Cooperation in Evolution (and in human nature)

[Dov]

Occasionaly (for example

http://www.the-scientist.com/yr2003/oct/research2_031006.html,

"Microbial Co-op in Evolution"), I come accross articles that "discover" in "scientifically sophisticated” verbiage, plainly ubiquitous phenomena of cooperation in evolution between cells or organisms or between their communities.

 

In my opinion co-op in evolution started, most probably, much earlier than in microbial communities; it started between individual pre-celled genes, who eventually formed and elaborated the cooperative associations we call genomes. Prior to this, even the genesis of Life itself is a product of cooperation, of molecules that were precursors to Life.

 

Life has always been and still is a fractal phenomenon and affair, a repetition of a framework of processes on ever more complex pattern. It cannot be otherwise;it is inherent in evolution.

 

And surviving-proliferating life has always been a cooperative affair since cooperation is the most successful route for overall survival/proliferation.

[Sayonara]

Login for the article: fyeasabnyodvo @ mailinator.com (remove spaces)

[admiral_ju00]

Or it won't kill anyone to register and create their own account and email notifiers

 

Speaking of which, I haven't been on that site in a while. Grrr

[admiral_ju00]

In my opinion co-op in evolution started' date=' most probably, much earlier than in microbial communities; it started between individual pre-celled genes, who eventually formed and elaborated the cooperative associations we call genomes. Prior to this, even the genesis of Life itself is a product of cooperation, of molecules that were precursors to Life.

[/quote']

 

I'm thinking along similar lines. What caused Organic Life to appear? Kind of like the Chichen or the Egg question, really, but a lot harder to answer.

 

It had to be the RNA that came first, then the DNA and lastly the Proteins were able to be manufactured(not any other way around).

[Dov]

Woese, a microbiology professor at the University of Illinois, with most provocative publications in the 1960s, traced sequence differences in microorganisms for the molecules he believed to be most central and conserved in life--the ribosomal RNAs responsible for protein translation, the universal language of cells.

 

By the way, in so doing, Woese made a then textbook-changing discovery, convincing many that archaea exist as a domain of life distinct from bacteria and eukaryotes. From this, he then constructed the first phylogenetic tree of microorganisms, leaving bacteria at the root, with archaea and eukaryotes branching off at a later date. This has later been contested with several different conjectures...

[Dov]

Enhancing the evolution calender RNA-to- DNA- to Proteins is the extensively expanding area of Viroids studies. The following accounts are from The Scientist ,Volume 18 | Issue 16 | 23 | Aug. 30, 2004, by Leslie A. Pray:

 

(A) Viroids are single-stranded, singular RNAs sized from 250 to 400 nucleotides, unprotected by any protein coat; they have no functional open-reading frame. So, unlike viral RNAs, viroids do not encode any proteins. This raises several questions: How do viroids cause disease? How do they replicate without the aid of a helper virus? And how do they move from cell to cell and host to host? Their self-complementary, circular nature and secondary structure (which allow viroids to self-cleave) provide some answers. Most recently, the identification of viroid-specific small interfering RNAs has led investigators to believe that RNA silencing also plays a role.

 

(B) There is growing evidence that small RNAs, believed to play an antiviral defense role in many organisms, may be acting as double agents. In March 2004, an international team of scientists reported that viroids, small infectious particles of naked RNA, may be employing RNA-silencing machinery to work their damage. Several weeks later, another international team announced the discovery of microRNAs in the Epstein-Barr virus (EBV), suggesting that miRNA-mediated gene suppression might play a role in animal-virus pathogenicity. Many researchers say this is just the beginning.

 

"In the past, all of these small RNAs were totally overlooked because they are so small in size. If they got any attention at all, they were considered unspecific degradation products. Now, we are starting to understand that they represent a sort of cross-talk between viral or viroidal sequences and endogenous genes," says Martin Tabler, Institute of Molecular Biology and Biotechnology, Crete.

 

EBV, a large DNA virus responsible for mononucleosis and a number of other diseases, including Burkitt lymphoma, is tough to beat; it hides from the human immune system and infects for life. Rockefeller University's Sebastien Pfeffer, lead author on the EBV study, says that he and his collaborators were looking for evidence that animals defend against viral infection using the same kind of posttranscriptional silencing pathways that plants, insects, and other organisms use. But instead of antiviral RNA activity, they discovered viral miRNA activity. According to Pfeffer, the data suggest that miRNAs could be involved in tumor formation and may explain how EBV hides so well. They also give scientists reason to look for miRNAs in other viruses. Says Pfeffer: "miRNAs are found in practically every eukaryotic organism. Other viruses could have them too."

 

RNA SILENCING: A WEAPON OF CHOICE? Viroids are single RNA molecules that have no protective protein coat and do not encode a single protein. While not all viroids inflict damage, some do so severely. A potato spindle tuber viroid (PSTVd) infection can reduce yields by 50% or more. As Ricardo Flores of the Valencia Polytechnical University, Spain, explains, "Viruses can induce disease by means of proteins encoded in their genomes, but viroids cannot. So the question is, how?"

 

For years, most researchers believed that the viroids induced disease by interrupting an unknown host factor (i.e., protein) and thereby disrupting normal cell functioning. This hypothesis was proposed in the mid-1980's, when scientists identified a region of the viroid genome, the "virulence-modulating" region, whose sequence, when altered, affected virulence. But the mechanistic details of this viroid-host interaction remained a mystery. In 2001 it was suggested that, rather than interacting directly with the host, perhaps viroids use small regulatory RNAs to influence host gene expression.

 

In March 2004, Ming-Bo Wang and colleagues from the Commonwealth Scientific and Industrial Research Organization in Canberra, Australia, provided the first experimental evidence suggesting that, similar to EBV, the key to viroid pathogenicity may indeed be RNA silencing, but in this case, siRNA-mediated, not miRNA-mediated. The investigators found that engineered tomato plants expressing viroid-derived, noninfectious hairpin RNA had symptoms mimicking those of viroid infection. Hairpin RNA is a key player in the RNA silencing pathway: When cleaved by a Dicer enzyme, it generates siRNAs, which in turn guide RISC complexes to degrade target RNA. In this case, the target RNA hasn't been identified, and Wang says this is a necessary next step.

 

"This is one of the most exciting things in the field," says Flores. "But more evidence is needed before deciding which of the two alternative hypotheses is correct. If you want to prove this hypothesis, you have to identify which host mRNA is degraded." For Tabler, the results are "surprising and actually a bit puzzling." They raise interesting questions about how nuclear-replicating viroids such as PSTVd exploit RNA-silencing machinery, which is located in the cytoplasm.

 

Future findings aside, both studies nonetheless confirm the ubiquitous nature of small RNAs and point to an additional, pathogenic function for RNA regulatory mechanisms. Says Andrew Ellington, University of Texas: "It's exciting to see the small RNA world sow its oats."

[Sorcerer]

My personal opinion is that abiogenesis required co-operation between abiotically formed proteins which had no genetic precursor and RNA strands, this is because the genes required for the production of tRNA and rRNA had not yet been synthesised, so by chance a protein(s) which dupilicated these roles came into existence and enhanced the fitness of RNA by adding to their ability to produce protein "offspring" which is how their fitness was enhanced.

 

I hypothesis that by chance a protein which catalysed the joining of ribose and phosphate to neucleotides thus allowing their spontaneous ploymerisation was the precursor requirement for all life. Once tRNA strands had arisen over time by chance they interacted with other RNA molecules to produce protein "offspring", now this process would be inefficient without ribosomes, so the most successful RNA strand in this case would be the ones which produce the proteins needed for ribosomes, and subsequently the RNA which formed a complex with these proteins to produce ribosomes.

 

It seems rather complex, but I cannot see any other way for life to be kickstarted without the catalytic function of ribosomes..... perhaps proto-ribosomes had RNA which also contained the information that encoded for the proteins they were associated with....

 

As a question, what role does rRNA play in protein polymerisation, and if that rRNA was used as mRNA what product would it produce. This is actually an experiment I would like to conduct.

[Dov]

If you have'nt yet seen it please look at the following site for a very brief precise updated review of the RNA world:

 

http://www.wordiq.com/definition/RNA_world_hypothesis

 

Of course experimental routes targeting simmulation/duplication of archaic occurences are problematic because of the very low probability of duplicating the then media constitution and energetic conditions...We might have to be forever satisfied by most scientifically probable conjectures...

[Sorcerer]

Thx, I knew that, just needed to be refreshed in it .... So rybozymes also help catalyse the production of tRNA? I imagine they would need to since tRNA forms hairpins which would need to be straighted in order to replicate without DNA.

 

By the way, do you know what peptide the 3 rRNA strands would encode if they were translated? If the two ribosomal subunits weren't around during abiogenesis, how would you account for 3 rRNA's being in the right place? Is only one the most important? Or do you invisage a folded larger strand, that was perhaps less efficeint that 3 seperate ones and protein, however efficient enough to suffice, then subsequently out-competed?

[Dov]

sorcerer, I would'nt presume to be able to comment on your points re the 3 rRNA strands, but I suggest you might find some hints in http://www.wordiq.com/definition/RRNA

[Sorcerer]

Right it says that the 23s is the functional site for peptide bond formation.... I wonder what part the other 2 rRNA and the protein play then, most likely an adaption that increases efficency, obviously an adaption that occured very early in lifes evolution. This is a fine example of cooperation between biochemicals in evolution.

[Dov]

You can now find an interesting RNA world view update by John S Mattic in the October issue of Scientific American.

 

And I can't resist pasting here three of many of my conjectural (how otherwise ?)postings on this world in another forum :

 

========================

From: "dovhenis"

Date: Sat Jul 19, 2003 7:41 am

Re: RNA update

 

Here is an RNA update review you should not miss :

 

http://www.nature.com/horizon/rna/background.html

 

Per my "armchair scientist" conception of Life, even prior to

any browsing in this review, each RNA is both a prime pre-DNA

archaic edition of a DNA gene and the DNA's tool. In pre-DNA

life this RNA edition lived independently and/or cooperatively

with other RNAs. The consequent more complex DNA life evolved

into symbiotically-associated collectively-dependent genes,

though, and the original primary RNA forms have been retained

as tools for their consequent collective-members DNA editions...

This is my gut feeling...

DH

====================

From: "dovhenis" <henisdov@n...>

Date: Mon Jul 22, 2002 6:53 am

Re: Nature of Life

 

Looking back at a couple of paras in a conjecture posted earlier at :

 

http://www.biobitfield.com/henis/

 

"The first time a peptide served as a template for its duplication

was the first appearance of an archaic gene, and the occurrence at

which the factors involved in the formation of the duplicate were

drawn to stay in a stable association, maybe in the form of a

nucleolus, was the occurrence leading to Cellular Life".

 

and

 

"Per Pasteur's "all life must come from previously existing life" the

pre-membraned pre-celled peptides were a form of life. If we regard

as an "organism" a unit element of a continuous lineage with an

individual evolutionary history this has applied also way back at the

earlier evolutionary phase of present-day organisms".

 

It is logical/reasonable to conjecture that throughout their

evolution from single archaic to chromosome-association-members genes

have been and are now as living organisms as the single or poly

celled organisms that evolved from/by them in their drive to

proliferate, in the process of accummulating-maintaining bubbles of

life-energy.

 

DH

========================

 

From: "dovhenis" <henisdov@n...>

Date: Sat Jun 1, 2002 9:28 am

Re: More On Genome Structure

 

The challenges of making sense of genome structure when chromosome

size and number vary widely between closely related organisms are

highlighted in this News Feature :

 

http://www.nature.com/nlink/v417/n6887/full/417374a_fs.html

 

http://www.nature.com/cgi-taf/DynaPage.taf?

file=/nature/journal/v417/n6887/full/417374a_fs.html

 

 

I do not tire and I am not exasperated in my effort to convince open

minded persons that all challenges of making sense of genome

structures, even facing widely varying chromosome sizes and number

within closely related organisms, are explainable when you adjust your

concep of Life. Again and again ad nausia: it is not the Cell that

is the base unit of life; the Cell is but the structural shell that

houses the Genes, which ARE the base units of Life and existed at

a pre-cellular era. The individual Genes have (and still do) evolved

and speciated and associated and competed and strove to survive and

replicate in the same way as mono- and poly-cell organisms evolved

and speciated, Life being a fractal phenomenon. We do not yet know

the Origin of Life earlier than the archaic gene era. This is not

different from not yet knowing the nature of the pre big banged

universe.

 

DH