Progress in Understanding Plant Longevity is Interesting, But is it in Any Way Relevant?

There is a portion of the life science community interested in the longevity of plants, though it is fairly disconnected from research into medicine and aging for the animal half of the planet. We can debate whether or not there is anything useful for medical research to be learned from comparing plant species and gaining a better understanding as to why some are much longer-lived than others. After all, researchers already reach for very difference species when beginning investigations of cellular biology relevant to medicine. In the animal-focused aging research familiar to this audience, a great deal of experimentation and exploration is carried out in studies of yeast, a fungus rather than an animal, and yet possessing so many similarities to mammals in its cellular processes that the data can be very useful. Yeast is a long evolutionary distance from humanity, but it is arguably a bigger leap from yeast to plants than it is from humans to yeast. Plants have chloroplasts, and that's just the start of a long list of differences. Early stage research into cellular biochemistry is always a trade-off: much more can be done for a given amount of funding in yeast, flies, and worms, but many of those results will fail to also prove relevant in mice, let alone in humans. So far the collective wisdom of the life science research community has declared that yeast passes the cost-benefit equation, while anything with a chloroplast does not.

There are of course, always heretics willing to argue the point, but that is the way science progresses. In the research noted here, a stem cell angle is pursued, and this is one of the areas where I could perhaps be persuaded there might be something useful to be learned from plant life science. If investigations of hydra and their continuous regeneration - and how that relates to mammalian stem cell biology - are worthwhile, then so might be research into the continuous regeneration of some plant species. Still, this is about as close to fundamental research as one can get, which means it is a part of the long-term gathering of information, with no presently plausible application to medical science, and we can only speculate as to where any part of it might prove useful in the decades ahead.

Mechanism Behind Extreme Longevity in Some Plants

Compared to humans' century-long life span, some plants - evergreens in particular - have the capacity to live for an exceptionally long time, even millennia. Researchers zeroed in the formation of axillary meristems - stem cells that give rise to branches - in Arabidopsis thaliana and tomato, finding few cell divisions between the apical meristem located at the very top of a plant and the axillary meristems. With such little proliferation comes less opportunity to accumulate potentially deleterious genetic mutations in somatic cells that could kill the organism, the authors reasoned. "Meristem aging is not a problem for perennial plants, in other words. The meristems are the growing units. If they don't senesce, then the plant will keep the capacity to grow and reproduce forever, at least potentially." Instead, structural defects or pathogens most often kill plants.

In tomato, "it turns out all the cells around are making lots of cell divisions to make leaves and stems, but few cells are destined to become the axillary meristem. Those really don't divide." If the same is true in other species, the results suggest that most plants have something akin to the germline in animals. "That is, plants seem to set aside some cells in such a way as to minimise the number of mutations they accumulate."

One project underway in Switzerland could lend empirical data to test the group's hypothesis. The Napoleome project is an effort to sequence the full genome of a 238-year-old oak tree. The team has actually sequenced two genomes, taken from different parts of the tree, to see how many mutations are present and whether these distant sites share any mutations. "This meristem hypothesis is what we're testing basically with our project. No one has an idea of how many somatic mutations are in an old tree that has lived outside for more than 200 years." Whether this mechanism to limit somatic mutations was selected for evolutionarily to increase longevity or protect the germline "remains an open question, and one that would be very tricky to answer."

Patterns of Stem Cell Divisions Contribute to Plant Longevity

The lifespan of plants ranges from a few weeks in annuals to thousands of years in trees. It is hard to explain such extreme longevity considering that DNA replication errors inevitably cause mutations. Without purging through meiotic recombination, the accumulation of somatic mutations will eventually result in mutational meltdown, a phenomenon known as Muller's ratchet. Nevertheless, the lifespan of trees is limited more often by incidental disease or structural damage than by genetic aging. The key determinants of tree architecture are the axillary meristems, which form in the axils of leaves and grow out to form branches. The number of branches is low in annual plants, but in perennial plants iterative branching can result in thousands of terminal branches.

Here, we use stem cell ablation and quantitative cell-lineage analysis to show that axillary meristems are set aside early, analogous to the metazoan germline. While neighboring cells divide vigorously, axillary meristem precursors maintain a quiescent state, with only 7-9 cell divisions occurring between the apical and axillary meristem. During iterative branching, the number of branches increases exponentially, while the number of cell divisions increases linearly. Moreover, computational modeling shows that stem cell arrangement and positioning of axillary meristems distribute somatic mutations around the main shoot, preventing their fixation and maximizing genetic heterogeneity. These features slow down Muller's ratchet and thereby extend lifespan.

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Progress in Understanding Plant Longevity is Interesting, But is it in Any Way Relevant?

''"This is an attractive hypothesis," Reymond said of Kuhlemeier's idea on branch heterogeneity. "This is what we're testing basically with our project. . . . No one has an idea of how many somatic mutations are in an old tree that has lived outside for more than 200 years."

Whether this mechanism to limit somatic mutations was selected for evolutionarily to increase longevity or protect the germline "remains an open question, and one that would be very tricky to answer," said Lanfear.

To Noodén's mind, it's possible the researchers' observations of the meristem constitute a mechanism for life span maintenance, but it is likely not the only mechanism. "The relationship of mutation accumulation to aging and death is not clear," he said.
''

Interesting. Yes, it's (more) relevant (than not), even if it may seem pointless or non-applicable/non-translatable to human specie since trees are ultra-basic with little resemblance besides a couple of cells.

It's relevant because some of the mechanism are still intact in us or in semi-eternal trees; evolution just 'refits' whatever adaptations/mechanism from one specie to another but the mechanism can be similar-like in their goal and method - becaus already share many ressembling building blocks (cells, mitochondrias, stem cells, etc).
Doesn't mean they are the 'same same' though, it's still quite different (genetically/morphologically...) but not That different that we can't relate At All or any research on plants or immortal trees is useless. No. I mean we do compare little flies to humans...how exactly are we so related. Ok we're animal and descend from bacterias, eukaryote, and ultra-old flies but that's where it ends. Still research on flies thought us so much; thus it's all valid and useful somehow.

They are *Living Alive organisms like us, full of Living cells, ECM, tissues and teach us lots, that may or may not be applicable (most likely the latter), but still is valuable.
I guess we are at the point where we think in terms of days, minutes and seconds in the amount 'of time' we will allow on something or some research. It's Slow-Mo like the Slow-Mo growing Forever Tree.
As such there is an imperative to 'forget about studying plants, trees, and insects'...but concentrate on creatign real therapies - for (saving) humans'lives from 100% assured death - like now - cause time is going
and we can learn and research on trees all we want....but we have to be 'alive' for that because one day we die anyway anyhow, all of us; a problem and problem of prioritizing. I rather they found
that eternal elixir from the immortal tree inside a human, then try to study plants and say : ''well, they are immortal. Fin.''. Thanks for stating the obvious, how do we 'apply' this knowledge to us so we can 'study them forever' while we are alive forever too in the first place (to study them :P.
I'm guessing we'll stop 'stuyding them' the moment we reach LEV without plants.

''To Noodén's mind, it's possible the researchers' observations of the meristem constitute a mechanism for life span maintenance''

Makes sense, plants and especially the roots of non-clonal semi-eternal trees (such as the 2000 year old If, Baobab, California Red Pine, Great Basin Bristlecone Pine, Iran Cypres and a few others) survive
for many centuries and over thousands of years. The meristem stem cell pool cycling is just enough to keep things going and replace the roots continuously as some of the parts of the tree dies (upper trunk, branches, leaves, fruits) and are replaced with ultra-slow renewal/growth of semi-eternal trees.
Most of these trees are Giant and demonstrate indefinite (but ultra-slow) growth (like a millimeter trunk ring increase per year). By being giant, they have massive reservoirs of glucose molecules inside their huge tons of reservoir of resistant starch which they use a lot during winter to thrive in dead vitamin-infertile ground (they suck and fabricate from their roots from the ground); it's what is needed to create sugary sap and Canadian Maple Tree Syrup (our special here! The Best thing when you want Diabetes faster than you can say, diabetes).
SEe we learn something from trees and plants : ).

''"This is what we're testing basically with our project. . . . No one has an idea of how many somatic mutations are in an old tree that has lived outside for more than 200 years."''
Well, actually yes, one study verified lipid integrity in a 1000 year old Lotus tree seed. They found out that the hermectic outer shell protected it from rust and destruction; peroxidation of its polyunsatures,

its mitochondrial membranes were perfectly preserved and its polyunsatures intact; thus the membrane was fluid -despite being over a 1000 year old by C-14 dating. Upon trying to germinate in lab, the seeds germinated but some died and many of them
showed 'veins' and 'damage' that was very obvious that the seeds were 'ancient'. This damage was due to daily cosmic, solar and earth radiation for a thousand years (obviously carbon dating is radiation dating and trees are UV absorbing to photosynthesis/chlorophyl and oxygen creation; they litterally 'breathe-in' UV radiation); but these had an severe cell damaging impact - despite it being shieled from oxygen - radiation exposure and progressive mutational damage had accumulated deep inside the DNA of ancient lotus seed.

This effectively created oxidative damage - not enough to kill them and not germinate - but seriously harm them/make them very 'ill/'aged'' looking upon birth like a 1000-year old progeria (like say a UV/X-ray radiation exposure, since its the same, just like Hiroshima bombing on the Japanese who were irradiates; same for Chernobyl radiation accident or recent Fukushima radiation explosion. Imagine this, but for a 1000 year and in a small 'daily' dose like smoking a daily cigarette)).
So we know that somatic mutations caused by oxidative stressors like radiation appear in trees - like the 1000-year old semi-eternal Lotus tree, and its forever-dormant seed. And any other tree or plant for that matter.

''Whether this mechanism to limit somatic mutations was selected for evolutionarily to increase longevity or protect the germline "remains an open question, and one that would be very tricky to answer," said Lanfear.
''

Interesting. I would wager that this is very close to the Hydra's germ cell line constant renewal (after sexual immaturity reversal) allowing it immortal life; and telomerase being the key element that allows its immortality.
It was found that when TERT gene was blocked inside germline of immortal jellyfish - no more immortal jellyfish, it became mortal. This is in line with another study that showed cyclic activation of telomerase each centuries in the meristem cells, tree's stem cells/germ cells and trunk of the non-clonal Great Basin Bristle Cone Pine which lives up to *5000 years*.
Like a perpetual ultra-slow growth and activation of telomerase in their stem cells/germ cells; allowing near-eternal life just like the Hydra and just like the Bristlecone Pine.
I don't know if it would 'limit' somatic mutations; this proliferation is so sllow that it doesn't make much difference; in a hydra it may be different as proliferation must be higher. A hydra grows faster than a slow growing tree. THough both share a 'forever maintenance' of their tissues via stem cells via telomerase - like immortal cancers.

The fact that these trees are huge means they can survive almost anything, break a big branch, no problem, cut them down, they grow back by their stem cells in meristem and their huge tons 'garde manger' of glucose starchy reservoir for energy along their 100 feet tall trunk, they never move, they have no natural predator, they survive in high altitude - fully irradiated, they survive draught and freezing, they are ultra-stress-hardened/tolerant...they never die (almost).

Hydras are not huge, they are small and simple, and simple, small-like and uncomplex being - generally end up with the immortality. Complex beings are a sacrifice and much too complex 'to make it work' (in exchange for immortality you obtain complexity). That doctor said it : ''The price for complexity in humans is mortalitity/the loss of immortality.'' Vice versa, the price for immortality in 'simple-like' animal, like Hydra or a Tree, is 'remaining simple/uncomplex beings with complex organs'. Why ? Because cancer mutation formation will happen in complex animals, not in simple ones like a Hydra or a Tree, it is an evolutionary trade-off and mechanism against cancer formation in complex animals. Evolution cannot allow immortality to a complex animal likely to develop cancer over time and compromise specie survival
- unlike an uncomplex animal. It makes much more sense to explain why trees can live thousands of years not getting cancer when they have telomerase in permanence. Their mutational load is small and organ simplicity smooths things out, like in Hydras, they can permit themselves to 'play around' with telomerase and attain immortality.

Another study showed something important, plants that survive produce more chlorophyll and chlorophyll production loss equals death soon, this is for all plants/trees.
Oxidative stress resistance of tobacco plants that survive harsh winter and draught showed that they have higher REDOX reduced potential (higher tissue glutatione and NAD+/NADH).
There's still a lot more to learn from plants and one day, we'll somehow be able to apply that knowledge.

It's already happening with BioViva Mrs.Parrish's telomerase tryout. It may not work like in BristleCone Pine or a Hydra to give them eternal life; but it's better than nothing. SENS will try to reach that with LEV, all types of damage reduction in 'repeat' mode.

Posted by: CANanonymity at May 6th, 2016 12:08 AM

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