

Extraordinary gene transfer between cells observed - Expez
http://www.malaghan.org.nz/news-and-events/extraordinary-gene-transfer-between-cells-observed/

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spiritplumber
This is very revolutionary, although as an EE I cannot comprehend the
ramifications fully (and hope someone enlightens me)

Just for fun, I'm going to post this on creationist forums and see what
pretzels they twist their heads into about it.

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reasonattlm
The paper isn't open access, unfortunately [1]. As I recall stem cells have
been shown to do this as well, a few years back, so there are probably a
couple of other papers out there on the same topic. Interestingly the example
I was thinking of was retracted, however. [2]

Nonetheless, university publicity people are very quick to claim "first" and
you should always be skeptical about that part of news releases.

There are demonstrations to show that cells will import free-roaming
mitochondria. If you put cells and mitochondria into a culture, the cells will
pull them in and use them [3]. Researchers have manipulated this mechanism to
some degree to obtain the import of specific mitochondria. [4]

So I think there has been the sense that it was expected for at least some
cells to be moving mitochondria around between one another under at least some
circumstances.

Some further commentary:

\-------

Mitochondria are the powerplants of the cell, more or less. There is a herd of
mitochondria in every cell, dividing like bacteria as necessary to keep up
their own numbers. Their most important - but by no means only - activity is
the generation of adenosine triphosphate (ATP) molecules used as chemical
energy stores to power cellular processes. Mitochondria have their own DNA
separate from that in the cell nucleus, and it encodes a few vital pieces of
protein machinery used in the process of generating ATP. Unfortunately this
DNA often becomes damaged in ways that evade cellular quality control
mechanisms and lead to a takeover of the cell by malfunctioning mitochondria.
The details of this takeover are still under investigation: researchers never
see it happening, only the before and after state, which suggests that it is
fairly rapid at least. Cells in this dysfunctional state are thought to
contribute to a range of age-related conditions by exporting a flood of
reactive molecules and damaged proteins into surrounding tissues.

One of the challenges in studying the progression of mitochondrial damage is
that mitochondrial dynamics are highly complex. Mitochondria are like bacteria
in that they multiply by division, copying their DNA and assembling new ATP-
creation machinery in the process. Equally they are also like other cell
components in that various complicated processes monitor them and destroy them
when they show signs of wear. Further, they can also fuse together, and any
two individual mitochondria can contain more than one copy of the
mitochondrial genome and differing amounts of molecular machinery. To make
matters even more entertaining individual mitochondria promiscuously swap
components of that molecular machinery between one another. So you can
probably see that it is not exactly straightforward to track the process by
which a few thousand of these entities in one cell move rapidly from a state
in which one mitochondrion has damaged DNA to that same DNA damage being
present in all of the mitochondria. There are dozens of distinct mechanisms at
work, few of which are fully understood at this time, and all of which have
their own particular constraints and reactions to circumstances.

As is the case for many areas in aging, however, researchers could skip over
all of this complexity and bypass full understanding in order to sprint down a
more direct path towards treatments. The SENS approach to work on rejuvenation
treatments, for example, picks out provision of proteins encoded in
mitochondrial DNA as the key point. Provided that those proteins are supplied,
it doesn't matter what happens to the mitochondrial DNA, as the necessary
machinery is still there. The mitochondria will continue to function correctly
rather than malfunction. On that basis there are a number of ways to go:
deliver replacement mitochondrial genomes while clearing out existing genomes,
put copies of mitochondrial genes into the cell nucleus (plus solve the thorny
problem of how to transport the proteins produced back into the mitochondria),
deliver RNA that will manufacture proteins at the mitochondria, and so forth.
None of these methods requires a full understanding of how mitochondrial
damage progresses in order to be effective, but as is usually the case in
these matters none of them are well funded in comparison to efforts to
generate the full understanding of mitochondrial dynamics. Science as
practiced is very much biased towards the generation of understanding first
and foremost, which sometimes leaves practical paths towards treatments lost
and languishing.

In any case, back to the complexity of mitochondrial dynamics: there is yet
another level to all of this that has come under investigation in recent
years, which is that cells can under some circumstances exchange components
such as mitochondria.

\-------

[1]:
[http://dx.doi.org/10.1016/j.cmet.2014.12.003](http://dx.doi.org/10.1016/j.cmet.2014.12.003)

[2]:
[http://impactaging.com/papers/v3/n6/full/100341.html](http://impactaging.com/papers/v3/n6/full/100341.html)

[3]:
[http://dx.doi.org/10.1016/j.transproceed.2013.11.133](http://dx.doi.org/10.1016/j.transproceed.2013.11.133)

[4]:
[http://onlinelibrary.wiley.com/doi/10.1111/jcmm.12316/full](http://onlinelibrary.wiley.com/doi/10.1111/jcmm.12316/full)

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mrfusion
Thanks for all the information. So how do you suppose immortal germ line cells
deal with mitochondria damage?

~~~
waps
It is becoming more and more established that human cells are not really
alive. They just are a cooperative of things that are alive. Mitochondria, for
instance, are alive. Our cells cannot survive without mitochondria, yet
mitochondria can live an thrive without human cells. In a way eukaryot cells
are like companies, as opposed to individuals : they're a collection of
cooperative agreements between various parties. If you're pedantic eukaryot
cells are fictional, like companies : there are no cells/companies, there are
only cooperating smaller components that (in theory) could decide to dissolve
at any time. But when walking around in the world you could easily be forgiven
for thinking they do exist, as they are present, you can interact with them,
they often look like they have coherent reactions (even though they don't),
there's a wall around them, ...

The article specifies how they deal with mitochondrial damage : the same way a
company would deal with a "defective" employee : have security escort them out
of the building. Well a cell does what I often think companies would like to
do : kill them first, then escort them out of the building, then find a new
one (usually by asking an existing one to reproduce, but it seems there are
other ways). It's even more similar than you'd think. A eukaryot cell doesn't
kill the mitochondria "itself", it asks the golgi apparatus to do it for it
(form a lysosome around it).

This research is groundbreaking because it shows our cells behave like
companies do in another way : every now and again, they try to replace even
perfectly functional employees with better ones.

~~~
mrfusion
Thanks. That's a really interesting analogy.

I guess my question is why mitochondria damage Leeds to aging in normal cells
but germ line cells must have some way to deal with it flawlessly.

