2 replies to this topic

[treonsverdery]

Many readers will remember That DNA makes the RNA That Ribosomes use as code to make Protein The quantity plus transport of these proteins could be said to happen at the Protein factory The endoplasmic reticulum which is the lotsalayered membrane where the ribosomes are at

Now rather simplistically if you have a double size radiator you can keep cooler Or if you have twice as big a factory you may make more products

Changing the size of the endoplasmic reticulum changes the number of ribosomes available to make protein

Thus creating organisms with different volumes of endoplasmic reticulum is a way to find the effect of giving cytes greater protein production capacity


Now there are readers that will say Perhaps CR goes with less protein with autophagy conserving protein promoting remodelling based longevity Those readers will be keen on finding out if less or differently active endoplasmic reticulum promotes longevity

I think the number of ribosomes available to make things provides blunt responsiveness to change Like with neurotransmitter receptors known as G coupled protein receptors some of these saturate then renew at a hundred hour period also long memory is associated with protein production which means ribosomes Thus organisms with bigger endoplasmic reticulums are able to make more kinds of protein more rapidly which benefits the bodys rapid adaption systems

If a scientist then went on to make some lab mammals with different size endoplasmic reticulum at variously neurons, endothelial cytes, cardiocytes to see if those particular systems do better at thinking, being absent vascular aging or heart disease that would be the direct application of a new longevity theory

I do not know the genes that effect endoplasmic reticulum size although wikigene http://www.wikigenes...esh/e/1843.html notes that 2E1 changes the amount of endoplasmic reticulum There is a recent paper on how endoplasmic reticulum stress affect hormesis plus longevity http://www.sciencedi...40a2d752def5230

New aging theory
Changing the size of the protein factory Changes the adaptiveness of the organism Changing the size of the protein factory at specific critical tissues like neurons as well as cardiovascular tissues brings benefit

rather strangely this appears to be new Most research is on varying the amount of genetic activity rather than the actual size of the product factory

Edited by treonsverdery, 16 July 2010 - 06:01 PM.

[treonsverdery]

also littler endoplasmic reticulum Notably littler smooth endoplasmic reticulum that makes lipid structures could cause adipocytes to prefer to shrink thus curing overweight which then minimizes illness
The same kind of modulation could also shrink oncocytes Another cure for cancer

also yeast as well as tissue culture could possibly tremendously benefit from multiplying the mass of endoplasmic reticulum Genentechs new yeast protein system now produces 2 4 8 16 or 32 times as much of the protein with New Reticulon technology

There is a move to tissue culture meat replacement known as Vatfood Its possible amping up the endoplasmic reticulum could make this 2 4 8 16 or 32 times as rapidly productive


I do not know the genes that effect endoplasmic reticulum size although wikigene notes that CYP2E1 changes the amount of endoplasmic reticulum There is a recent paper on how endoplasmic reticulum stress affects hormesis plus longevity

New aging theory Changing the size of the protein factory Changes the adaptiveness of the organism Changing the size of the protein factory at specific critical tissues like neurons as well as cardiovascular tissues brings benefit

Now there are readers that will say Perhaps CR goes with less protein with autophagy conserving protein that goes with remodelling based longevity Those readers will be keen on finding out if less or differently active endoplasmic reticulum promotes longevity

Most research is on varying the amount of genetic activity rather than the actual size of the product factory

Technologies that change the size of the endoplasmic reticulum

siRNA to cyp2e1 or possibly the thrilling idea that you could use yeast (eukaryotic have endoplasmic reticulum) plus siRNA to endoplasmic reticulum Then screen on which yeast live through the process to find other genes that affect the size of endoplasmic reticulum with the idea of finding new drug molecules

[vaelrenx]

First, what you have is a hypothesis, not a theory. A theory is an explanation with a large body of evidence to support it, such as the theory of evolution by natural selection or the theory of special relativity.

Second, proteins are not only manufactured by ribosomes docked to the ER. Ribosomes are found all throughout the cell in the cytoplasm. The ER is primarily responsible for the production of proteins that are destined to find themselves embedded in membranes, inside vesicles, or to be exported to the outside of the cell.

Lastly, caloric restriction is known to lead to a broad reduction in translation (read mRNA being turned into proteins, i.e. what a ribosome DOES), through the TOR signaling pathway. When nutrients falls there is a reduction in TOR signaling which decreases the activity of S6 kinase (which, when active, phosphorylates thus increasing the activity of the small ribosomal subunit S6). The reduced TOR signaling also increases the activity of 4EBP, a translation inhibitor. Although one might think reduced translation is simply a consequence of CR, and not responsible for increased longevity, these experiments have also be done and show the opposite. By artificially reducing translation without CR(gene knockouts ect), lifespan is also extended, suggesting that the reduction of translation itself plays a role in the increase longevity seen with CR, and is not a mere side effect.


For a great review on the genetics of aging by Cynthia Kenyon (who has created C. elegans that lives 6 times longer) see http://www.nature.co...ature08980.html

She also has a lectures series which is fabulous