Biologists are performing significant studies on "life" forms. As we get more involved in the details -- the cells, the smaller and constituent parts of the cellular entities, the chemistry of life -- we come closer to "non-life" forms. And we get right next to that miracle distinction between the crystal and the colloid, the unliving and the living. And right there, we find VIRUSES. They are basically protein shells, and most biologists do not regard them as "living". In fact they need cells of the living in order to reproduce.
But...what were viruses doing before there were cells? And what are they really doing now?
It will become increasingly apparent that the "protein" chemistry of viruses and cells is interactive and even interchangeable. Viruses are go from cell to cell injecting protein which the cell actually incorporates, and in so doing, makes its own responsive changes. Different proteins make different reactions. The relations between cells and viruses are an engine of change.
We would not be here without viruses.
Wednesday, December 28, 2005
Protein Transmission
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Experimental testing of libraries of artificial WW domain sequences shows that a simple statistical energy function capturing coevolution between amino acid residues is necessary and sufficient to specify sequences that fold into native structures. These tests suggest that the potential complexity of the protein-folding problem may be exaggerated.
ReplyDeleteAlso, since the amino acid sequence of a protein specifies its atomic structure and biochemical function, the existence of the protein appears to be the bridge between life and nonlife structures. Compare, Socolich, Lockless, Russ, Lee, Gardner, Ganganathan - article: Evolutionary information for specifying a protein fold, NATURE (22 Sept 2005) 512.
Nota Bene - I should qualify the "compare" reference - the NATURE article does not mention the suggested role of viruses.
ReplyDeleteGenetic mutations can be tracked. Embedded in stretches of DNA, a mutation can be traced, and measured. Now we are pretty certain that a single "founder" is the source of variants in our DNA. But explaining the variant by finding a "founder" -- obviously long-dead -- does not explain the variant. What happened to the original "founder" DNA?
ReplyDeleteWhile it is true that a mutation might provide a possible advantage -- Sickle cell protects from malaria, cystic fibrosis protects from diarrhea, hemochromatosis protects from anemia. The protection or advantage, or even the diversification, may explain the survival of the gene. But the subsequent benefit does not explain the genesis.
A viral "messenger" making a slight mistake would always explain the genesis, as well as the diversification within limits.
In order for a virus to inject a cell with its own protein, it needs to secure or attach itself to the cell membrane, breach and penetrate the membrane, and unload without leaving itself ripped open, perhaps re-sealing itself after releasing from the cell.
ReplyDeleteSome viruses -- some of the most dangerous to us -- are also clearly protected by a membrane. In other words, their own "wall" or barrier must also be breached in order to fuse with and penetrate a cell.
Can we block the fusion?
Can we interfere with the viral means of locating-anchoring-fusing- penetrating process? Peptides or other chemicals that "communicate" with proteins should do the trick.
The key is the fact that viruses have to use their outer membranes to perform their "repro" trick, and that outer wall or husk is a protein.
VIRAL COUNTER-ATTACK. You mentioned peptides, but enzymes might be more practical. Production of a specific peptide by partial hydrolysis of protein does not sound "easy" in situ. Cells can control and distribute enzymes by locking them up in nucleoli. For example, an activated ubiquitin ligase could alter a protein's destiny by signaling its destruction.
ReplyDeleteApparently there is some mechanism within the cell which can regulate protein function by switching the enzymes between free and static states.
Sam points out that viruses cannot survive without cells, the interior of which viruses require to reproduce. "The first life forms were not viruses because there were no other life forms to live off of."
ReplyDeleteThis does make it appear that the cells therefore developed first, and then the virus came on the scene to exploit this fertile "interior" sea.
Just because the virus is "simpler" does not mean it precedes the cell, and being parasitic does not necessarily require succession. The sea in which the virus once reproduced may be extinct, and the only remnant may be cells.
We do not know which came first, or if the cell and the virus are pleiotropic or so interrelated that they developed each other. This is what I suggest. It is Chicken AND Egg, never one in a vaccuum.