird and proves once again that the more we discover, the less we know. It’s sort of a built-in feature of science that keeps us coming back for more.
Science Daily nicely illustrates this weirdness that is scientific study generally and epigenetics specifically in the title of their 2009 article, “100 Reasons to Change the Way We Think About Genetics.”
Sue Lange
Sue Lange’s latest ebook, Tritcheon Hash, is full of lapses of logic and weird science. Get your copy from Amazon or read a couple of free chapters at the publisher’s website.
Some genes appear to have an effect on lifespan. This shouldn’t be too surprising news. But now, a research team from Stanford has shown that there are epigenetic effects on longevity as well. Using the nematode Caenorhabditis elegans, a beloved model organism in aging research, they have shown that some changes in chromatin states in a parental generation can affect the lifespan of their descendants.
More specifically, they looked at the regulatory complex H3K4me3, which is composed out of ASH-2, WDR-5 and SET-2, and responsible for adding methyl-groups to the H3 histone. It has been shown that deficiencies in this complex extend lifespan. So, the researchers proceeded by ‘knocking out’ each of the components of this complex separately and determine whether or not this had an effect on the lifespan of the little worms.
The disturbance of each of the components significantly increased lifespan. Not only of the worms in which the components were disabled, but, and this is the important part, also in their descendants up to three generations later (the increase ranged from 20 to 30%) (see figure 1). So, even without changes in the DNA, the descendants somehow inherited the epigenetic markers of the parental generation. These markers are thought to be ‘reset’ each generation, and yet some epigenetic markers are transferred to the next generation. How exactly this happens is one of the big questions in epigenetics.
Figure 1: (a) Breeding schedule of the worms, where +/+ is the wild-type and wdr-5/wdr-5 the worms where WDR-5 is 'knocked out', (b), (c) and (d) represent the lifespan of the descendants after 3, 4 and generations respectivley. (Similar results were obtained for ASH-2 and SET-2.)
(Source: Greer et al., 2011)
This study shows that even traits as complex as lifespan can be significantly influenced by epigenetic markers.
The authors conclude:
Our study provides the first example of epigenetic inheritance of longevity. Histone methylation marks and DNA methylation are generally, but not always, erased between generations with epigenetic reprogramming. Our observations are consistent with the notion that H3K4me3 at specific loci may not be completely erased and replenished. … As the ASH-2 H3K4me3 regulatory complex is conserved from yeast to humans, manipulations of this complex in parents might have a heritable effect on longevity in mammals.
To test this, the lab is currently testing this in African killfish and mice. While this might not be as relevant in vertebrates as in nematodes, it’s certainly worth taking a look, isn’t it?
Reference
Greer, E.L.; Maures, T.J.; Ucar, D.; Hauswirth, A.G.; Mancini, E.; Lim, J.P.; Benayoun, B.A.; Shi, Y. and Brunet, A. (2011). Transgenerational epigenetic inheritance of longevity in Caenorhabditis elegans. Nature. Published online 19 October. doi:10.1038/nature10572.
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