I have a general question for anybody. 4 mutations were required for the virus to attach to the Omp protein. Had the virus also - in the past I presume - also mutated to attach to the LamB?
I don’t know the answer to that, but it is entirely possible. At least in modern times, lambda phage was only known to attach to LamB:
Lenski says, “Natural selection did its thing, in other words, discovering mutations that provided an advantage to the viruses.”
He brings up natural selection and “advantage to the viruses”. Was there some kind of threat to the virus if it did not mutate?
The bacteria they were using did not have LamB on their surface. If the virus does not have anywhere to attach to the bacteria then it can’t inject its genome into the bacteria and replicate. The virus wasn’t threatened directly, but it had nowhere to reproduce. However, mutations in the virus did allow it to bind to OmpF, a different protein on the surface of the bacteria. Only the viruses with this mutation could reproduce which is how selection works.
Lenski said, " This evolved lambda virus could now infect E. coli cells through the original receptor, LamB, or this new one, OmpF" …
…but you said, the LamB receptor was now absent. Were both in fact present or not?
After further reading, LamB was present in very low amounts which allowed for a very low level of viral replication:
However, there were other proteins on the surface of the bacteria that were much more numerous. One of those was OmpF. The virus was able to replicate much faster if it bound to that bacterial surface protein.
So the virus was able to bind to both LamB and OmpF. The viruses that were able to bind to both reproduced at a much higher rate because LamB was in such low amounts on the bacterial surface.
Lenski states, " Of course, E. coli doesn’t make LamB for the sake of the virus."
How are we certain of this? Not a trick question. Are we certain that the bacteria do not in fact work somehow with the virus to ‘invite’ an infection.
It states the function of LamB right there in the article:
Getting sugars into the bacteria where they can be used for food is a very important function.
Was the OmpF a new receptor port? If yes, how did it come about?
OmpF already existed on the surface of the bacteria. The virus mutated so that it could bind to the already existing OmpF.
What does Lenski mean here
“LamB, or this new one, OmpF”
He means the old target vs. the new target. The virus used to bind to LamB, but now it has a new target in OmpF.
Is evolution about ascendancy? or mere survival?
Evolution is not about ascendancy. Ascendancy is a subjective human value judgment. Evolution is simply the inevitable result of organisms who reproduce with mutations and compete for limited resources. When those two conditions are met you will get evolution.
Which were what [for the virus] in this experiment?
Bacteria are the limited resource in this experiment.
And the bacteria in turn are limited by the available nutrients.
Exactly. With the added pressure of phage (aka bacterial virus), those bacteria that were able to reduce phage infection were better able to acquire nutrients. This is why the authors saw mutations in the bacteria’s malT gene that reduced surface expression of LamB, the protein the phage were using to infect the bacteria.
In the article Lenski refers to finite numbers of genetic materials available to the virus. Genes, codons, DNA bases, amino acids. The experiment ultimately centered on 4 mutations, also a finite number. In your opinion, do you believe that since only finite genetic resources exist for the lambda virus, that we might only expect a finite number of mutations to be expressed no matter the number of environments for natural selection to operate?
The number of mutations will always be limited by the number of virus since mutations occur at a certain rate.