Epigenetics: changes don't have to be do mutation

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Humans kept Red Junglefowl as livestock about 8000 years ago. Evolutionarily speaking, the sudden emergence of an enormous variety of domestic fowl of different colours, shapes and sizes has occurred in record time. The traditional Darwinian explanation is that over thousands of years, people have bred properties that have arisen through random, spontaneous mutations in the chickens' genes.

Linköping zoologists, with Daniel Nätt and Per Jensen at the forefront, demonstrate in their study that so-called epigenetic factors play a greater role than previously thought. The study was published in the high-ranking journal BMC Genomics.

They studied how individual patterns of gene activity in the brain were different for modern laying chickens than the original form of the species, the red jungle fowl. Furthermore they discovered hundreds of genes in which the activity was markedly different.

Degrees of a kind of epigenetic modification, DNA methylation, were measured in several thousand genes. This is a chemical alteration of the DNA molecule that can affect gene expression, but unlike a mutation it does not appear in the DNA structure. The results show clear differences in hundreds of genes.

Researchers also examined whether the epigenetic differences were hereditary. The answer was yes; the chickens inherited both methylation and gene activity from their parentages. After eight generations of cross breeding the two types of chickens, the differences were still evident.

The results suggest that domestication has led to epigenetic changes. For more than 70 % of the genes, domesticated chickens retained a higher degree of methylation. Since methylation is a much faster process than random mutations, and may occur as a result of stress and other experiences, this may explain how variation within a species can increase so dramatically in just a short time. Nätt and Jensen's research may lead to a review of the important foundations for the theory of evolution.

More information: Heritable genome-wide variation of gene expression and promoter methylation between wild and domesticated chickens by Daniel Nätt, Carl-Johan Rubin, Dominic Wright, Martin Johnsson, Johan Bel
 
If it isn't in the genes it is not inherited, it will not be maintained within the population.

Grumpy:cool:
 
Grumpy said:
If it isn't in the genes it is not inherited, it will not be maintained within the population.
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That is not quite correct. Epigenetic inheritance mechanisms have been discovered and are a very active area of genetics research. I’m not all that familiar with the field; as far as I know epigenetic inheritance has been discovered only in ‘lower’ model organisms like plants, yeast, C.elegans and Drosophila. But, as is so often the case, if it’s happening in those organisms it is very likely to also be happening in ‘higher’ organisms like us.
 
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Hercules Rockefeller said:
That is not quite correct. Epigenetic inheritance mechanisms have been discovered and are a very active area of genetics research. I’m not all that familiar with the field; as far as I know epigenetic inheritance has been discovered only in ‘lower’ model organisms like plants, yeast, C.elegans and Drosophila. But, as is so often the case, if it’s happening in those organisms it is very likely to also be happening in ‘higher’ organisms like us.
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"In every cell, DNA wraps itself around proteins called histones. Chemical groups such as methyl and acetyl can bind to histones and affect DNA expression. HDAC2 is a histone deacetylase, an enzyme that removes acetyl groups from the histone, effectively turning off nearby genes.

In 2007, Tsai's group reported in Nature that this so-called epigenetic change can contribute to cognitive decline. They used a strain of mutant mice developed in her lab called CK-p25, which shows a profound loss of neurons and synapses, the junctions between neurons. The animals also carry the amyloid-beta plaques thought to cause Alzheimer's disease and show impaired learning and memory. When Tsai's team gave the mice drugs that block all HDACs, the animals sprouted more synapses and showed better memory function.

There are 19 known HDACs. In 2009, the researchers found that one of these, HDAC2, can cause a loss of synapses and memory function in normal mice.

The new study pulls from both of these previous findings, investigating HDAC2's affect on CK-p25 mice.

The researchers showed that the mutant animals have an elevated level of HDAC2 in two regions known to be affected in neurodegenerative disease: the hippocampus, important for learning and memory, and part of the temporal lobe called the entorhinal cortex. In these regions, the researchers also found that HDAC2 binds to a host of memory genes and dampens their expression.

Tsai's team then used a technique called RNA interference to silence the expression of HDAC2 in neurons in the hippocampus. Four weeks later, they found a dramatic increase in synaptic density. What's more, when given two different memory tests, the treated animals were indistinguishable from normal controls.

Blocking HDAC2 expression did not change the number of dying neurons. Still, the findings suggest that memory can be improved even in later stages of the disease, Tsai says.

"The neurons that are still alive are essentially zombies: they're not really functioning properly because of the epigenetic blockade," Tsai says. "What we're showing is that, if we can get some of those neurons to wake up, we can get cognitive function to recover to a certain extent."
 
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Hercules Rockefeller said:
That is not quite correct. Epigenetic inheritance mechanisms have been discovered and are a very active area of genetics research. I’m not all that familiar with the field; as far as I know epigenetic inheritance has been discovered only in ‘lower’ model organisms like plants, yeast, C.elegans and Drosophila. But, as is so often the case, if it’s happening in those organisms it is very likely to also be happening in ‘higher’ organisms like us.
Click to expand...

Happens in higher-orders also.
 
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