It seems plausible that our DNA hosts a myriad of capable dormant viruses than be triggered by some external activator (or binder), much the same way we have receptors for plants found in the wild (cannabis, nicotine etc...). It also seems perfectly reasonable that the (m)(b)(tr)illions of viruses on the planet are waiting in the wings for a host to get infected to start the process on a new epidemic. I'd like to think this is some form of regulation but of course that would necessitate the world as we know it as a part of a single system that can regulate even the tiniest of members.
For a hypothetical we could imagine the scenario where viruses existing in say a remote rain-forest, generally innocuous and self-contained. When deforestation occurs the virus is now open and can potentially infect whatever mechanism (human) that has disrupted it, binding to the same virus DNA that has existed for millions of years.
It's not that far-fetched to think unintelligent systems have defenses that we are largely unaware of - or cannot understand.
You're affirming the consequent. We don't have receptors for plants found in the wild (cannibis, nicotine, etc). Rather, compounds formed by those plants match up with receptors we already have.
There's an entire endocannabinoid system, and it's not because pot is natural. Nicotine broadly matches up with acetylcholine and nicotonic acetylcholine receptors.
It's far more likely that plants evolved and selected for compounds which have beneficial/detrimental effects on possible consumers, like nicotine as a pesticide, than it is that we have receptors for plants found in the wild on the off chance that we may have consumed them or that they would have been so prevalent in the past that receptors for them would have been selected for.
Read the book twice. Excellent. Dawkins can be a little long-winded and repetitive at time. For me the book got better after the first third or so. Highly recommended.
I also recommend "Evolutionary Psychology: A Critical Introduction" which echoes many of the themes in "The Selfish Gene" from a different perspective.
Well, the author of this article mentions he has a book on the same topic called "A Planet of Viruses." So that might be worth checking out. (I haven't read it myself.)
"The Selfish Gene" is explicitly directed at the layman, and absolutely no knowledge of biology is assumed. While this presents a danger of boring readers (such as myself) who are already familiar with DNA and meiosis, the colorful metaphors Dawkins uses throughout the book do much to keep the reading engrossing and entertaining.
After a lengthy exploration of basic biology, covering topics such as DNA and the origin of life, Dawkins introduces the gene-centered view of evolution that has long been textbook orthodoxy. Dawkins uses the remainder of the book to look at various types of animal behavior in an effort to convey some general conclusions and tools to help the reader understand evolution and natural selection. Much of his effort is devoted to explaining behavior in terms of the 'selfish gene' - especially social behavior that has long been held to have evolved 'for the good of the species.' Dawkins shows that how fundamental axiom of natural selection (that the genes best at surviving and reproducing will eventually spread through the gene pool) leads directly to the selfish gene and the behavior exhibited by nearly all animals (humans being the prime exception).
I should warn that conservatives would probably not enjoy the book nearly as much as I did. Dawkins is an open secular humanist with socialist leanings, and is not worried about offending the delicate sensibilities of creationists and fundamentalists. This book should only be read by those willing to 'accept' the validity of natural selection and evolution; others would only waste their time. I would direct readers seeking a more scientific discussion of these issues to G. C. Williams's "Adaptation and Natural Selection." All others will most likely enjoy "The Selfish Gene" a great deal and finish the book with a new appreciation for and understanding of evolution and biology.
The unit of selection is the gene; not the individual, much less a group of individuals. The reproduction of an allele is not necessarily aligned with the well-being and reproduction of an individual carrying the allele.
note for the future: Amazon is a tab away and will give you summaries and more of millions of books. mostly a solved problem. would not be surprised if Wikipedia had a summary of it too.
if I wanted a summary from a non HN user I would've gone there. I think people often miss the importance of someone summarizing it in their own words on a network.
It would be interesting to see if we could clean up (refactor) the human genetic code into a more efficient form with less baggage, and maybe less chance at getting hit by viruses just by virtue of having fewer random flaws to exploit.
If we could simulate human cells completely, we could try to simulate an embryo's initial formation and see what falls apart if you remove various sequences.
Besides that... we need to understand how a cell recognizes its purpose in its local environment - some kind of local communication probably. If we knew what the various environments that control cell responses are, we would have the basis for something like unit tests... and then we could try randomly removing parts of the DNA and see if its failing to perform as expected or not.
I think it's a mistake to consider a "clean" version of the human genome that "got polluted" along the way. We co-evolved with these other factors all together. Tinker at your own risk.
Yeah but chimps and denisovans lived fine without as many copies. Certainly I don't advise knocking about indiscriminately. But we have 100 copies - wouldn't 50 do? 20? 1?
Actually that's an incredibly terrible idea.
You see single base-pair (and other) errors are very common during DNA replication. By having a lot of "useless" (allegedly) zones in our DNA, decreases, statistically speaking, chances of that error occurring in more important areas.
The animations I've seen that purport to show the general public how DNA replication works indicate that it is a sequential process. The DNA is split into two strands, kind of like a zipper unzipping, and then bases are added to the two strands to form the two new complete DNA molecules. One strand (the leading strand) has the new bases added one after the other in the same direction. The other strand (the lagging strand) has them added in short called Okazaki fragments.
Errors on the leading strand should be independent and occur at a constant rate, and so having useless zones should have no effect on the number of errors a given useful zone gets.
The lagging strand is more complicated, because you have at least 3 distinct things going on: finding where to start on Okazaki fragment, filling it in, and recognizing the end. I suppose that allows for a different kind of error on the lagging strand (messing up recognizing the start or end of an Okazaki fragment) that would affect multiple consecutive base pairs. Useless segments would increase the average spacing between useful segments, and so would decrease the chance that a given multi-base error in a useful fragment affects multiple segments.
However, the problem here is that the enzymes aren't perfect and coding errors are quite common (they get fixed, sometimes). A big problem is that some chemicals can look like a nucleotide (A or T or C or G) and after insertion it can "decay" into a different one, hence causing an error. During replication it is possible for a DNA fragment to be cleaved (once again, it is often repaired, but thats how the Y chromosome came to be AFAIK) however sometimes enzymes "mess up" and reattach them at wrong positions. At other times base-pairs are deleted or inserted shifting the whole strand. There is a lot of things that could go wrong.
I don't believe that argument. Why would an error transcribing a virus dna segment affect in any way, the probability of error transcribing useful dna? They would be independent variables.
Removing duplicates of Useful segments could be bad - one gets mis-copied, the other is still there and so partial function would remain.
Imagine a general with a finite amount of artillery shells and a Howitzer on the fritz (i.e. the intended trajectory of the shots are somewhat off the mark today). Given the choice of where to deploy the artillery, the general may choose to concentrate their fire on the narrow beachhead landing instead of upon a widely scattered formation of units approaching across a vast plain.
The artillery that lands on the plain may strike an advancing unit, or it may fall (possibly harmlessly) between a set of advancing units. The artillery that lands on the narrow beachhead is more likely to hit a unit.
This analogy is far from perfect: sometimes mutations are good, which is one primary driver of evolution. Non-coding regions and/or "baggage to be refactored" (paraphrased great-great-gp comment) in DNA (the regions of the plain/beach not occupied by an advancing unit) can absorb "errors". Also, there are other types of mutations (insertions, deletions, ...), aside from the single point mutations that this analogy was attempting to help convey.
The point is: it's like bunching up a lot of important things over a few points of failure. If you increase "the genetic surface area", you lower the chance of the important thing getting hit.
On evolutionary scales, viable DNA has been selected with a lot of non-coding (and sometimes useful) regions, we know that if we reduce that down, we are more likely to be susceptible to fatal mutations on coding regions (e.g. a region that codes for a vital protein).
I think that's not the best analogy. You're imagining a constant amount of mutations (artillery shells) spreading over the size of the genome (the beach). It doesn't quite work like that, which is why mutation rates are usually measured in errors per base pair per generation.
In fact, copying DNA is more like downloading a large file over an unreliable network. There's a certain chance that each individual bit is flipped and the file becomes useless. You can reduce that chance by sending it multiple times, or introducing checksums, both of which add redundant data. But simply adding an extra TB of junk bytes to your download won't help preserve the integrity of the original file.
Does the number of mutations in a genome increase with the size of the genome, or with the length of time the genome is "in use?" Let's assume that the mutations are evenly distributed throughout the genome. If genetic mutation count is dependent on the size of the genome then it fits your "unreliable transmission" model.
However, if genetic mutation count is time-dependent but totally independent of the size of the genome, then having a larger genome actually does protect you from individual mutations, and it would do so exactly using the mechanisms described previously.
Think of two genomes, one large and one small, both existing throughout time. Both will accumulate a similar quantity of mutations from mutagenic processes which are time-dependent like radiation exposure.
I was more trying to explain the intuition of why single nucleotide mutations (resulting in non-viability or undesired effects) are probably more likely in a strand of DNA with regions removed versus a strand of DNA left as-is.
Basically, trying to give an example of the grandparent's point. (i.e. fewer nucleotides to be flipped -> more likely that an important one will be). I agree that it was a poorly executed analogy. The metaphor I was trying to make is that on the 'vast field' a random single point mutation is probably going to land on an individually unimportant nucleotide, and in the 'narrow beach' (the smaller strand/higher geninfo density) an individually important nucleotide is more likely to be hit. I'm still probably not articulating my point well, sorry.
But I think your analogy is better for a subtly different point; describing how DNA replication works in a system, where stands can be selected out, errors corrected, and genetic information can be preserved at a systemic level.
For a hypothetical we could imagine the scenario where viruses existing in say a remote rain-forest, generally innocuous and self-contained. When deforestation occurs the virus is now open and can potentially infect whatever mechanism (human) that has disrupted it, binding to the same virus DNA that has existed for millions of years.
It's not that far-fetched to think unintelligent systems have defenses that we are largely unaware of - or cannot understand.