Humans With Green Skin Could Live Off Sunlight.

DRZion said:
This is assuming we use sunlight as a source of energy. It could be just as helpful to use specialized lightbulbs as a means of efficiently converting electricity to nutrition.
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Very silly idea. We already have plants that do not waste energy moving around collecting solar energy, and then animals to concentrate the chemically stored energy for us to eat - that is efficient 100 times more for our energy requirements compared to us moving to the bottom of the food chain or becoming the primary converters. Only way we could do that is to become plant like - I.e. take roots where we were born and never move.

Not to even mention the huge energy losses trying to make electric power in caloric intake via skin absorbed light from lamps (only a small fraction of the light would even hit the skin and much that does would not hit the photoconverter cells or be reflected!).
 
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draqon said:
that will require astronomical amounts of water...the whole process will be extremely inefficient for moving organisms like us.
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Frank Ryan said:
Very interesting stuff! While still thinking about all this, and reading around it, I would like to contribute to the discussion about why viruses sometimes kill their hosts.

It depends on a number of factors and dynamics. Viruses are obligate genetic parasites. They form two different levels of partnership with hosts. In acute viral infections, virus and host will often have a relatively fleeting level of interaction, with selection operating at mainly selfish level in both virus and host, and here there will be the real potential for viruses killing some of the host population. If the dynamics of viral evolution favour rapid spread, this can maximise disease manifestations, eg coughing, sneezing, infectious skin lesions, etc, and the evolutionary drive towards maximising symptoms in host can lead to lethality. Nowhere is this more dangerous to host than in the initial interaction between a highly infectious virus and a virgin host -- a so-called emerging virus infection. This is a situation where the virus might even cause the extinction of the virgin host. But one needs to take a step backwards and really think it through to realise that in such circumstances the virus itself may not be threatened with extinction in a broader sense.

A virus invading a virgin host will probably have hopped species (even families) to do so. In other words it is coming from another host with which it may well have established a long-term partnership.

Let us take the squirrel pox virus that is currently threatening the UK red squirrel with extinction. This virus is a persistent partner with the grey squirrel. In persistent infections -- partnerships where the virus never leaves the host (think myxomatosis, hantaviruses, AIDS, etc) -- the partnership dynamics are very different. Here virus and host must enter into a long-term interaction where selection is operating to a significant degree at partnership (in symbiological parlance, holobiontic) level. The virus has already culled the species genotype of the grey squirrel to one that allows longterm coexistence of virus and host, so it causes no overt disease while yet multiplying freely in the species. The extinction of the red squirrel would not cause the virus itself to become extinct. On the contrary the virus would benefit from the success of its partner, the grey squirrel, taking over the entire ecological niche of the red squirrel. This is one aspect of an evolutionary dynamic of plague viruses I termed "aggressive symbiosis".

In AIDS, even at the very peak of the present pandemic, and where HIV-1 and the human species are interacting mainly at selfish individual (or gene) level, there is the beginnings of such an aggressive symbiotic interaction, with virus and host influencing one another's evolution. This interaction, which is evolutionarily intense, involves the human HLA-B antigens -- coded by our Major Histocompatibility Complex (xMHC), which governs both our immune respones and our determination of self. (see Kiepiela P, et al, 2004. Nature 432: 769-74.). By the time the AIDS pandemic settles, it will have significantly changed the human species gene pool in populations where the epidemic has infected a large proportion of the population. What was formerly a small minority of people within those populations who were genetically more adapted to live with the persistent presence of the virus will survive and multiply, thus greatly increasing their proportion within the host population. In these the virus will be able to reproduce and spread without causing serious disease, an essential step to viral persistence. Moreover, since lentiviruses are capable of invading the germ line of mammals, and primates, HIV-1 could potentially enter into a long-term holobiontic union with the human genome, as have very large numbers of retroviruses with our human and pre-human ancestors.

This would take it to a new and powerful symbiogenetic stage where selection, operating at the holobiontic level of combined vertebrate and viral inheritance within the genome, would open up new evolutionary possibilities in the future.
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This is a fascinating new area of science I wasn't aware of before. I think you're right about the need for a summary of it all. Is this getting close to the boundary between the physical forces of atoms & molecules w.r.t how they perform within living cells?
 
Billy T said:
Very silly idea. We already have plants that do not waste energy moving around collecting solar energy, and then animals to concentrate the chemically stored energy for us to eat - that is efficient 100 times more for our energy requirements compared to us moving to the bottom of the food chain or becoming the primary converters. Only way we could do that is to become plant like - I.e. take roots where we were born and never move.
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No reason why we would have to take root.. I'm not sure how we would supply the nutrients to our photocenters - the chemicals are very likely not present in the blood. However, the sea slug does do it.

Every time we feed animals we lose about 95% of the caloric value in the feedstock. We first grow wheat that is maybe 10% efficient at converting sunlight and then we feed livestock which is .1x.05 you do the math. Very ineffcient.

If we had lets say a patch of photosynthetic skin on our backs - somehow placed there using a skin graft - that would work well with certain lightbulbs.

Billy T said:
Not to even mention the huge energy losses trying to make electric power in caloric intake via skin absorbed light from lamps (only a small fraction of the light would even hit the skin and much that does would not hit the photoconverter cells or be reflected!).
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Hmm. I'm not an expert in photosynthetic systems but it seems that we could top the efficiency of plants if we engineered the system to work with specific wavelengths of light- as made by a halogen lamp.

At 15% efficiency we would need something like 2000 watts on a patch .4 m^2. With increasing efficiency the light would not have to be so concentrated- that is my main concern. Overheating may be a big issue if you are receiving so much energy.


It would be interesting if people no longer had to eat. Instead of wasting time going to restaurants we could just work work work all day long. :D
 
getting back to reality

Hi Guys,

But all of this is beside the point. What I wrote about in Virolution was the fact that viruses have made a huge contribution to the evolution of our human genome. This has very important implications to our human embryology, and day to day genetic chemistry. And it is of major importance to our understanding of important disease groups, like the autoimmune diseases and cancer.

If some of the participants in this lively debate really want to debate this, and maybe understand a little more of what must seem a bit startling to start with, I would be glad to open up onto some very interesting supportive information.

A series of medical reviews are currently going through on this in the Journal of the Royal Society of Medicine. On October 1 the first review of the importance to the autoimmune diseases will appear. One in twenty people suffer from these, which makes understanding kind of important.

Are you guys interested in delving into some real, cusp of the advance science?
 
Frank Ryan said:
... If some of the participants in this lively debate really want to debate this, and maybe understand a little more of what must seem a bit startling to start with, I would be glad to open up onto some very interesting supportive information. ...
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I hope you will. Not active in this thread are some posters here who can fully understand your points. Perhaps they can be attracted to this thread. More than half of the active posters here just misunderstand and pick up some minor out of context comment and soon have you advocating green people with no need to eat and somehow magically exhaling much more carbon (in CO2) with each breath than they inhaled.

To better judge who can follow you - you can click on their name then get list of posts they have started etc. to see the nonsense common to several active here. But don't let that discourage you from posting more of your POV - just be prepared for it to be twisted into things I am sure you do not intend, like green non-eating people.

For example CharonZ knows a great deal in the area you are discussing, works in it or closely related field, but seldom bothers refuting the nonsense posted here. I am retired but still like to teach so I do.
 
AlphaNumeric said:
Let me guess, your explanation for galaxy rotation curves has something to do with a cure for cancer?
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Let's not be quite so negative, shall we? How about trying to keep Frank's serious discussion just that i.e. without the insults and inane lame jokes. It'll never happen, I know.

New and stirring things are belittled because if they are not belittled, the humiliating question arises, 'Why then are you not taking part in them?'
- H. G. Wells
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a startling piece of real science

I'm going to introduce you to the first viral gene discovered to play a critical role in human evolution. If some of you have trouble interpreting the picture, let me know and I'll see what I can do to explain it further.

Okay, so can I suggest that any of you guys who wants to visit this site do so. You may find it strange, even baffling at first, but focus entire on the picture within the site. Download it and blow it up if it will help. It is multi-layered and each layer tells you a different part of the story. I will guide those who are interested enough to understand it. When you do you will find it rewarding - or at least I hope you do.

I am not allowed to post links so you will have to google for it, as follows:

ERVWE1 (Endogenous Retroviral family W, Env(C7), member 1)

Maybe some member who can post links could put it up for you after locating it.

This is the genetic region of your human genome that codes for a protein known as syncytin. Syncytin fuses the cells of the human placenta into a confluent monolayer, studded with nuclei but no cells walls between them. This is an essential thing to do since it forces all the goodies going into the embryo to pass through cytoplasm and the same applies to the waste products coming out. Think about the fact that half the embryo's genes are coming from the father, hence alien to the mother. If antibodies could get through the placental barrier, which is only one cell thick in humans, they would kill off every embryo.

So what you are looking at is a virus, known as a HERV-W (human endogenous retrovirus W), whose envelope gene codes for syncytin. The HERV-W is labelled ERVWE1 on the picture. You will also notice that it is not a viral gene captured by the vertebrate part of the human genome, but a viral envelope gene within a virus, with the viral LTR on the left (the 5' long terminal repeat) acting as the gene promoter.

The viral genes in between the two LTRs are labelled Agag, Apol, and env (coloured yellow). This internal structure of three genetic domains, gag pol and env, is the normal genomic structure of any retrovirus. So this tells us we are dealing with a complete retrovirus, though the gag and pol genes have been switched off by stop codons (mutations that switch off unwanted genes as part of the selection process). The yellow coloured env gene is the fully active one coding for syncytin.

Lower down the picture, in the third layer you see a blow-up of the regulatory regions for syncytin production. The HERV-W LTRs are colored white. LTRs are regulatory dynamos that will take over the control of neighboring genes, regardless of whether they were originally vertebrate or viral in their origins. They are very powerful and fulfill multiple regulatory functions. You will also notice that the HERV-W is further flanked by the LTRs of a second endogenous retrovirus (MalR), whose left sided LTR (the 5' LTR coloured red) is also an upstream regulator of syncytin.

So you are looking at a virus that is an integral component within the genome whose env gene has been conserved by natural selection for more than twenty million years, and whose regulation is through two viral LTRs. The evolutionary story is also told in the second layer of the picture. As you will see, we share the syncytin evolutionary story with chimps, gorillas and orangutans.

No human has been found to be without this important genetic structure in their genomes, which is is thought to be essential for normal pregnancy.

I would thus like to open the debate now -- I would welcome a few wisecracks, so don't hold back -- and ask if anybody looking at this extraordinary genetic locus could offer a logical explanation as to how this evolved (we know the viruses enter the genome from outside, it didn't grow out of nothing there) other than through viral symbiogenesis? In essence symbiogenesis means that this virus entered a symbiotic genome-to-genome union with the host genome, with selection now operating at the level of the united (holobiontic) genome.

If you think about it, the fact the viral env gene, and the whole structure, has been conserved by selection over this vast time period, can only mean that the virus has been selected for at the level of the holobiontic genome.

But maybe some of you have other ideas?
 
Ervwe1 url

Hi Billy,

If you visit my fprbooks website you will find that I have put in a page linked to this website and on the page I have inserted a picture of a typical retrovirus genomic structure and a direct link to the ERVWE1 URL.

P.S. There's this rather aggressive character pretending to be cool who is trying to muscle in on the story, claiming that it's his own. He goes by the name HERV Dubya. He wants to know if this is a private party or can any virus join in.
 
Here's the link to Frank's official Virolution website: fprbooks and here's a shortcut to the diagram in 'Endogenous Retroviral family W, Env(C7), member 1' or ERVWE1 for short.
 
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getting the hang of it

Okay -- many thanks!

Can I now suggest that those who are interested, even if they know nothing about viruses and have never visited a genetic locus before, will, with a little help, understand the ERVWE1 locus. And when you do you will have discovered a good deal of the history of a retrovirus that hit the primates sometime betweeen 20 and 40 million years ago. So devastating was that historic pandemic, which would have taken place when all the human related primates inhabited the hinterland of the African rainforest, that all humans today inherit its descendants in the form of the HERV-W. I'll explain a little more of its history -- if the virus doesn't do it for me -- when people have digested the basics. Download the pic off my website that shows you the basic genome of all retroviruses, look at what the various bits of the genome do, focus on the env (envelope) "gene", which is actually a genetic domain with more than one coding capacity. Take in the positions of the regulatory dynamos, the LTRs, which flank the three genetic domains. Then visit the ERVWE1 site and download the figure. Within the figure focus on the illustration that consists of a genetic structure running across the top in many colours. That's the first layer. Below this is an evolutionary history of the virus and its spread in the early primates and below that is a blow-up of the genetic regions that control expression of the virus env gene in the human genome today.

You can ignore all the rest because the main part of the history is contained in those three layers.

If you have any difficulty understanding what you are looking at, just ask away. It's really fairly basic but quite an education in terms of modern evolutionary biology and the real genetic make-up of our human genome.
 
Frank Ryan said:
...a retrovirus that hit the primates sometime betweeen 20 and 40 million years ago. So devastating was that historic pandemic, which would have taken place when all the human related primates inhabited the hinterland of the African rainforest, that all humans today inherit its descendants in the form of the HERV-W.
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This is the only bit that I understand! The figures are daunting to the uninitiated; it can't just be me!

btw, what do you make of this article: Did Prehistoric Viruses Trigger Human Evolution? A Galaxy Classic (Sept 2009)?
 
Rather than just a link, here are the four figures found there. (All in one drawing):

ERVWE1Fig1.jpg

I have deleted prior incorrect drawing that was posted as post 91.
 
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common_sense_seeker said:
Sounds ludicrous at first, I know, but a sea slug has managed to do just that. To quote Frank Ryan from his excellent groundbreaking book 'Virolution':



Has anyone read his fascinating book on evolution?
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This is how "God" should of designed nature. It's more civil to have your life forms feeding off the sun, then to have them decapitate each other and consume them alive in some cases.
 
clearing a path through the confusion

Hi,

Can I re-explain what is clearly confusing people in the figure of the ERVWE1 locus?

Okay. First let me explain that for a virus that is embedded in a genome to contribute to the evolution, and physiology, of the host it doesn’t have to make whole viruses. It only needs to express whatever parts of its genetic make-up that might contribute in an important way to host evolution or physiology.

Now, with this in mind, can I ask those who are confused by the figure to look only at the top section, which is labeled Figure 1. The left hand side of the genetic sequence comprises a virus, HERV-H (in purple) flanked by the solitary LTRs (long terminal repeats = viral regulatory dynamos) of another virus, called HERV-P, which are shown as green vertical bars. I’m just explaining what these are before telling you to put them aside and now focus on the right hand side of the genetic sequence, which is enclosed within two bright red vertical bars.

Okay?

The red vertical bars are the solitary LTRs (viral regulatory dynamos) of a human endogenous retrovirus called MaLR. This means that all of the normal viral genes of the MaLR have been deleted by selection, leaving just the flanking regulatory regions. The little pointy arrows, which look like triangles on their sides, merely show the flow of genetic transcription, or readout to proteins, and so they can also be ignored. Within the MaLR regulatory regions, you discover a complete endogenous retrovirus, which is labeled ERVWE1.

If you mentally add an “H” to ERVWE1, you will get the picture. It is merely a code term for one specific viral insert of the family of endogenous retroviruses known as HERV-Ws. This insert is on human chromosome 7.

Okay?

Now if you look more closely at the HERV-W, known as ERVWE1, you will observe, running from left to right within the two red MaLR bars, that it begins with a white vertical bar. This is the left flanking LTR of the HERV-W. This is followed by two bars of different tones of grey, followed by an intron (a non-viral genetic insert into the virus), shown as a thick black line, followed by three viral genes, labeled A-gag, A-pro-pol, and env. The env gene, which is more accurately the env genetic domain of the virus, is followed by the white vertical bar of the right side flanking LTR of the HERV-W.

Okay?

If we now focus down onto the HERV-W per se, we see that, ignoring the intron insert, it comprises a complete endogenous retrovirus, made up of flanking LTRs (its own regulatory dynamos) which contain within them the three normal genetic domains (gag, pol, env). The env domain (or gene) codes for the protein syncytin-1, which plays an essential role in fusing the single layer of placental interface cells into a confluent monolayer – a membrane devoid of cell walls studded with nuclei.

Okay?

So what we are looking at is a complete retrovirus (selection has switched off the gag and pol genes but they are still there) whose envelope gene has become integrated in a vital way into human evolution and day to day physiology of reproduction.

Now if we look at the left hand side HERV-W LTR and also the left hand side MaLR LTR, we discover that between them, these flanking viral regulatory regions play important roles in promotion and further regulation of the viral env gene, and thus the timing and expression of syncytin-1.

I don’t want to over simplify it, and there must be vertebrate regulatory factors that will link up with this, but in essence you are looking not just at a viral gene but at a virus, wrapped by the regulatory apparatus of another virus, which is an integral and important component of the human genome.

The only logical evolutionary mechanism that could explain such an extraordinary event is genetic symbiosis – in other words the symbiotic union of whole but very different pre-evolved genomes. In symbiological terms, this would be terms holobiontic genomic union. The env gene codes for a protein whose function does not exist in the vertebrate genetic inheritance. But the viral env gene is pre-evolved to fuse cells (amongst other things). You are looking at two genomes combining pre-evolved evolutionary lineages, which is quintessential genetic symbiogenesis. This is a very rapid and powerful genetic force for hereditary change, but it does not contradict classical Darwinism. It is additional to it, and essentially complementary to it.

Once you grasp the basic principles, and they are really quite simple, it opens the door to understanding the very strange make-up of the human genome.
 
That was an essential step-by-step commentary. And I'm beginning to get it. I'll have another look tomorrow. Thanks for that.
 
more anon

You're very welcome.

I'll wait to see if others get it and then show how this opens up a very interesting line of exploration, and conclusion.
 
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