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Epigenetics: Biologists discover 71 new “imprinted” genes in the mouse genome


Some of us recall a science writer wondering when the “epigenetics” anomaly would finally come to an end, bringing us back to yer old biology teacher’s Darwinism. Not soon, it seems:

Most of the thirty trillion cells in a person’s body contain genes that come from both their mother and father, with each parent contributing one version of each gene. The unique combination of genes goes part of the way to making an individual unique. Usually, each gene in a pair is equally active or inactive in a given cell. This is not the case for imprinted genes. These genes — which make up less than one percent of the total of 20,000+ genes — tend to be more active (sometimes much more active) in one parental version than the other.

Until now, researchers were aware of around 130 well-documented imprinted genes in the mouse genome — the new additions take this number to over 200…

Close examination of the newly identified genes has allowed Professor Perry and his colleagues to make a second important discovery: the switching on and off of imprinted genes is not always related to DNA methylation, where methyl groups are added to genomic DNA- a process that is known to repress gene activity, switching them off). DNA methylation was the first known type of imprint, and was discovered around thirty years ago. From the results of the new work, it seems that a greater contribution to imprinting is made by histones — structures that are wrapped up with genomic DNA in chromosomes.

Although scientists have known for some time that histones act as ‘dimmer’ switches for genes, fading them off (or back on), until now it was thought that DNA methylation provided the major switch for imprinted gene activity. The findings from the new study cast doubt on this assumption: many of the newly identified genes were found to be associated with changes to the histone 3 lysine 27 (H3K27me3), and only a minority with DNA methylation.


Scientists have yet to work out how one parental version of a given gene can be switched (or faded) on or off and maintained that way while the other is in the opposite state. It is known that much of the on/off switching occurs during the formation of gametes (sperm and egg), but the precise mechanisms remain unclear. This new study points to the intriguing possibility that some imprinted genes may not be marked in gametes, but become active later in development, or even in adulthood.

Although it only involves a small proportion of genes, imprinting is important in later life. If it goes wrong, and the imprinted gene copy from one parent is switched on when it should be off (or vice versa), disease or death occur. Faulty imprinted genes are associated with many diseases, including neurological and metabolic disorders, and cancer.

University of Bath, “There’s more to genes than DNA: How Mum and Dad add something extra, just for you” at ScienceDaily The paper is open access.

Given that cancer is more likely to strike later in life, it would surely be no surprise if epigenetic factors played a role.

See also: Epigenetic change: Lamarck, wake up, you’re wanted in the conference room!

PaV @2
Histones are not just some outside layer protecting DNA and involved in its packaging, but it is also involved with gene regulation.
I am glad you have mentioned this. i am an engineer, and here is what bothers me: we hear all the time, that there are many parts of the cell, that have more than 1 function. If this is not a textbook example of purposeful engineering and design optimization, then i don't know... When you are a Darwinist, you need a lot of faith to believe that a blind unguided process can evolve a thing with multiple functions ... and like i said, there are many parts of the cell that have multiple functions... Darwinists believe in miracles ... martin_r
What is most interesting is that this 'imprinting' is regulated by histones. We are beginning to see what has, I believe, already been called the "Histone Code," or something to that effect. Histones are not just some outside layer protecting DNA and involved in its packaging, but it is also involved with gene regulation. This experimental result ties the histones into the overall epigenetic framework of the genome. And, of course, the question arises: how did this code arise? Along with: how did this code integrate itself synthetically with the genetic code? By chance? How improbable is that? PaV
I just purchased 36 lectures from two courses of The Great Courses titled “ Biology and Human Behavior: The Neurological Origins of Individuality, 2nd Edition” and “ Being Human: Life Lessons from the Frontiers of Science” https://www.thegreatcourses.com/courses/biology-and-human-behavior-the-neurological-origins-of-individuality-2nd-edition They were on sale today for a total of $42 for 36 lectures. Essentially they are explaining how the natural law plays out in humans. We are affected by our genes but not determined. Will find out if epigenetics is covered. jerry

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