Is the 'Randomness' of Evolution Really Random?

[ShayanJ]

(In order to ask my question, I need to explain a little bit. But I don't have a background in biology, so I may make some mistakes along the way. corrections are welcome.)

Recently I've been thinking a lot about evolution. Its really fascinating. The random exploration of the life "phase space" through mutations and settling on regions that provide the most adaptive traits for the current environment through natural selection.

But what does this "randomness" really mean? and how random is "random"?
I think when people call evolution random, they just mean that the mutations have no preferred direction, let alone a direction that gives the species more adaptive traits. But could it be that the "randomness" of evolution itself, is subject to evolution and so after some generations, the species actually evolves in a more adaptive direction?

Apparently yes. Because evolution is based on mutations and mutations are mistakes in the process of copying the DNA, you can accelerate evolution by making copying process more error prone, which can be achieved by a few patterns in the DNA(like a sequence of repeating letters).

My question is, how can evolution develop these patterns? I mean, natural selection is crucial for evolution. So if a trait is not going to make the species more adaptive in an environment, evolution can not drive that species towards that trait. these error prone patterns in the DNA are an example of such a trait. These patterns are good for the species as a whole because they make the evolution of adaptive traits more efficient, but they are not more adaptive traits for the species at an individual level and so they will not increase the probability of an individual's mating.

So how can evolution evolve these patterns without any help from natural selection?
Thanks

 

[pinball1970]

How random is random?

This link pf explores some of the questions

https://www.physicsforums.com/threads/a-few-questions-about-evolution.952006/
edit- randomness is discussed

 

[jim mcnamara]

What you are talking about is called the Gaia Hypothesis first stipulated by Lynn Margulis.
Example: life transformed the environment from one without free oxygen to one with free oxygen.
Lovelock, James, (1995) "The Ages of Gaia: A Biography of Our Living Earth" is one reference.

A general overview:
https://en.wikipedia.org/wiki/Gaia_hypothesis

For the example I mentioned about oxygen:
https://en.wikipedia.org/wiki/Great_Oxidation_Event
This event changed everything on Earth from minerals in the crust to the current dominant form of aerobic respiration in living cells.

Critics of Gaia point to the fact that changes like oxygenation of the biosphere were toxic and not necessarily to the benefit of the current living organisms - in contrast to what Gaia says:

... that living organisms interact with their inorganic surroundings on Earth to form a synergistic and self-regulating, complex system that helps to maintain and perpetuate the conditions for life on the planet.

Plus you need to note that you are on the more "touchy feely" end of Biology so everyone who has a position on this thinks they understand it correctly.

Fair warning - that sentence above means: please keep this thread out of speculation. It has lots of interesting aspects.

 

[ShayanJ]

It seems I should clarify my question.
Fundamentally, evolution is the result of random mutations+natural selection. When we say mutations are random, we mean that they don't care about whether the mutation is constructive, destructive or benign to the species.

But it seems that the process of evolution itself has evolved in a way that traits that are more likely to be important in a particular environment, are more likely to be mutated.

From what I understand, a mutation is a mistake in copying the DNA. So if you want to make mutation more likely in a particular place in the DNA, you should use patterns in that area that make mistakes in copying the DNA more likely, like a sequence of repeating letters(CACACACACA...).

So basically, life not only has evolved adaptive traits for species in their environments, but it has also evolved the process of evolution itself in a way that makes constructive mutations more likely, by making sure that important areas of DNA are more likely to be mutated.

My question is that how is that possible? The evolution of an adaptive trait is possible because it immediately affects the distribution of offsprings among various groups of the same species with different phenotypes.

But the above mentioned mechanism to make constructive mutations more likely, has no such effect on the species which means natural selection won't be able to select groups with such a trait. So how is this mechanism created?

 

[Drakkith]

My question is, how can evolution develop these patterns? I mean, natural selection is crucial for evolution. So if a trait is not going to make the species more adaptive in an environment, evolution can not drive that species towards that trait. these error prone patterns in the DNA are an example of such a trait. These patterns are good for the species as a whole because they make the evolution of adaptive traits more efficient, but they are not more adaptive traits for the species at an individual level and so they will not increase the probability of an individual's mating.

I'm not sure I quite understand what you're getting at. Let's look at an example, perhaps a virus. Specifically a retrovirus. Retroviruses are notorious for having especially error prone copying mechanisms. This is beneficial to the species because it enables the virus population to adapt to its host species immune system or antiviral drugs quite rapidly, as shown by viruses like HIV.

The evolution (through natural selection) of an efficient error-checking mechanism is suppressed because it would end up reducing the virus's ability to mutate as rapidly, reducing its ability to adapt to changes in its environment. So a population of viruses with such an error-checking mechanism would most likely end up being out competed by populations without one.

The only thing happening at an individual level is whether the virion (one complete virus particle) has one allele or another and how that affects its ability to survive and reproduce inside the host. The lack of error-checking machinery isn't itself an adaptive trait that helps a virion survive and reproduce, but it helps create traits that do. Hence it can be selected for by natural selection.

 

[ShayanJ]

I'm not sure I quite understand what you're getting at. Let's look at an example, perhaps a virus. Specifically a retrovirus. Retroviruses are notorious for having especially error prone copying mechanisms. This is beneficial to the species because it enables the virus population to adapt to its host species immune system or antiviral drugs quite rapidly, as shown by viruses like HIV.

The evolution (through natural selection) of an efficient error-checking mechanism is suppressed because it would end up reducing the virus's ability to mutate as rapidly, reducing its ability to adapt to changes in its environment. So a population of viruses with such an error-checking mechanism would most likely end up being out competed by populations without one.

The only thing happening at an individual level is whether the virion (one complete virus particle) has one allele or another and how that affects its ability to survive and reproduce inside the host. The lack of error-checking machinery isn't itself an adaptive trait that helps a virion survive and reproduce, but it helps create traits that do. Hence it can be selected for by natural selection.

I think this explanation falls in the trap of assuming that mutations have a goal in mind. The fact that such a trait is beneficial to the species across several generations has no effect on whether this trait is selected or not. Natural selection can only select a trait if it's beneficial to the group with that trait in the number of offsprings they have.

 

[Drakkith]

I think this explanation falls in the trap of assuming that mutations have a goal in mind. The fact that such a trait is beneficial to the species across several generations has no effect on whether this trait is selected or not.

Of course it does. Population A has a mutation that reduces its ability to adapt to changes in its environment, while population B doesn't have that mutation. Over time, population B out competes population A and becomes the dominant, if not sole, population.

Natural selection can only select a trait if it's beneficial to the group with that trait in the number of offsprings they have.

Which is exactly what is happening in my example of viruses. Over time, population A has fewer offspring in total because they can't adapt to their environment as well as population B.

 

[BillTre]

Recently I've been thinking a lot about evolution. Its really fascinating.

This is a complex subject which is probably why you find it interesting.
I think about it a lot as well (thus my long response).

The random exploration of the life "phase space" through mutations and settling on regions that provide the most adaptive traits for the current environment through natural selection.

This is one way many people conceive of evolutionary changes. Your phase space is often called an adaptive landscape, usually with adaptiveness increasing along the z-axis, leading adapting population to migrate "up hill". However, one should remember that the landscape would be multi-dimensional.
At the bottom of this wikipedia page is animation of the process, shown in a static and dynamic adaptive landscape. The spots in the animation represent individuals of the population which have different locations on the landscape due to their different genetic make-ups. The spots should be disappearing each generation (due to death), and being replaced by new spots in slightly different positions (the previous generation's offspring) on the population's landscape.
It should also be noted that the adaptive landscape will differ for each species (or even each individual, due to their unique composition), otherwise everything would be moving toward the same set of adaptations and other nitches would be left unoccupied.

But what does this "randomness" really mean? and how random is "random"?
I think when people call evolution random, they just mean that the mutations have no preferred direction, let alone a direction that gives the species more adaptive traits. But could it be that the "randomness" of evolution itself, is subject to evolution and so after some generations, the species actually evolves in a more adaptive direction?

So basically, life not only has evolved adaptive traits for species in their environments, but it has also evolved the process of evolution itself in a way that makes constructive mutations more likely, by making sure that important areas of DNA are more likely to be mutated.

Much of the "randomness" of evolution is attributed to the generation of mutations and the mechanisms that generate them. But as you suggest, there are cases where certain mutations can be affected by the genetic composition of the organism in question.
Genetic variation is the fuel of evolutionary change. Without variation, there would be nothing for selection to choose among. No change would happen. Mutations provide that variation, but different kinds of mutations can be limited in several ways. There are many levels at which this can happen.
These levels extend from the molecular, through the cellular, to the complex multi-cellular organisms, and even to societies that might emerge from interactions of populations.

In common (non-scientific) talk, random would just mean can't predict much what will happen ahead of time. And biological things are so complex, covering several levels of organization, each with their own set of emergent phenomena, that this is often the case. However, science likes to divid into smaller categories and examine them independently. More order can often be found there.

Here is a partial list of possible kinds of mutations.

Cause of mutations: There are many possible causes of mutations, some with the same set of effects on the sequence, some with different kinds of effects.

• Chemical of Radiation caused sequence change: single nucleotide base changes are often considered pretty much random in what they affect. These are often used in mutagenic searches for new mutations because they are considered unbiased. DNA breaks (breakpoint mutations) rearrange chunks of DNA. This can have a more complex set of effects on genes and their activity.
• Copying Mistakes like you mention, where there is slippage of repetitive sequences and repeated elements are either increased or decreased. These are known to underlie some disease states. Some of these mechanisms are limited to specific sequences as you point out.
• Changes due to Biological Activity: Including changes in sequence due to things like viral insetions, activated transposons, and other "weird things". These can have a direction toward particular kinds of genomic locations due to their complex nature, involving many molecular elements some of which may have either sequence recognition of be limited to locations where the DNA is available enough for their rather large molecules to physically access particular DNA sites.

There are probably some others I am forgetting.
The point is that there are a lot of sources of genomic sequence change. These might vary independently for a variety of reasons.

Mutations vs. Phenotypes:
The relationship between particular mutations and their effects (phenotypes) is not always simple and direct.
Changes in sequence can affect molecular gene products directly in cases of transcribed RNA and translated some proteins, however some sequence changes will not effect amino acid sequences in proteins due to the redundancy of the triplet code. This means some changes will have no effect.
Effecting more complicated things like developmental systems that might require intricate controls on the development a cell. This would probably involve regulating the control of hundreds of different genes, at different times in different cells (some based on position). This could be very complex and subtle, but could still be selected for because it affects something adaptively important (reproduction, behavior, ...).
Some phenotypes (like an adult morphology) are may not be easily achievable by many genomes because they lack important genes of functional and generative systems. In genome space, they would be very far away. An example might be: If you start with an insect and mutate it (I've done this), it would be extremely unlikely you would get something with a vertebrate feature like a vertebrate CNS. It would require thousands of simultaneous changes that would be required to establish new developmental processes to generate the CNS. Within reasonable odds, each organism would have a limited set of phenotypes that it could reach. Losing functions is a lot easier than making new ones.

Other more-weird sources of mutations (changes in genome sequence) can be:

• Hybridization: introduces a half of a genome of new stuff, could be very similar or very different in sequence, as well as copy number of particular genes, and ploidy (numbers of copies of the whole genome (normally 2 in metazoans, but can get 16 or higher). Something like 5% of the your genome, if you ancestry is from Europe, Asia, Australia, is Neanderthal. Then there's the Desenovans. Some of those transferred genes are important.
• Some groups of fish have been shown to be the result of hybridzation, repeatedly within a group.
• Endosymbiosis: The mitochondria had to come from somewhere (chloroplasts too). When it did, it had a big effect on the genome. Not just the addition of the mitochondrial genome, followed by it drastic reduction. Many of the bacterial genes of the mitochondrian, invaded the genome of the Archaean host cell and altered it by adding well formed functional units. But, it is also thought to have introduced a pack of molecular parasites (like transposons) that went through a period of rampant expansion, messing things up by inserting in different places in the genome, until restraining systems were evolved. This may have involved the formation of the nucleus and other eukaryotic features. Thus a set of repeated sequences were created.
  This was an important mutation (the mitochondrial endosymbiosis), but extremely rare. Life got started from inanimate matter less than 500 million years after water could form on the planet's surface (some say as rapidly as 100 million years), but it then took another 1.5 to 2 billion years for the eukaryots to evolve.
• Lateral or Horizontal Gene Transfer: Small numbers of genes moving among populations, in bacteria and a lesser extent in eukaryotes. This is often the source of genes better adapted in a new environmental condition.
• Genome Duplications: which have happened several times in the vertebrate lineage (and plants and insects), generate extra copies of each gene. One of the gene copies gene can then evolve completely independent functions, while leaving the older, still required functions, to the other copies.

Balancing out all of these effects on a population's genetics could result in some biasing of the mutation rate. Presumably these effects would be small in most cases. However, assuming these is a genetic basis underlying these kind of differences, it should be possible for selection to effect then, if there were consistent environmental reasons for that selection to happen.

Example (Scenario):
a small aquatic invertebrate dries up in a small temporary pond (this happena lot in this environment) and gets blown away. The local area (within wind blowing range) has a very diverse set of related but very different aquatic environments. You fall out of the sky into a situation different from that where you came. Your genes are not so good a match for the environment. Organismal and cellular stress results, both provide internal cell signals. This in turn might trigger a response (change in gene expression), which could include changes in the expression of genes effecting mutation rates. Such a control would make adaptive sense.

Molecular systems underlying these differences have been identified. Selection has been demonstrated. And cases of increasing or decreasing general rates of mutation have been found.
There are also well defined molecular systems for making directed and restrained mutations in specific genes, in the immune system. However, I can't think of anything like this that is inherited (inter-generational inheritance in metazoans, runs through the reproductive cells, which are a small population of cells that are not part of the immune system where these genes are being mutated)).

My question is, how can evolution develop these patterns? I mean, natural selection is crucial for evolution. So if a trait is not going to make the species more adaptive in an environment, evolution can not drive that species towards that trait. these error prone patterns in the DNA are an example of such a trait. These patterns are good for the species as a whole because they make the evolution of adaptive traits more efficient, but they are not more adaptive traits for the species at an individual level and so they will not increase the probability of an individual's mating.

There are many ways things like this can happen:
Not all sequences are under really stringent (meaning strong) selection. In the last maybe 50 years, random genetic drift has become more appreciate aas important in sequence evolution. Some sequence change will just happen with no apparent effect on viability. This means that although any gene can be mutated, not all of those mutations will have either a positive or negative effect of equal size. Some will be neutral (extreme case) and just ride along with the selection for other nearby (linked) genes in their particular that genome, which might be under strong (or weak) selection.
In addition, most eukaryotic (more complex than a bacterium) organisms will be at least diploid which can hide the effects of recessive deleterious (or advantageous) alleles in a proportion of the breeding population, due to their pairing with non-recessive non-deleterious alleles. Thus, a lot of alleles could hide, to some extent, from selection. Example: the Sickle Cell gene

There are also several levels at which biological entities can be selected for:

• Gene selection : (selfish gene stuff)
• Organismal (Whole Plant or Animal) Selection: that which is normally considered evolution
• Selection among Organelles (like selection for faster reproducing mitochondria (due to their smaller more quickly copied genomes) within a cell)
• Cell Selection with in an organism: cancer cells reproduce with a selective advantage within an organism (their environment) because they have escaped the normal controls on cell growth and movement, until their environment (the host body) dies, then they are a dead end (except for things like Tasmanian Devils and their nose cancer).
• Group Selection: kin selection, altruism among group members
• Selection of Taxonomic Lineages: some evolutionary lineages are very good at making more species and leave more descendant species than others. These will bush out rapidly (repeatedly) leading to more species of that taxonomic group (taxa is the general term) over longer evolutionary time periods. Those lineages that (over long periods of time) do not speciate much, could well eventually die out (some won't, due to some reason).

Species have average life spans and if they are not making new species, a species of average lifespan will die out without leaving any decedents (extinction of both the species, but possibly also the larger taxonomic lineage in which it is found). Exceptionally long lived species (like the coelacanth) can survive long periods without generating daughter species, but they are the exception. Most species that ever were, are extinct.

So, to answer your questions:
There are a lot of different ways that mutagenic rates might be controlled. In some cases, but probably not most, it is probably not dynamically regulated.
New phenotypes could be generated through either along series of simple or a few complex sets of changes. Some kinds of changes occur so infrequently that they might be considered the result of chance.
There are a lot of ways that an genetic components of an incipient trait (set of genes) may lay around the genome (involved in other processes) prior to its being recruited for some new function.
Genome duplications can provide lots of sequences that can be relatively easily adapted to new functions.
There are a lot of ways to work around these apparent barriers to evolving new traits.

 

[atyy]

But what does this "randomness" really mean? and how random is "random"?
I think when people call evolution random, they just mean that the mutations have no preferred direction, let alone a direction that gives the species more adaptive traits. But could it be that the "randomness" of evolution itself, is subject to evolution and so after some generations, the species actually evolves in a more adaptive direction?

Randomness includes deterministic behaviour. Randomness is specified by the measure, and the delta measure is deterministic.

. Because evolution is based on mutations and mutations are mistakes in the process of copying the DNA, you can accelerate evolution by making copying process more error prone, which can be achieved by a few patterns in the DNA(like a sequence of repeating letters).

Mutations are not necessarily mistakes. In meiosis, chromosomes assort independently, and there are crossovers.

My question is, how can evolution develop these patterns? I mean, natural selection is crucial for evolution. So if a trait is not going to make the species more adaptive in an environment, evolution can not drive that species towards that trait. these error prone patterns in the DNA are an example of such a trait. These patterns are good for the species as a whole because they make the evolution of adaptive traits more efficient, but they are not more adaptive traits for the species at an individual level and so they will not increase the probability of an individual's mating.

Evolution is more general than natural selection. Natural selection is only one mechanism of evolution, and explains how adaptive traits (one definition of an adaptive trait is that it increases survivorship) evolve. However, there are other mechanisms of evolution that drive non-adaptive traits, eg. sexual selection. https://www.nature.com/scitable/knowledge/library/sexual-selection-13255240

Does evolution select at the level of an individual or at the level of a group or at the level of a gene? There cannot be a single answer (there are persistent debates). However, think of these things from the point of view that it is physics that is fundamental. Selection is an emergent, approximate concept, so there is no reason to expect it to be absolute.

Edit: Also, you should not mix-up the concepts of fitness (leaving offspring to the next generation) and adpativeness (survivorship). https://evolution.berkeley.edu/evolibrary/article/evo_27

 

[Chris S]

If you are asking how can supposedly random mutations mutate more often in a manner favorable to adapting to the being's environment, I believe it may be possible for the mutations to be more adaptive to the environment that 100% random due to an offspring inheriting some of the same/similar genetic mutation tenancies/aspects that the parent benefited from. Parents who survive due to adaptive mutations pass their genes on, so the odds of the offspring having environmentally beneficial mutations is increased, not random.

 

[haruspex]

But it seems that the process of evolution itself has evolved in a way that traits that are more likely to be important in a particular environment, are more likely to be mutated.

What is your evidence is for that?
As I understand it some pathogens do seem to have evolved to be quite unstable in some genes. The advantage is rapid mutation to overcome evolving defences. Can't see that applying to more general environmental changes, though.

 

[cmb]

I like the style of the OPs question and I am hoping very much if this thread could begin to expand into discussing what must be a new set of evolutionary theories that main stream science must be coming up with.

I mean, we get the basic 150 year old plot of Darwinian evolution; one individual survives better than another, and hey presto they have more kids... repeat a million times ...

But that doesn't address all the issues and I am confident that other people have augmented that basic theory with 'add-ons' and really I don't know what they are. Can biologists here tell us what those are?

Here are a couple of things I think someone in the field must have thought about and come up with answers for;-

1. In answer to the OP's point, I think one of the points that has to arrive is that, surely, the theory is actually 'survival of the generally fit' rather than the fittest. I mean, if mutation is random, as the OP proposal (which seems to make sense to me), this will give a range of characteristics, some of which may not be particularly beneficial at a given point in time. But as environments and predation changes those 'hidden' characteristics may manifest and all of a sudden within the generic mix of those individuals, those that 'had been' the fittest all of a sudden, possibly instantaneously, die out. For example, say a species living in an arid area has some of its individuals 'uselessly' born with webbed feet but it doesn't disadvantage them too much and it just happens to be a characteristic, some have more webbed feet than others. The fastest runners don't have webbed feet and so do a bit better and slowly the population are moving towards 'no webbed feet', but still it is not such a disadvantage that those individuals die out. ... and then their habitat floods ...! So I think the substance of this is not merely 'the fittest' and 'survival' but actually if a species can successfully maintain the widest set of random characteristics then it is more likely to survive. As such, this is not survival of the fittest individuals, this is survival of the species with the widest set of tolerances to environmental changes. I am sure this has been proposed by evolutionary biologists and already has a name, which would address the OPs question.

2. Trans-species jumps; if species can't interbreed (my understanding of what defines a 'species') then this means we cannot evolve 'from' another extant species that then carries on its own evolutionary path. What it means is that we can have long-gone ancestors in common with current day species, but one species evolving from another and then continuing to co-exist is excluded. I think that is fairly obvious but it is not excluded from Darwin's original proposition as far as I can tell. I'd have thought there would be some theoretical expansion of this point, and if anyone can say what the current thinking/theories are that would be good.

3. Rate of change of species; A common ancestor of ours to other primates (as far as I know) is the Miocene Proconsul (https://www2.palomar.edu/anthro/earlyprimates/early_2.htm) which is said to have lived from 21 to 14 million years ago. But if it took 7 million years to become a new species then why is that an unrepresentative timescale for the 14 million years since then? I mean, surely there are more than two evolutionary 'species' steps from proconsul ape to us? Maybe not? I don't know? What do updated evolutionary theories say about this? I mean, taking that thought further, if we look at the first 'modern humans' 250,000 years ago, if one was here today they could integrate into society, we'd be able to have offspring with them and (presumably with training!) talk together. Yet that is 'only' 1/40th or so between proconsul ape and us, and it looks to me like there are going to be more than 40 times the number of differences between early homo sapiens and proconsul ape? Again are there any modern theories to explain what would initially appear to be, presumably, sudden accelerations in changes of species?

4. Given the total number of species on the planet, and that evolution occurs by seeing new species coming into existence, what does statistics of the past say about the rate of bifurcation of one species into two species, and are we seeing that rate of bifurcation today? I mean, just for primates alone, there appear to be a few hundred known species (https://en.wikipedia.org/wiki/List_of_primates) so is there some statistical inference when we should see the next bifurcation of a primate species, and when was the last? Is there a theory which quantifies this?

 

[cmb]

What you are talking about is called the Gaia Hypothesis first stipulated by Lynn Margulis.
Example: life transformed the environment from one without free oxygen to one with free oxygen.
Lovelock, James, (1995) "The Ages of Gaia: A Biography of Our Living Earth" is one reference.

A general overview:
https://en.wikipedia.org/wiki/Gaia_hypothesis

For the example I mentioned about oxygen:
https://en.wikipedia.org/wiki/Great_Oxidation_Event
This event changed everything on Earth from minerals in the crust to the current dominant form of aerobic respiration in living cells.

Critics of Gaia point to the fact that changes like oxygenation of the biosphere were toxic and not necessarily to the benefit of the current living organisms - in contrast to what Gaia says:Plus you need to note that you are on the more "touchy feely" end of Biology so everyone who has a position on this thinks they understand it correctly.

Fair warning - that sentence above means: please keep this thread out of speculation. It has lots of interesting aspects.

Something I came across just recently is the proposal that, actually, one of the dominant sources of oxygen at certain times in Earth's history was not biological in nature but radiological. I had assumed it would 'only' have been biological, but I can see that is in error now. What the proportion of bio- to radio-logical is, I guess is for future research?

https://web.archive.org/web/20050226115725/http://www.kirj.ee/oilshale/7_pihlak_2002_1.pdf

 

[Rap]

This has been covered above, but here is a simplified model.

If you consider a hypothetical organism that evolves by mutation alone, you have to take into account the variations in the environment. For example, suppose there are two food sources (A and B) available to an organism, and its DNA can conform to utilize only one at a time. (Maybe later it will evolve the ability to use both, but not now). The DNA to utilize A or B can be "protected" - The DNA can be encoded in such a way that it is relatively immune to mutation. Or, it could be less protected - more susceptible to mutation.

If you have an environment where, for a long time, A is the only food available, organisms which use protective encoding for A will reproduce more successfully than those that use unprotected encoding. They may reproduce at a 100% rate, while the unprotected organisms reproduce at only a 50% rate. Unprotected organisms will represent less and less of the population, percentagewise. However, if the environment is cyclical, such that the A food source is plentiful, while B is not, and some time later, B is plentiful, A is not, and then some time later... etc. etc. In this case those organisms that use protected DNA are at a disadvantage - Those encoded to utilize A get wiped out when the environment goes to B. The organisms that use unprotected DNA, will still only reproduce at a 50% rate, but they will be able to do so no matter which food source is more plentiful.

When you say that evolving adaptability does not benefit the individual, you are right, if the food source is static. If it is not, then unprotected DNA may in fact benefit the individual, and therefore be inherited by its offspring.

 

[Drakkith]

1. In answer to the OP's point, I think one of the points that has to arrive is that, surely, the theory is actually 'survival of the generally fit' rather than the fittest.

That's right. "Fittest" shouldn't be taken as the extreme end of a fit to not-fit scale. It just refers to the fact that the more fit an organism is, the better chance it has of surviving and reproducing.

I mean, if mutation is random, as the OP proposal (which seems to make sense to me), this will give a range of characteristics, some of which may not be particularly beneficial at a given point in time. But as environments and predation changes those 'hidden' characteristics may manifest and all of a sudden within the generic mix of those individuals, those that 'had been' the fittest all of a sudden, possibly instantaneously, die out.

That's also right. That's why genetic diversity is so important. It preserves neutral traits which are potentially positive if the environment changes.

2. Trans-species jumps; if species can't interbreed (my understanding of what defines a 'species') then this means we cannot evolve 'from' another extant species that then carries on its own evolutionary path. What it means is that we can have long-gone ancestors in common with current day species, but one species evolving from another and then continuing to co-exist is excluded.

Not true. Some species last for millions of years with relatively few changes, and a population of this species could potentially be isolated from the parent population and evolve into its own separate species. This new species could then, at a later date, be reintroduced into the original environment and the two species would then coexist.

3. Rate of change of species; A common ancestor of ours to other primates (as far as I know) is the Miocene Proconsul (https://www2.palomar.edu/anthro/earlyprimates/early_2.htm) which is said to have lived from 21 to 14 million years ago. But if it took 7 million years to become a new species then why is that an unrepresentative timescale for the 14 million years since then? I mean, surely there are more than two evolutionary 'species' steps from proconsul ape to us?

It doesn't take 7 million years to form a new species. This can happen in as little as a couple hundred thousand years. This new species would still be very similar to the original species, as even a few hundred-thousand years isn't long enough for drastic changes, but it would still be a new species. For bacteria, new species can happen very, very quickly. Just a few years even. Does that answer your question?

 

[Mark Harder]

...you should use patterns in that area that make mistakes in copying the DNA more likely, like a sequence of repeating letters(CACACACACA...).

It's true that there are a lot of repeating sequences, sometimes known - erroneously or not - as 'junk' DNA and presumably mutations in such sequences would be silent. Assuming, that is, the mutated sequence truly has no sequence-sensitive function. Last I heard, this question has not been answered in the general case and we should be cautious, since absence of evidence is not evidence of absence. Perhaps we are just talking about our own ignorance when we call some DNA sequences 'junk'.

I believe that your observation that life may have evolved mechanisms that make evolution easier has at least one positive answer, namely that there are redundancies in some gene sequences. Some genes are replicated, or at least their products can exist with slight variations in structure and function. That means that unfavorable or neutral mutations, which are more common than favorable ones, will not necessarily kill their host organism if they affect only one of the redundant forms. In this way, nature has granted some space in which mutations can experiment without fatal consequences.

I also wonder just what you mean by 'random'. Often people use that word assuming that the random events are independent of each other - that one event doesn't affect the probability that any other event will happen. I believe that the probabilities that certain lines of evolution will be followed are most certainly not independent of earlier events. Probabilities of events at the genomic level - single nucleotide mutations for example - are independent of each other. But I don't believe that phenotypic changes are independent of each other. Crudely speaking, which is more likely to evolve fingernails, a cephalopod like an octopus, or a clawed animal?

Species evolve inside valleys in the sequence 'phase space' into which they were led by previous phenotypic changes, not on the flat plains where every direction is equally adaptive. Which raises the question, "Are some valleys blind canyons from which a species must devolve before it finds another path?" If so, such a species may find itself trapped when externalities, like the climate, change and make their phenotype newly maladaptive and ways out even more so. Some species, eg. Homo Sapiens, are more adaptive than others and are well suited for surviving such an event. But there are limits. If the environment changes too rapidly, even the most adaptable species may find itself trapped in an evolutionary dead end.

 

[confusedhome]

There are many external effects which introduce randomness in any process, including evolution.
Cosmic rays and natural background (including our own internal) radiations tend to shake up the mix so to speak, preventing broken DNA chains from recombining properly and happens more often than many pay attention to.
These types of interactions affect all forms in the Universe.

 

[Mark Harder]

Population A has a mutation that reduces its ability to adapt to changes in its environment, while population B doesn't have that mutation. Over time, population B out competes population A and becomes the dominant, if not sole, population.

Reference___

I have no issue with your statement as far as it goes; but we must remember that mutations often result in a trade-off. Population A may be resistant to an antibiotic, for instance; but that mutation might also slow the growth and reproduction of A or cause it to use up more energy in order to neutralize the antibiotic. In the wild, population B would ordinarily have the adaptive advantage over A. However, the presence of the antibiotic may be invariably fatal to B, leaving the slow-poke A as the successful reproducer in such an environment. Later, it may find ways to speed its growth, but it has to survive the antibiotic onslaught first.

If this sounds like an improbable combination of events, and it may very well be such in nature, it's a technique that was very commonly used in laboratories to choose clones of mutant bacteria that would ordinarily be out-competed by the wild type lines. Penicillin is an antibiotic that kills cells that are actively dividing by inhibiting an enzyme responsible for knitting together expanding cell walls. In order to divide, some bacteria must break bonds in the cell wall before adding to it while the cell grows in size. When penicillin stops the growth enzyme, clipping still takes place. Consequently, affected cells rupture without an intact cell wall. But cells that contain a desirable mutation that ordinarily stops their growth are commonly resistant to penicillin because the wall-clipping mechanism is not needed and ceases operating. After allowing the wild-types to die, the remaining cells are rescued by changing the growth conditions (eg. changing temperature or adding to the culture a nutrient that the mutants can't make for themselves). (Of course, some healthy cells might evolve a mechanism that inhibits the action of penicillin, as often happens in nature or inside us when we don't handle our treatment correctly. But these can be weeded out of the surviving population. How?)

 

[cmb]

Does that answer your question?

Not exactly. I was just posing 'the sorts of questions' which I don't think Darwin's theory addresses, and asking if there are new theories in science that augment it?

We can all throw in our thoughts and new hypotheses, but this site only deals with mainstream, written material. It is not for the likes of you and I to add our theoretical opinions here.

 

[Drakkith]

We can all throw in our thoughts and new hypotheses, but this site only deals with mainstream, written material. It is not for the likes of you and I to add our theoretical opinions here.

Those weren't 'theoretical opinions', they were examples of how evolution really works. If you're looking for a single reference that explains all of this I'm afraid I don't have it, as my knowledge has been gained over several years and many different sources, both online and offline.

I was just posing 'the sorts of questions' which I don't think Darwin's theory addresses, and asking if there are new theories in science that augment it?

Yes, there has been a great deal of advancement in our understanding of evolution since Darwin's time. Some of the main developments have been the 'modern synthesis' of the 1920's-1930's, the rise of molecular biology, and the creation of evolutionary development biology (evo-devo). Recently a further synthesis has been suggested in order to account for non-genetic inheritance modes.

Most advancements don't come packaged as their own theories. They tend to get incorporated into existing theories unless they clearly fall outside all existing theories. Once enough of these latter advances have been made, they are then commonly incorporated into their own 'master' theory. So in the middle-late of the 20th century, the advancements made in what we now call evolutionary development biology probably didn't really fit into any existing theories at the time. It was only once a large body of knowledge in this area was developed that it got its own proper theory that was then incorporated into modern evolutionary theory.

 

[cmb]

Those weren't 'theoretical opinions', they were examples of how evolution really works.

They have to be citeable examples, for the purpose of the forum's rules (which seem quite flexible/inflexible depending on who is saying what, it seems?).

Can you give me a cited example of a species which has become isolated from its evolutionary lineage, and two species co-exist, one evolved from the other?

I am sure you are right, but the point is that you might also be wrong. If it can be either it is just a speculation.

I was hoping to see 'Theory X covers that stuff' and 'Theory Y covers that stuff'.

 

[DavidSnider]

I was hoping to see 'Theory X covers that stuff' and 'Theory Y covers that stuff'.

I think all of the questions you had in post #12 are covered is one way or another in Richard Dawkins "The Greatest Show on Earth: The Evidence for Evolution".

 

[Drakkith]

They have to be citeable examples, for the purpose of the forum's rules (which seem quite flexible/inflexible depending on who is saying what, it seems?).

Can you give me a cited example of a species which has become isolated from its evolutionary lineage, and two species co-exist, one evolved from the other?

I am sure you are right, but the point is that you might also be wrong. If it can be either it is just a speculation.

I'm not giving my personal opinion or speculation. I'm giving you the generally accepted principles of evolution as I understand them. I could be wrong, but it's not because I'm speculating. An additional problem is that evolution happens over very long timescales and we can't be certain if two closely related species both split off from a now extinct ancestor species, or if one of them split off from the other. So you're wanting something that is extremely difficult, if not impossible, to provide. We may in fact have evidence of such a split, but if so, I don't know about it.

The best I can do is to suggest further reading into the subject, as I'm afraid I don't have a specific reference for you at this time.

I was hoping to see 'Theory X covers that stuff' and 'Theory Y covers that stuff'.

Unfortunately things aren't really classified like that in biology. I mean, they are all already under 'large' or 'master' theories like the Theory of Evolution, but they don't always have sub-theories that they fall under. Mostly because these other theories already cover most of the general rules and principles that evolution follows.

In any case, this is just a matter of classification. An immense number of papers get published every year adding to our body of knowledge of evolution, and there is no need to invent new theories for each one when they already fit within the theory of evolution as a whole. We can get by just fine by calling many of these 'principles' and adding them to the theory. This last part is important. We don't have to constantly create new theories when modifying one works just as well, if not better. The scientific theory of evolution has been added to and refined by 150 years of work. There was never a need to stop adding to it and start a new theory.

Also, instead of asking about which theory covers what, perhaps you're looking for different fields of research involved in evolution, of which evo-devo is one example.

 

[metastable]

Recently I've been thinking a lot about evolution. Its really fascinating. The random exploration of the life "phase space" through mutations and settling on regions that provide the most adaptive traits for the current environment through natural selection.

But what does this "randomness" really mean? and how random is "random"?

Considering the process of "sexual selection," and by sexual selection I mean -- "natural selection arising through preference by one sex for certain characteristics in individuals of the other sex" -- can we really say that natural selection is "random?"

 

[Ophiolite]

Considering the process of "sexual selection," and by sexual selection I mean -- "natural selection arising through preference by one sex for certain characteristics in individuals of the other sex" -- can we really say that natural selection is "random?"

I don't understand your question. No biologist considers natural selection to be random. That's the whole point. Was that the point you were trying to make?

 

[Ygggdrasil]

A few notes:

But that doesn't address all the issues and I am confident that other people have augmented that basic theory with 'add-ons' and really I don't know what they are. Can biologists here tell us what those are?

As noted, while evolutionary theory certainly originated with Darwin, you are correct that his thoughts on evolution are quite old (they pre-date knowledge of genes and genetics, which are crucial to our modern understanding of evolution). If modern evolutionary theory has a name, it would be generally referred to as the "modern synthesis," referring to a theory that synthesizes Darwin's model of natural selection with our modern understanding of genetics and molecular biology. A brief description of the modern synthesis can be found here: http://www.talkorigins.org/faqs/modern-synthesis.html

1. In answer to the OP's point, I think one of the points that has to arrive is that, surely, the theory is actually 'survival of the generally fit' rather than the fittest. I mean, if mutation is random, as the OP proposal (which seems to make sense to me), this will give a range of characteristics, some of which may not be particularly beneficial at a given point in time. But as environments and predation changes those 'hidden' characteristics may manifest and all of a sudden within the generic mix of those individuals, those that 'had been' the fittest all of a sudden, possibly instantaneously, die out. For example, say a species living in an arid area has some of its individuals 'uselessly' born with webbed feet but it doesn't disadvantage them too much and it just happens to be a characteristic, some have more webbed feet than others. The fastest runners don't have webbed feet and so do a bit better and slowly the population are moving towards 'no webbed feet', but still it is not such a disadvantage that those individuals die out. ... and then their habitat floods ...! So I think the substance of this is not merely 'the fittest' and 'survival' but actually if a species can successfully maintain the widest set of random characteristics then it is more likely to survive. As such, this is not survival of the fittest individuals, this is survival of the species with the widest set of tolerances to environmental changes. I am sure this has been proposed by evolutionary biologists and already has a name, which would address the OPs question.

It is important to remember that the fitness of an organism is a function of its environment. An organism that is the most fit in one environment is not necessarily the most fit in a different environment. Sometime, specialization to gain fitness advantages in one particular environment may cause fitness disadvantages in a different environment (e.g. the example of the cost of antibiotic resistance genes in an antibiotic free environment which was mentioned earlier). These trade offs between fitness and "robustness" or "evolvability" (i.e. ability to withstand environmental change) have been experimentally observed in laboratory models of evolution, for example in the following studies:

Stiffler, Hekstra and Ranganathan (2015) Evolvability as a Function of Purifying Selection in TEM-1 β-Lactamase. Cell 160:882 2015 https://www.sciencedirect.com/science/article/pii/S0092867415000781?via=ihub

Johnson et al. (2019) Higher fitness yeast genotypes are less robust to deleterious mutations. bioRxiv. https://www.biorxiv.org/content/10.1101/675314v1

3. Rate of change of species; A common ancestor of ours to other primates (as far as I know) is the Miocene Proconsul (https://www2.palomar.edu/anthro/earlyprimates/early_2.htm) which is said to have lived from 21 to 14 million years ago. But if it took 7 million years to become a new species then why is that an unrepresentative timescale for the 14 million years since then? I mean, surely there are more than two evolutionary 'species' steps from proconsul ape to us? Maybe not? I don't know? What do updated evolutionary theories say about this? I mean, taking that thought further, if we look at the first 'modern humans' 250,000 years ago, if one was here today they could integrate into society, we'd be able to have offspring with them and (presumably with training!) talk together. Yet that is 'only' 1/40th or so between proconsul ape and us, and it looks to me like there are going to be more than 40 times the number of differences between early homo sapiens and proconsul ape? Again are there any modern theories to explain what would initially appear to be, presumably, sudden accelerations in changes of species?

The rate of evolution is definitely not linear and there are periods (especially those associated with widespread environmental changes) that are associated with much higher rates of speciation (e.g. the Cambrian explosion). This relates to the previous point about the role of environment in determining fitness. Changes to the environment will alter the relative fitness of the populations in an ecosystem, precipitating changes in the populations in that environment. The idea that evolutionary change can happen in intense bursts of change followed by relative periods of stability is known as punctuated equilibrium (https://en.wikipedia.org/wiki/Punctuated_equilibrium). The extent to which "evolution by jerks" (punctuated equilibrium) vs "evolution by creeps" (gradualism) describes most evolutionary change is a subject of debate in the field.

 

[FactChecker]

So basically, life not only has evolved adaptive traits for species in their environments, but it has also evolved the process of evolution itself in a way that makes constructive mutations more likely, by making sure that important areas of DNA are more likely to be mutated.

How would the DNA know which parts to protect and which should it should allow to be changed for the better? IMHO, duplication would just slow down the process of evolution -- both for good changes and for bad changes. That might be a great weakness compared to organisms that evolve more rapidly for the better. I think that evolution would eliminate this weakness.

 

[Mary Conrads Sanburn]

Excerpt from the National Science Foundation:

Human Evolution's Winding Path

“Tim White is a world renowned paleoanthropologist and professor of Integrative Biology at the University of California at Berkeley. His work frequently takes him to study sites in Afar, Ethiopia, Jordan, Kenya, Malawi, Tanzania (at Olduvai Gorge and Laetoli) and Turkey. His primary research involves human evolution in all its dimensions and he and his colleagues are credited with the discovery in Ethiopia in 1995 of perhaps the oldest known human ancestor, Ardipithecus ramidus, dated to 4.4 million years ago. The National Science Foundation supports his work on a Middle Awash research project in Ethiopia.”

https://www.nsf.gov/news/special_reports/darwin/textonly/anthro_essay2.jsp

 

[Ophiolite]

Excerpt from the National Science Foundation:

Human Evolution's Winding Path

“Tim White is a world renowned paleoanthropologist and professor of Integrative Biology at the University of California at Berkeley. His work frequently takes him to study sites in Afar, Ethiopia, Jordan, Kenya, Malawi, Tanzania (at Olduvai Gorge and Laetoli) and Turkey. His primary research involves human evolution in all its dimensions and he and his colleagues are credited with the discovery in Ethiopia in 1995 of perhaps the oldest known human ancestor, Ardipithecus ramidus, dated to 4.4 million years ago. The National Science Foundation supports his work on a Middle Awash research project in Ethiopia.”

https://www.nsf.gov/news/special_reports/darwin/textonly/anthro_essay2.jsp

Would you elaborate on how this article is relevant to the specific questions the OP has? It's not clear to me.

 

[Mary Conrads Sanburn]

Excerpt from article Science Direct

HighlightsRandomness effects in the evolution of tag-based cooperation were studied.
•
An agent-based evolutionary model with memory, heritable traits, and asexual reproduction was employed.
•
Competition between dominant cooperating strategies (ethnocentrism and altruism) was analyzed.
•
Stochastically established indiscriminate altruism can permanently outweigh ethnocentrism.
•
Randomness plays an important role in promoting non-ethnocentric cooperation.

https://www.sciencedirect.com/science/article/abs/pii/S0376635715000042?via=ihub

 

[Ophiolite]

Excerpt from article Science Direct

HighlightsRandomness effects in the evolution of tag-based cooperation were studied.
•
An agent-based evolutionary model with memory, heritable traits, and asexual reproduction was employed.
•
Competition between dominant cooperating strategies (ethnocentrism and altruism) was analyzed.
•
Stochastically established indiscriminate altruism can permanently outweigh ethnocentrism.
•
Randomness plays an important role in promoting non-ethnocentric cooperation.

https://www.sciencedirect.com/science/article/abs/pii/S0376635715000042?via=ihub

Well, those are certainly relevant, however none of them appear in your original linked item which is not from Science Direct, but from the National Science Foundation.

 

[fresh_42]

Please stay on topic and consider the references. Just because a publisher has scientific textbooks in their portfolio doesn't mean that any publication is peer reviewed. A discussion about the seriousity of a publisher is not necessary and misleading. Individual journals count, not the company.

 

[BillTre]

IMHO, duplication would just slow down the process of evolution -- both for good changes and for bad changes. That might be a great weakness compared to organisms that evolve more rapidly for the better. I think that evolution would eliminate this weakness.

Gene duplications, and on a larger scale, genome duplications in particular have provided important material (usefully structured sequences) for evolution to modify and use. As a result, they let evolution happen faster in many cases.

Whole genome duplications have occurred several times, in several lineages during evolution.
In the evolutionary lineage leading to use (humans (and related animals)), two obvious whole genome duplications have occurred, after the branch point between the amphioxus (kind of like a fish without a head (its head is actually there, just not very distinctive from neighboring axial body regions)) and more familiar vertebrate animals (like fish, amphibians, reptiles, mammals, primates, humans).

Complex sets of genes (Hox gene clusters), that have been identified (by sequence) and seem appear to be obviously the result of whole genome duplications.
There clusters of genes contain several genes with several properties that vary colinearly with their position in the overall cluster.

• body areas (along the anterior-posterior body axis) are effected by mutations at colinear positions within the cluster
• genes are expressed in different anterior-posterior locations in the body
• Transcription usually (but not always) goes in the same direction along the DNA

The gene clusters, clearly show a history, in the vertebrate evolutionary lineage, of two genome doublings, followed by the different genes and clusters of genes taking on different regulator functions (often more anatomically refinded within the embryo)

About 20 years ago, NeoFunctionalization and SubFunctionalization was proposed to explain why genome duplications and single gene duplications could be useful in evolution, briefly:
All genes duplicated:

• lots of extra new copies of all genes
• Continued selection for the traditional gene function (of the original parental gene, in the unduplicated genome) should maintain one copy of the gene.
• The other copy is available for evolutionary tinkering (without strong selection to preserve its original function or prevent its elimination). This copy would be under no selective pressure to not change and variation could arise.
• If the modified version of the gene develops some function that is distinct and useful, it could be selected for and be maintained (over the generations). In development (where Hox genes work), this can involve things like: some sequence change, expression in different (perhaps subsets of) anatomical locations or at different times.

 

[mswzebo]

cmb - interesting thoughts. Some of this is actually far more fascinating than you are tempted to imagine.

First, the sequences like CAGCAGCAGCAG (simple, repetitive sequences) are in fact more likely to mutate. This is because of two processes called replication slippage and strand mismatch crossover which occur during DNA replication. However, these sequences are almost always found in regions that are transcriptionally silent - the DNA is never made into RNA, and there aren't any observed consequences of the mutations - so they don't contribute to changes in fitness. Perhaps these higher mutation rates are tolerated evolutionarily because there aren't any consequences so there is no pressure to fix it (at least in plants and animals, with huge genomes most of which are transcriptionally silent; bacteria don't have these repetitive sequences because their genomes need to be replicated rapidly so there is selective pressure to get rid of nonfunctional regions).

TOTAL ASIDE NUMBER ONE: sometimes they do matter - in fact- there is a whole set of diseases that are called trinucleotide repeat disorders. These include Huntington's and Fragile X syndrome. Here, the changes that occur are increases in the number of repeats...which increases the likelihood that offspring will have even more repeats...and the more repeats you have the more likely your cells are to methylate and transcriptionally silence the gene...which is ultimately the cause of the diseases.

BACK TO OP/OR MAYBE TOTAL ASIDE NUMBER TWO: Mutations are generally thought to happen at random - ie the probability of a mutation happening is independent of the effect on fitness. However, in 1988 John Cairns published a paper saying sometimes this wasn't true, at least in E. coli. There is an interesting, but rare, set of subcases where certain mutations will happen at higher rates in genes that have stopped working normally. Here is a review paper of this very cool phenomenon:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2747772/
From the review:

"In a stimulating but controversial paper published in 1988, Cairns et al. (1988) described experiments suggesting that a population under selection had access to a process that could direct mutagenic change to the very genes that would relieve the selective pressure. Such a process, of course, would be a great boon to adaptive evolution (Fitch, 1982). After nearly 20 years of research, evidence now suggests that various types of stresses induce responses that have mutagenic consequences, and that sometimes this essentially random process can appear to be directed. Originally it was also thought that there was just one mechanism for all cases of adaptive mutation. This idea also proved to be wrong–it seems there are many mechanisms by which genetic change can be produced when organisms are under stress.

This review concentrates on stress-induced mutagenesis in Escherichia coli and related bacteria with a few examples from other organisms."

But, the phenomenon is simply not widespread enough to claim that it is a major force in evolution, which does in fact seem to be random and undirected.

OK, but TOTAL ASIDE NUMBER TWO OR THREE: Sometimes the creation of a new species happens instantaneously. This happens ALL THE TIME in plants, and is thought to be the case for something like half of extant flowering plants. The mechanisms have to do with polyploidy and hybridization. The classic example was Hugo de Vries, who found an evening primrose in his greenhouse that was bigger and more vigorous than the other evening primrose he had...and ultimately he figured out that it had twice as many chromosomes as the other plants and couldn't interbreed with them, but was self-fertile. Voila! Anew species in 1 generation. Check out autopolyplody and allopolyploidy as search terms for other examples.

OK BUT THE FLIPPIN COOL THING IS THAT THERE ARE HUMAN EXAMPLES TOO! Via an unrelated chromosome change mechanism (Robertsonian translocation) there can be instantaneous human speciation and there is actually an example of it having happened within the last ten years. Link to paper is here:
http://www.alliedacademies.org/arti...ans-involving-robertsoniantranslocations.html
Ok, sorry about all the allcaps but cool stuff.

 

[Drakkith]

OK BUT THE FLIPPIN COOL THING IS THAT THERE ARE HUMAN EXAMPLES TOO! Via an unrelated chromosome change mechanism (Robertsonian translocation) there can be instantaneous human speciation and there is actually an example of it having happened within the last ten years. Link to paper is here:

From the paper:

Although a Robertsonian translocation carrier has a full genetic complement, their fitness is reduced due to high probability of genetically imbalanced gametes. However, this type of translocation can provide material for human evolution. Long term isolation of a group of individuals who are homozygous for a particular Robertsonian translocation chromosome could theoretically lead to the establishment of a new human subspecies having a full genetic complement in 44 chromosomes.

So there's not really an instantaneous speciation event in humans. It would take the isolation of a population with this type of translocation to create a new species/sub-species.