Epigenetic Components of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome Uncover Potential Transposable Element Activation (Almenar-Pérez 2019)

EloyAlmenar-PérezMSc TamaraOvejeroPhD TeresaSánchez-FitoMSc José A.EspejoBSc LubovNathansonPhD ElisaOltraPhD

Abstract:

FULL: https://sci-hub.tw/10.1016/j.clinthera.2019.02.012
https://www.sciencedirect.com/science/article/abs/pii/S0149291819300724

 

Alternative sci-hub link

 

I am very grateful to Elisa Oltra for her commitment with ME patients and also to “Universidad Católica de Valencia” for the research grant.

Unfortunately this paper is too technical for me. I would love if anyone could summarize for us the conclusions in plain words if posible.

 

I won't even pretend to understand what this paper really is about, but looks interesting.

 

does this in any way relate to Lipkind'/ Light's ( sorry can't remember whom) view on epigenetic modulation?

 

Bumping this one. Do any of our science brains have an opinion on this paper?

 

I am not sure I really understand it, unfortunately.

 

Could we ask the authors for an explanation and Q&A on forum?

 

Transposons are bits of DNA that contain coding sequences that allow themselves to be cut out and then inserted into the genome at a different spot.

Transposons can be a source of genetic diversity, and it can also cause disease or other problems. It seems like they can also have a positive effect. They're found in all organisms.

Because a lot of lengths of DNA are used not to code protein by themselves, but to regulate how and when other sequences will be used, snipping bits of DNA out and putting them somewhere else can change DNA expression (what things get made in the cell and when). Also some of the transposons are complete regulatory sequences.

Methylation is a system of packing and tagging genetic information to regulate how and when it will be used. There's evidently methylation systems that affect transposons, too.

I am not clear on how they found transposon information from a literature review, but I didn't read the full paper.

Epigenetics is stuff that is not DNA itself but associated to DNA ("upon" is the literal meaning of the prefix epi-), and regulates how and when the DNA is used (including by how it's packed--DNA in a long strand would reach from here to the moon and back, many times over, and it has to be packed and organized in order to fit into and be used by the cell, but it can be more or less tightly packed in order to be more or less available). So methylation and I forgot what else.

They're saying maybe something turns on a transposon that had previously been inactive (something that's known to occur in some well-studied transposons).

Sounds like they could be saying RNA (maybe miRNA?) could be involved in the epigenetics of this.

So without there being an infection, they figure the innate immune system is activated.

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I am not sure how much evidence there is for innate immune activity in ME.

The transposon stuff is super interesting but as they said in the abstract, one would need a very large genetic study to have any good evidence for or against something like this.

 

It's not something I would get to for quite some time. I'd be more than happy if someone else wanted to send a polite request to them asking if a laypersons summary was possible, perhaps pointing them towards this thread as well.

 

Thanks @WillowJ