Register | Sign In


Understanding through Discussion


EvC Forum active members: 64 (9163 total)
5 online now:
Newest Member: ChatGPT
Post Volume: Total: 916,419 Year: 3,676/9,624 Month: 547/974 Week: 160/276 Day: 0/34 Hour: 0/0


Thread  Details

Email This Thread
Newer Topic | Older Topic
  
Author Topic:   Cellular Creativity and the Unselfish Gene
Nova
Inactive Member


Message 1 of 47 (248119)
10-02-2005 8:07 AM


Cellular Creativity and the Unselfish Gene
One of the greatest wonders in the known Universe is the eukaryotic cell. Once thought to be a simple blob of protoplasm, the brilliant work of modern biochemists has shown that...
“A living cell is a self-assembling, self-adjusting, self-perpetuating isothermal system of organic molecules which extracts free energy and raw materials from its environment.
It carries out many consecutive organic reactions promoted by organic catalysts which it produces itself. It maintains itself in a dynamic steady state, far from equilibrium with its surroundings. It functions on the principle of maximum economy of parts and processes. Its nearly precise self-replication through many generations is assured by a self-repairing linear coding system”. (Lehninger, Principles of Biochemistry p12)
How could the blind forces of Nature have created an entity of such incredible complexity and fantastic efficiency?
I would like to suggest a model that may make comprehensible the causal mechanism for the evolution of the design-like structures and processes of the eukaryotic cell.
For reasons that will become apparent, I have called this model ”the Eureka Hypothesis’. The model consists of three parts:
1) Intracellular Biochemical Pathway Selection.
2) Cellular Experimentation.
3) Intercellular Gene Transmission.
Intracellular Biochemical Pathway Selection
Intracellular Biochemical Pathway Selection is a simple consequence of the fact that the eukaryotic cell functions on the principle of maximum efficiency of parts and processes. Assume a new, unique enzyme is expressed by the genome of a living cell. Assume also that the new enzyme catalyses the last step of a biochemical reaction to produce a useful current biomolecule, and that the new pathway synthesizes the biomolecule with greater efficiency. The ”newly discovered’ pathway will automatically be selected, since the new pathway effectively ”short-circuits’ the less efficient pathway. This will occur even if the new process requires more steps than the less efficient pathway.
Thus, a simple, less efficient pathway will be ”short-circuited’ by a more efficient, but more complex pathway. This means that complex biochemical pathways can form in a cell if there is some system for introducing new, unique macromolecules into the biochemical system. Where might these new macromolecules come from?
Cellular Experimentation
The Eureka Hypothesis postulates the existence of a special ”experimenter’ gene in the genome. When each new cell forms, the experimenter gene constructs a new gene at a specific site (the ”signature’ site). After removing the previously unsuccessful signature gene from this site, the experimenter gene selects a random sequence of introns and exons from an existing chromosome for the new signature gene.
The signature gene, when expressed as a polypeptide chain forms a new and unique ”test protein’ which interacts with the rest of the cellular machinery.
Each cell is thus provided with the standard genome for the organism, plus one unique protein encoded in the signature gene. Of course, there is very little probability that any particular test protein will increase the overall efficiency of the cell it occurs in. The cell is already so intricately finely tuned that the vast majority of test proteins will have either no effect or a detrimental effect. But when we consider that there are 10exp14 cells in one human body, and 6.2exp9 people now on Earth, then we realise there are a total of 600,000,000,000,000,000,000,000 independent, unique experiments in human cellular physiology occurring right at this instant.
This means that even if there is only one chance in a hundred thousand million trillion of the test protein having the effect of increasing overall cellular efficiency, then around six such new proteins will occur in today’s human cellular population.
These rare ”successful’ tests will be called 'Eureka events'.
A cell that has undergone a Eureka event is operating more efficiently than the cells that surround it. We will assume this is recognized, either by the Eureka cell itself, or by the cells that surround the Eureka cell. (Presumably by the difference in the basal metabolic rate of the Eureka cell as compared to the surrounding cells). Perhaps the Eureka cell receives chemical ”congratulations!’ signals from the surrounding cells, and on receiving enough of these signals it yells “Eureka!!”.
Intercellular Gene Transmission
When a cell yells “Eureka!!”, it undergoes a radical transformation.
The virus producing subsystem of the cell is activated, and the test gene at the signature loci is copied and packaged into protein coats for distribution to other cells. A cell that is producing viruses also secretes small quantities of the virus inhibiting biomolecule interferon. When interferon binds at the receptor site of an ”uninfected’ cell, it is sending a message to that cell that says “when you receive the incoming viral message, don’t produce more viruses, just write my message into your genome”. Cells that have not received the interferon message begin synthesizing more viruses, in addition to more interferon.
In this way, the organism sacrifices some of its cells to edit the new gene into the genomes of the rest.
In common editing viruses, such as colds and ”flu, viruses are embedded in mucous in the nose and throat, which is then atomized and forcibly sprayed into the air to facilitate the spread of the good news to other people (finally making it understandable why we bless people who sneeze on us!).
In this way, the efficiency improvement, the discovery of one single cell becomes part of the genetic machinery of every cell in the population.
After the new gene has been edited into the genome, the ”immune’ system finally clears away and recycles the debris of protein coats left by the editing viruses.
Note that random mutations play no part in the process. The random element is introduced in an orderly and controlled manner by the cell itself.
So, if the Eureka Hypothesis is correct, every time you ”catch a cold’, viruses from a Eureka event in someone are editing a new, more efficient cellular process into your genome. After every cold, your cells are just a little more complex and efficient.
If the hypothesis is correct, you can think of yourself as a super-biocomputer carrying out a hundred million billion empirical organic calculations simultaneously.
It is by these empirical experiments that cells have discovered the most efficient processes. It is by viral transmission that the blueprints of proteins enhancing cellular efficiency are communicated to other cells of the species.
In this way, the intricate design-like structures and processes of eukaryotic cells have been, and are continuing to evolve, molecule by molecule, in every living organism.
Released from PNT. --Admin

Replies to this message:
 Message 2 by sidelined, posted 10-02-2005 12:01 PM Nova has replied
 Message 5 by wj, posted 10-05-2005 5:19 AM Nova has not replied
 Message 6 by Ooook!, posted 10-05-2005 10:46 AM Nova has replied

  
sidelined
Member (Idle past 5929 days)
Posts: 3435
From: Edmonton Alberta Canada
Joined: 08-30-2003


Message 2 of 47 (248175)
10-02-2005 12:01 PM
Reply to: Message 1 by Nova
10-02-2005 8:07 AM


Nova
The Eureka Hypothesis postulates the existence of a special ”experimenter’ gene in the genome. When each new cell forms, the experimenter gene constructs a new gene at a specific site (the ”signature’ site). After removing the previously unsuccessful signature gene from this site, the experimenter gene selects a random sequence of introns and exons from an existing chromosome for the new signature gene.
So you have a candidate in mind for the hypothetical experimenter gene? How does this experimenter gene get formed in the first place? What is the mechanism by which this construction of new genes would be accomplished?
In short what experimenter gene constructed the present more efficient experimenter gene?
This message has been edited by sidelined, Sun, 2005-10-02 10:03 AM

But I realize now that these people were not in science; they didn’t understand it. They didn’t understand technology; they didn’t understand their time.

This message is a reply to:
 Message 1 by Nova, posted 10-02-2005 8:07 AM Nova has replied

Replies to this message:
 Message 3 by RAZD, posted 10-02-2005 12:10 PM sidelined has replied
 Message 7 by Nova, posted 10-06-2005 5:41 AM sidelined has not replied

  
RAZD
Member (Idle past 1426 days)
Posts: 20714
From: the other end of the sidewalk
Joined: 03-14-2004


Message 3 of 47 (248179)
10-02-2005 12:10 PM
Reply to: Message 2 by sidelined
10-02-2005 12:01 PM


this looks like a proposed ID mechanism
problem is that it does not match observation to date: should be easy to invalidate imho.
so far the evidence is that all the genetic material transported to others via virus is pathological ...

This message is a reply to:
 Message 2 by sidelined, posted 10-02-2005 12:01 PM sidelined has replied

Replies to this message:
 Message 4 by sidelined, posted 10-05-2005 1:56 AM RAZD has not replied
 Message 8 by Nova, posted 10-12-2005 8:04 PM RAZD has replied

  
sidelined
Member (Idle past 5929 days)
Posts: 3435
From: Edmonton Alberta Canada
Joined: 08-30-2003


Message 4 of 47 (248999)
10-05-2005 1:56 AM
Reply to: Message 3 by RAZD
10-02-2005 12:10 PM


RAZD
this looks like a proposed ID mechanism
Oh, I agree. I posed these questions to see if any thought has gone into the consequences of this Eureka Hypothesis. It is one thing to postulate an existence it is all together different to question the possible weaknesses of the hypothesis to see if the model stands up to investigation.
I think it is key to the validity of this hypothesis to ask the mechanism and origin of the experimenter gene. Of course it is necessary on the part of Nova to check the real world for the presence of this hypothetical experimenter gene in order to provide evidence of such.
I am quite certain that Nova putting an actual effort into trying to find evidence for the hypothesis would gain valuable lessons on the workings of biology and they would be the fruit of his own labour and not yours or my opinion on it.I wish him luck though I highly doubt the probabilty for success.

This message is a reply to:
 Message 3 by RAZD, posted 10-02-2005 12:10 PM RAZD has not replied

  
wj
Inactive Member


Message 5 of 47 (249007)
10-05-2005 5:19 AM
Reply to: Message 1 by Nova
10-02-2005 8:07 AM


Strange that the procaryote cell doesn't get a mention. Why no fantasy hypothesis for them as well?

This message is a reply to:
 Message 1 by Nova, posted 10-02-2005 8:07 AM Nova has not replied

  
Ooook!
Member (Idle past 5836 days)
Posts: 340
From: London, UK
Joined: 09-29-2003


Message 6 of 47 (249084)
10-05-2005 10:46 AM
Reply to: Message 1 by Nova
10-02-2005 8:07 AM


Why do we need an experimenter gene?
Hi Nova,
Like Sidelined, I would like you to go back and consider the consequences of having organisms full of experimenting cells pumping out viruses. I'm also keen to hear how far back into evolutionary history your proposed system would go. In addition, I'd like you to explain why we need to invoke an experimenter gene in the first place.
For example:
Thus, a simple, less efficient pathway will be ”short-circuited’ by a more efficient, but more complex pathway. This means that complex biochemical pathways can form in a cell if there is some system for introducing new, unique macromolecules into the biochemical system. Where might these new macromolecules come from
But we already have a mechanism for that: it's called an imperfect DNA replication system! It can explain the introduction of novel genes with novel functions and it has been observed. What aspect of this is inadequate in your opinion?
This message has been edited by Ooook!, 05-10-2005 03:46 PM

Si hoc signum legere potes, operis boni in rebus Latinis alacribus et fructuosis potiri potes!

This message is a reply to:
 Message 1 by Nova, posted 10-02-2005 8:07 AM Nova has replied

Replies to this message:
 Message 25 by Nova, posted 10-28-2005 8:15 PM Ooook! has not replied

  
Nova
Inactive Member


Message 7 of 47 (249374)
10-06-2005 5:41 AM
Reply to: Message 2 by sidelined
10-02-2005 12:01 PM


No I do not have a specific candidate for the experimenter gene, nor the knowledge and resources to determine where it would be on the chromosome, or what its precise mode of operation would be. Indeed, I have no idea whether the experimenter gene even exists or not.
What I wanted to point out was that if a gene with the properties of the experimenter gene did exist, then the development of what seems to be intelligently designed structures and processes in the eukaryotic cell could be explained without reference to any intelligent designer.
The concept can be simply extended to explain the design-like characteristics of species
Just as a cell is an integrated assemblage of diverse molecules, the organism is an integrated assemblage of diverse cell types.
Almost every organism begins its life as a single eukaryotic cell that contains the machinery and instructions for the expression of the organism. Organisms are ”colonies’ of eukaryotic cells that develop and function as integrated wholes. Like the individual cells, organisms function on the principle of maximum efficiency.
A species is a population of organisms capable of interbreeding to produce viable offspring. There are already more than a million described species that together integrate to form the biosphere. Each is a marvel of design, construction and behavior.
By what causal mechanism have all these species come into existence?
In my previous essay ”Cellular Experimentation and the Unselfish Gene’ it was explained how, by postulating an experimenter gene, the intricate design-like characteristics of eukaryotic cells could be understood as arising from an iterative process of gene additions that increase cellular efficiency.
Organisms evolve in a two tiered selection process. The first selection process increases cellular efficiency and generates phenotypic variation. The second selection process removes inefficient phenotypes. The second selection process is simply Darwinian Natural Selection, with the source of variation supplied by the experimenter gene instead of random mutations.
The second selection process can operate if we assume that when a new gene is added to the genome of a species by viral transmission, only a proportion of the population initially acquires the new gene.
If the new gene, expressed at the phenotypic level causes a decrease in an organism’s efficiency, then the organisms without the gene will out-compete those with it, and the gene will be eliminated.
If however, the new gene causes an efficiency improvement in the phenotype, then the organisms with the new gene will out-compete and eliminate those individuals without it.
In this way, the species will either accept or reject the new gene.
If the species accepts it, it will have advanced one rung up its evolutionary ladder.
Thus the evolution of species is also an iterative process of experimentation where the organism is the experiment, and death before reproduction is the selective force.
Again, random mutations play no part, and the species can be thought of as the production of a long sequence of successful experiments rather than an accumulation of random errors.

This message is a reply to:
 Message 2 by sidelined, posted 10-02-2005 12:01 PM sidelined has not replied

  
Nova
Inactive Member


Message 8 of 47 (251295)
10-12-2005 8:04 PM
Reply to: Message 3 by RAZD
10-02-2005 12:10 PM


If all genetic material transported via viruses were pathological, then Natural Selection would select organisms with the greatest resistance to viruses.
Vertebrates have the genetic blueprint for the biomolecule interferon, which "binds to the plasma membrane of uninfected cells and renders them immune to infection by the same or other viruses." (Lehninger, Principles of Biochemistry p.939)
Why isn't there a bank of interferon secreting cells to stop viral infections before they happen? If it was in the interest of our species to stop viruses, then we could easily do it.
"Interferons are proteins that are secreted by certain cells of vertebrates when they are infected by a virus." (ibid p.939)
Thus interferons, which could be used to completely prevent viral infections, are merely used to self-regulate total virus production within an organism.
The fact that our bodies allow viral infections to occur when they could be prevented implies that viruses must do something for us that enhances our overall survivability. The fact that viruses can sometimes kill the organism they 'infect' implies that viruses must do something very good for us to be positively selected for in the face of such a negative.
Nova

This message is a reply to:
 Message 3 by RAZD, posted 10-02-2005 12:10 PM RAZD has replied

Replies to this message:
 Message 9 by RAZD, posted 10-12-2005 8:41 PM Nova has replied
 Message 10 by Ooook!, posted 10-13-2005 8:20 AM Nova has replied

  
RAZD
Member (Idle past 1426 days)
Posts: 20714
From: the other end of the sidewalk
Joined: 03-14-2004


Message 9 of 47 (251307)
10-12-2005 8:41 PM
Reply to: Message 8 by Nova
10-12-2005 8:04 PM


Consider both sides of the design controversy.
The fact that our bodies allow viral infections to occur when they could be prevented implies that viruses must do something for us that enhances our overall survivability. The fact that viruses can sometimes kill the organism they 'infect' implies that viruses must do something very good for us to be positively selected for in the face of such a negative.
Begging the question (they must be doing good because you assume they are doing good?) plus a bit of a post hoc ergo propter hoc fallacy (those who survive infection demonstrate that the virus is not there to kill us but to make us better) there.
The fact that infection still occurs when there is a good design mechanism to prevent it, plus the fact that the evidence shows such infection to be a negative (with the body evolving new defenses to such infectuous agents that evolve new ways to infect us), and NO evidence of your assumed "must do something for us" shows that the concept of this being a design mechanism does not involve intelligent design.
It may involve Silly Design: both sides of the design controversy should be considered to see which has the better applicability.
Enjoy.

we are limited in our ability to understand
by our ability to understand
RebelAAmerican.Zen[Deist
... to learn ... to think ... to live ... to laugh ...
to share.

This message is a reply to:
 Message 8 by Nova, posted 10-12-2005 8:04 PM Nova has replied

Replies to this message:
 Message 11 by Nova, posted 10-17-2005 8:45 PM RAZD has replied

  
Ooook!
Member (Idle past 5836 days)
Posts: 340
From: London, UK
Joined: 09-29-2003


Message 10 of 47 (251395)
10-13-2005 8:20 AM
Reply to: Message 8 by Nova
10-12-2005 8:04 PM


Nova,
You don't seem to have thought about the implications of what you are proposing very carefully and/or have misunderstood a few things about cell biology and evolution.
If all genetic material transported via viruses were pathological, then Natural Selection would select organisms with the greatest resistance to viruses.
RAZD has aready mentioned this, but I feel that it needs to be underlined. In the virus/host relationship it's not just the host that changes over time; viruses are evolving like crazy! It's a classic example of the Red Queen effect (running to stay in the same place): an organism evolves a defence against a virus, the virus evolves a way to get around the defence, the host develops a new way of impeding the virus...etc, etc.
Why isn't there a bank of interferon secreting cells to stop viral infections before they happen? If it was in the interest of our species to stop viruses, then we could easily do it.
Maybe because it is not in the best interest of an individual organism for cells to be pumping out interferon all the time.
Cell signalling in the immune sytem (like so many aspects of cell biology) is never a case of having a series of on/off switches. It is a delicate balancing act between contrasting signals. The actions of inflammatory cytokines are counterd by the pathways triggered by anti-inflammatory ones. Don't forget that what is good for defeating viruses is not necessarily good for being a healthy fully functioning cell.
For example (from Alberts et al)
quote:
The binding of the interferons to their cell-surface receptors stimulates specific gene transcription by the Jak/STAT intracellular signaling pathway (see Figure 15-63), leading to the activation of a latent ribonuclease, which nonspecifically degrades ssRNA. It also leads to the activation of a protein kinase that phosphorylates and inactivates the protein synthesis initiation factor eIF-2, shutting down most protein synthesis in the embattled host cell.
emphasis mine
If a cell loses its ssRNA and most of its ability to produce proteins it ain't gonna last that long. Interferon signalling has to be transient.
Vertebrates have the genetic blueprint for the biomolecule interferon,
Does this mean that the 'eureka hypothesis' only extends to vertebrates now? How did all of the other eukaryotes evolve? This is what I mean about thinking things through and making sure they make sense in line with the facts.

This message is a reply to:
 Message 8 by Nova, posted 10-12-2005 8:04 PM Nova has replied

Replies to this message:
 Message 13 by Nova, posted 10-17-2005 9:31 PM Ooook! has replied
 Message 14 by Nova, posted 10-17-2005 9:40 PM Ooook! has not replied

  
Nova
Inactive Member


Message 11 of 47 (252516)
10-17-2005 8:45 PM
Reply to: Message 9 by RAZD
10-12-2005 8:41 PM


Re: Confirm no Intelligent Designer necessary.
...the concept of this being a design mechanism does not involve intelligent design
Hi RAZD
I have tried to stress this point. The mechanism proposed here allows complex design-like structures and processes to evolve without the intervention of any hypothetical Intelligent Designer.
If the Eureka Hypothesis is correct then evolution can be understood as being driven by the second law of thermodynamics like all other physical processes.
Nova

This message is a reply to:
 Message 9 by RAZD, posted 10-12-2005 8:41 PM RAZD has replied

Replies to this message:
 Message 12 by RAZD, posted 10-17-2005 9:01 PM Nova has not replied

  
RAZD
Member (Idle past 1426 days)
Posts: 20714
From: the other end of the sidewalk
Joined: 03-14-2004


Message 12 of 47 (252519)
10-17-2005 9:01 PM
Reply to: Message 11 by Nova
10-17-2005 8:45 PM


Re: Confirm no Intelligent Designer necessary.
Why is it necessary?
If the Eureka Hypothesis is correct then evolution can be understood as being driven by the second law of thermodynamics like all other physical processes.
2nd T has no bearing anyway, not a closed system. Mutation accounts for change observed, what you are proposing has not been observed and would actually tend to contradict evolution by breaking the nested genetics that creates genetic trees of life similar to the others we've developed from other sources.
Occam's bloody razor takes it out.

we are limited in our ability to understand
by our ability to understand
RebelAAmerican.Zen[Deist
... to learn ... to think ... to live ... to laugh ...
to share.

This message is a reply to:
 Message 11 by Nova, posted 10-17-2005 8:45 PM Nova has not replied

  
Nova
Inactive Member


Message 13 of 47 (252530)
10-17-2005 9:31 PM
Reply to: Message 10 by Ooook!
10-13-2005 8:20 AM


If a cell loses its ssRNA and most of its ability to produce proteins it ain't gonna last that long. Interferon signalling has to be transient.
Hi Ooook!
Interferon injections are used as a treatment for a variety of illnesses. Experience has shown that:
quote:
The amount of interferon that occurs naturally in the body is very small. When interferon injections are given the amount in the body increases greatly. For this reason, it causes side effects, even though it is a naturally occurring substance. However, the side effects of interferon are not usually severe.
The physicians recommend what could have been naturally supplied by a bank of interferon secreting cells without unusually severe side effects.
Does this mean that the 'eureka hypothesis' only extends to vertebrates now? How did all of the other eukaryotes evolve?
Vertebrates are the most complex products of evolution and have, by cellular experimentation, found more efficient solutions to biochemical problems. Porifera, one of the most simple of eukaryotic metazoan phyla use more less well evolved versions of interferon system:
quote:
In addition, sponges are provided with an interferon-related system, with the (2-5)A synthetase as controlling enzyme.
Thus invertebrates do not synthesise interferon, they simply use a more primitive method of acheiving the same result.

This message is a reply to:
 Message 10 by Ooook!, posted 10-13-2005 8:20 AM Ooook! has replied

Replies to this message:
 Message 18 by Ooook!, posted 10-18-2005 2:43 AM Nova has replied

  
Nova
Inactive Member


Message 14 of 47 (252533)
10-17-2005 9:40 PM
Reply to: Message 10 by Ooook!
10-13-2005 8:20 AM


Re: Evolving Viruses
viruses are evolving like crazy!
This is an interesting assertion Ooook!. Could you please explain by what mechanism viruses are supposed to 'evolve like crazy'?
Also some evidence that they do actually evolve like crazy would be nice.

This message is a reply to:
 Message 10 by Ooook!, posted 10-13-2005 8:20 AM Ooook! has not replied

Replies to this message:
 Message 15 by RAZD, posted 10-17-2005 9:43 PM Nova has not replied
 Message 19 by Carson O'Genic, posted 10-18-2005 8:59 PM Nova has not replied

  
RAZD
Member (Idle past 1426 days)
Posts: 20714
From: the other end of the sidewalk
Joined: 03-14-2004


Message 15 of 47 (252536)
10-17-2005 9:43 PM
Reply to: Message 14 by Nova
10-17-2005 9:40 PM


Re: Evolving Viruses
AIDS

we are limited in our ability to understand
by our ability to understand
RebelAAmerican.Zen[Deist
... to learn ... to think ... to live ... to laugh ...
to share.

This message is a reply to:
 Message 14 by Nova, posted 10-17-2005 9:40 PM Nova has not replied

Replies to this message:
 Message 16 by jar, posted 10-17-2005 9:45 PM RAZD has replied

  
Newer Topic | Older Topic
Jump to:


Copyright 2001-2023 by EvC Forum, All Rights Reserved

™ Version 4.2
Innovative software from Qwixotic © 2024