One common objection to the theory of evolution claims that the theory is self contradictory. It says that it is impossible for complex features such as wings, eyes etc to evolve because they will require a series of mutations that do not individually confer any evolutionary advantage. Since they do not have any evolutionary advantage, they cannot spread in the population. Therefore the chance of these mutations appearing in series is almost as small as these mutations appearing simultaneously. The chance of these mutations appearing simultaneously is, of course, astronomically small.
The usual counterargument says that just one mutation is usually enough to create a functional prototype of a complex feature/organ (MVP, if you please). A series of mutations is not required.
This study provides yet another example backing this counterargument. One single mutation can change an unicellular entity and make it behave like a multi cellular organism. Intuitively, one would think this would take many mutations. However, intuition is wrong in this case, and in many others.
I'm a math biology (in other words, I use math to model biology problems) student, and not an evolution nay-sayer, and...the scientific work isn't at all about showing how the amazingly (I'm a student, I learn to respect my opponent) complex phenomena underlying the emergence of organs can be neatly associated with single events.
In particular, this article was of interest to me simply because of how grand a claim it makes.
In general, grand claims are something to approach with skepticism, because of laws of probability number 35, which states that: "few complex non-linear phenomena have a beautifully simple explanation, and if a grand claim purports to be such an explanation, then it most likely is not such an explanation".
It is worth reading law 36 of probability as well: "the maker of a grand claim is more likely to be a 'journalist' or a PR department person, than a scientist".
How do the laws of probability hold up? Pretty darn well, I'd say.
Here's the abstract (by the way, eLife IS an open source journal, so the journalist had no excuse here):
> To form and maintain organized tissues, multicellular organisms orient their mitotic spindles relative to neighboring cells. A molecular complex scaffolded by the GK protein-interaction domain (GKPID) mediates spindle orientation in diverse animal taxa by linking microtubule motor proteins to a marker protein on the cell cortex localized by external cues. Here we illuminate how this complex evolved and commandeered control of spindle orientation from a more ancient mechanism. The complex was assembled through a series of molecular exploitation events, one of which – the evolution of GKPID’s capacity to bind the cortical marker protein – can be recapitulated by reintroducing a single historical substitution into the reconstructed ancestral GKPID. This change revealed and repurposed an ancient molecular surface that previously had a radically different function. We show how the physical simplicity of this binding interface enabled the evolution of a new protein function now essential to the biological complexity of many animals.
Key takeaways:
1) "A molecular complex scaffolded by the GK protein-interaction domain (GKPID) mediates spindle orientation in diverse animal taxa by linking microtubule motor proteins to a marker protein on the cell cortex localized by external cues"
Explanation: in this sentence, the scientists are carefully pointing out where the 'thing' (a protein domain) they are going to make a claim about fits into the biological picture. No, there isn't one superhero -- there's a carefully choreographed concert that their 'thing' is a part of.
2) "we illuminate how this complex evolved and commandeered control of spindle orientation from a more ancient mechanism"
Very cool. Simple statement. Interesting, but no grand claim.
3) "The complex was assembled through a series of molecular exploitation events, one of which – the evolution of GKPID’s capacity to bind the cortical marker protein – can be recapitulated by reintroducing a single historical substitution into the reconstructed ancestral GKPID."
Again, they reiterate how there was actually a bunch of things happening ("a series of molecular exploitation events"), ONE of which is the cool one they want to talk about.
4) "This change revealed and repurposed an ancient molecular surface that previously had a radically different function."
If you were wondering what's cool, this is what's cool.
5) In conclusion: "We show how the physical simplicity of this binding interface enabled the evolution of a new protein function now essential to the biological complexity of many animals."
Hmm...no grand claim finishing claim made regarding how this ONE thing changed EVERYTHING. Again, we are reminded of the whole picture: "so yeah guys, here's how this protein function, which is essential (because it's part of a super complex dance number) for so many living things, probably came about".
I'm going to go commission a gold filigree copy of the laws of probability.
Indeed, the old local maxima problem. Why doesn't evolution get stuck in local maxima; what pushes it out of those valleys and into the mountains? Why have all our evolution simulations gotten stuck?
Luckily machine learning came along and has shown empirically that the solution is to increase the number of dimensions. Our tiny neural nets of the 90s also got stuck in local maxima. But when we could finally make huge and deep networks, the problem more or less disappeared.
I believe this is the real solution to the local maxima problem in evolution. Real evolution works with a massive number of parameters, which means exploration of the problem space doesn't get stuck in local maxima, just as it doesn't in Deep Learning. When the number of tweakable parameters outstrips the dimensionality of the problem space then there is always some angle pointing up out of the valleys.
This is a different, and I think more general way of expressing the typical counterargument which you explained. "There is always some angle pointing up" is a more general way of saying "just one mutation is usually enough to create a functional prototype".
it is impossible for complex features such as wings, eyes etc to evolve because they will require a series of mutations that do not individually confer any evolutionary advantage
The answer to this proposition is that the fact we aren't aware of the evolutionary advantages which were obtained en route doesn't mean there weren't any.
The feathered wing is very complex and it won't fly until it has fully evolved, for example -- but as we learned quite recently, feathers evolved (and were an evolutionary advantage) because dinosaurs needed to stay warm. Birds can fly because a feather which is efficient at capturing air and keeping a giant lizard warm also turns out to be very efficient at pushing air and keeping a proto-avian aloft.
> do not individually confer any evolutionary advantage
Genes which do not confer any advantage are just as likely to spread as ones that do. Evolution doesn't select for advantages, it selects against disadvantages. Evolution is just an emergent property of death.
>Since they do not have any evolutionary advantage, they cannot spread in the population
This is not true, the question isn't whether neutral changes can spread, but simply what percentage of molecular changes that spread are neutral. In fact I think that molecular evidence has shown pretty convincingly that on the genome scale most changes are neutral, vindicating the Neutral theory of evolution:
> It says that it is impossible for complex features such as wings, eyes etc to evolve because they will require a series of mutations that do not individually confer any evolutionary advantage.
This is just false. Evolutionary theory requires no such thing and there's plenty evidence that each step towards the evolution of things like the eye provides marginal advantage to the organism even though it's not fully an eye.
Speaking of the evolution of the eye, recently I began reading the book The Vital Question (Nick Lane), and incidentally, last night I closed my reading on a discussion on that exact topic.
Allow me to quote [topic: 'The missing steps to complexity', page-45]:
"In The Origin of Species Darwin made the point that that natural selection actually predicts that intermediates should be lost. In that context, it is not terribly surprising that there are no surviving intermediates between bacteria and eukaryotes [e.g. plants, humans]. What is more surprising, though, is that the same traits do not keep on
arising, time and time again -- like eyes.
We do not see the historical steps in the evolution of eyes, but we do see an ecological spectrum. From a rudimentary light-sensitive spot on some early worm-like creature, eyes have arisen independently on scores of occasions. That is exactly what natural selection predicts. Each small step offers a small advantage in one particular environment, with
the precise advantage depending on the precise environment.
Morphologically distinct types of eye evolve in different environments, as divergent as the compound eyes of flies and mirror eyes of scallops,or as convergent as the camera eyes that are so similar in humans and octopuses. Every conceivable intermediate from pinholes to accommodating
lenses, is found in one species or another. We even see miniature eyes, replete with a 'lens' and a 'retina', in some single-celled protists [e.g. amoeba]."
One common counterargument I ever head when talking to evolutionists is that some mutations are linked to others, so a mutation can spread through the population even though it does not confer any evolutionary advantage because it genetically linked to another evolution somewhere else that indeed confer advantage.
What do you think of it? Is it serious enough? Because I think there is an obvious flaw in it, the question: why are these mutations linked?
But why would a single mutation immediately disappear? Isn't it possible that several generations carried on without significant advantage or disadvantage, experiencing series of mutations until the last one provided the true advantage? (I would love to know if this is completely wrong)
The usual counterargument says that just one mutation is usually enough to create a functional prototype of a complex feature/organ (MVP, if you please). A series of mutations is not required.
If this seriously _had_ happened all on its own (apparently it didn't) then I'd be thinking the exact opposite -- this would tend to make me re-consider intelligent design.
the article over generalizes the find to be basically bereft of real information.
"Instead of working as enzymes (proteins that facilitate reactions inside the cell) the proteins were now what’s known as an interaction domain. They could communicate with and bind to other proteins, a useful skill for cells that have decided to trade the rugged individualist life for the collaboration of a group"
Enzymes switch between being enzymes and interaction domians across all taxa everywhere in the tree of life, so this is not the "money shot". Moreover, unicellular life do plenty of intracellular, collaborative communication (e.g. quorum sensing).
Reading the paper, the specific switch enabled the orientation of cell division to be communicated from one cell to another. This is interesting because this communication is not over an anisotropic chemical gradient, but encodes directional and spatial information.
This is the closest that article gets to an "explanation":
> A single mutation that repurposed a certain type of protein. Instead of working as enzymes (proteins that facilitate reactions inside the cell) the proteins were now what’s known as an interaction domain. They could communicate with and bind to other proteins, a useful skill for cells that have decided to trade the rugged individualist life for the collaboration of a group.
Which is total gibberish. Yet unsurprisingly the abstract to the actual paper (helpfully linked in the wapo article: http://elifesciences.org/content/5/e10147) is gibberish to me for different reasons.
Is anyone expert enough to attempt a "for technical dummies" reading?
I'll have a go. Disclaimer: I'm not a biologist; corrections welcome.
Consider a growing multicellular organism. It grows by a process of cell division. Each division turns one cell into two adjacent cells. The structure it ends up with will depend on the orientation of those dividing cells (you'll tend to get growth "along the axis of division", so to speak).
A wide variety of multicellular organisms have a mechanism that orients cells according to features on the outside of neighbouring cells. (It "mediates spindle orientation in diverse animal taxa by linking microtubule motor proteins to a marker protein on the cell cortex localized by external cues", as the abstract puts it. The "mitotic spindle" is a structure involved in cell division, also called mitosis. It's mostly made out of long thin things called microtubules, and its job is to separate the chromosomes for the two new cells, which it does using "motor proteins". The cell cortex is the inner surface of the boundary of the cell.)
One part of this process is the way in which a protein involved in the mitotic spindle attaches itself to that thing on the cell cortex. The relevant bit of that protein is called the "guanylate kinase protein interaction domain" or GK_PID for short. A protein interaction domain is a bit of protein that interacts with other things; multiple different proteins can contain instances of the same interaction domain, just as multiple different programs can contain (say) the same code for computing SHA-256 checksums.
The paper reports evidence that a single mutation enabled the GK_PID to attach itself to the marker on the cell cortex. ("The complex was assembled through a series of molecular exploitation events, one of which – the evolution of GK_PID’s capacity to bind the cortical marker protein – can be recapitulated by reintroducing a single historical substitution into the reconstructed ancestral GK_PID."
So. This doesn't say that multicellularity was enabled by a single mutation. It says that one small but important part of a process that's necessary for complex multicellular organisms was enabled by a single mutation. Still pretty cool, but the journalistic science->hype conversion machine is clearly operating as usual here.
As another comment noted, some of the participants in this thread about the interesting article kindly submitted here appear to be unaware of the factual basis for evolutionary theory. For anyone who wonders how we know that the earth is much more than 600 million years old, or how we know that current living things descended from a common ancestor, more or less remote depending on how closely related the current living things are, see 29+ Evidences for Macroevolution: The Scientific Case for Common Descent,[1] which is a very informative and interesting website with a lot of information about biological facts and geological facts that have been discovered since you and I graduated from high school.
How does it impact the probability of extraterrestrial life? I mean, after 4 billion years of relative peace, Earth still had only single-celled organisms. And it would have stayed that way, if not for this particular mutation. So it is not just how many planets can support life. First, it will need to continuously keep supporting life for billions of years before any form of intelligent life can emerge. THEN it has to wait till such a pathbreaking mutation occurs, which might take a random amount of time. I am starting to gravitate towards the lower bound of what the Drake equation estimates to be the number of planets with intelligent life. (= we are probably alone in the universe)
Is there another way than a mutation, propagation to an offspring(s), survival and successful reproduction of these, then over-reproducing others due to this adaptation (or by a pure chance) etc?
I thought multicellularity on Earth evolved independently around 50 times? So it does kind of make sense that it would be the result of something as simple as a single SNP that changes a function of a protein from whatever to binding to proteins of external organisms. Perhaps more complex mechanisms (multiple mutations) wouldn't have the likelyhood of occuring so many times
Obviously important to understand actual modern problems like cancer, but in a broad sense this is just the beginning of coming to a complete picture of the origin of metazoa. This was a single mutation that ends up in all animals, but perhaps other mechanisms were also involved in making the mutation survive and win.
The scientific article makes a far from convincing case for the purported importance of this mutation. The journal its published in (eLife) is not exactly known for high-quality comparative genomics / molecular evolution work either. The Washington Post article is misleading at best. Hyperbole.
The Cambrian Explosion has been known for quite some time. This is a theory of HOW the Cambrian Explosion happened. One single mutation. Interesting ideas for sure!
insights into life at that time rely on researchers’ imaginations
Where is this 600M years taken from? big claims based on assumptions, I don't like this kind of science, building on too many assumptions and you are going too far from the truth and this is the opposite of what science tries to achieve.
Since the researcher was reconstructing the evolution of a protein I would say the date was determined using a technique called the molecular clock: https://en.wikipedia.org/wiki/Molecular_clock
That and the rise of multi-cellular life marks the beginning of the Cambrian explosion (542M years ago). That gives 60M years for the mutation to spread and specialize.
Are you folks aware that 1000 years is already a very long time? Any number bigger than, say 100.000 years is just the same as infinity, regarding to time.
This "infinity" problem simply requires too much faith, and will never have real evidence. Not very good attributes for a credible theory.
Maybe it's about time to get a better one, with less time involved? This way the faith required would be at a real human reachable level.
> Any number bigger than, say 100.000 years is just the same as infinity, regarding to time.
Tell that to a geologist or an astrophysicist and you'll be laughed out of the room. There's plenty of evidence of timescales in the millions and billions of years.
[+] [-] steinsgate|10 years ago|reply
The usual counterargument says that just one mutation is usually enough to create a functional prototype of a complex feature/organ (MVP, if you please). A series of mutations is not required.
This study provides yet another example backing this counterargument. One single mutation can change an unicellular entity and make it behave like a multi cellular organism. Intuitively, one would think this would take many mutations. However, intuition is wrong in this case, and in many others.
[+] [-] bmer|10 years ago|reply
In particular, this article was of interest to me simply because of how grand a claim it makes.
In general, grand claims are something to approach with skepticism, because of laws of probability number 35, which states that: "few complex non-linear phenomena have a beautifully simple explanation, and if a grand claim purports to be such an explanation, then it most likely is not such an explanation".
It is worth reading law 36 of probability as well: "the maker of a grand claim is more likely to be a 'journalist' or a PR department person, than a scientist".
How do the laws of probability hold up? Pretty darn well, I'd say.
Here's the abstract (by the way, eLife IS an open source journal, so the journalist had no excuse here):
> To form and maintain organized tissues, multicellular organisms orient their mitotic spindles relative to neighboring cells. A molecular complex scaffolded by the GK protein-interaction domain (GKPID) mediates spindle orientation in diverse animal taxa by linking microtubule motor proteins to a marker protein on the cell cortex localized by external cues. Here we illuminate how this complex evolved and commandeered control of spindle orientation from a more ancient mechanism. The complex was assembled through a series of molecular exploitation events, one of which – the evolution of GKPID’s capacity to bind the cortical marker protein – can be recapitulated by reintroducing a single historical substitution into the reconstructed ancestral GKPID. This change revealed and repurposed an ancient molecular surface that previously had a radically different function. We show how the physical simplicity of this binding interface enabled the evolution of a new protein function now essential to the biological complexity of many animals.
Key takeaways:
1) "A molecular complex scaffolded by the GK protein-interaction domain (GKPID) mediates spindle orientation in diverse animal taxa by linking microtubule motor proteins to a marker protein on the cell cortex localized by external cues"
Explanation: in this sentence, the scientists are carefully pointing out where the 'thing' (a protein domain) they are going to make a claim about fits into the biological picture. No, there isn't one superhero -- there's a carefully choreographed concert that their 'thing' is a part of.
2) "we illuminate how this complex evolved and commandeered control of spindle orientation from a more ancient mechanism"
Very cool. Simple statement. Interesting, but no grand claim.
3) "The complex was assembled through a series of molecular exploitation events, one of which – the evolution of GKPID’s capacity to bind the cortical marker protein – can be recapitulated by reintroducing a single historical substitution into the reconstructed ancestral GKPID."
Again, they reiterate how there was actually a bunch of things happening ("a series of molecular exploitation events"), ONE of which is the cool one they want to talk about.
4) "This change revealed and repurposed an ancient molecular surface that previously had a radically different function."
If you were wondering what's cool, this is what's cool.
5) In conclusion: "We show how the physical simplicity of this binding interface enabled the evolution of a new protein function now essential to the biological complexity of many animals."
Hmm...no grand claim finishing claim made regarding how this ONE thing changed EVERYTHING. Again, we are reminded of the whole picture: "so yeah guys, here's how this protein function, which is essential (because it's part of a super complex dance number) for so many living things, probably came about".
I'm going to go commission a gold filigree copy of the laws of probability.
[+] [-] fpgaminer|10 years ago|reply
Luckily machine learning came along and has shown empirically that the solution is to increase the number of dimensions. Our tiny neural nets of the 90s also got stuck in local maxima. But when we could finally make huge and deep networks, the problem more or less disappeared.
I believe this is the real solution to the local maxima problem in evolution. Real evolution works with a massive number of parameters, which means exploration of the problem space doesn't get stuck in local maxima, just as it doesn't in Deep Learning. When the number of tweakable parameters outstrips the dimensionality of the problem space then there is always some angle pointing up out of the valleys.
This is a different, and I think more general way of expressing the typical counterargument which you explained. "There is always some angle pointing up" is a more general way of saying "just one mutation is usually enough to create a functional prototype".
[+] [-] cperciva|10 years ago|reply
The answer to this proposition is that the fact we aren't aware of the evolutionary advantages which were obtained en route doesn't mean there weren't any.
The feathered wing is very complex and it won't fly until it has fully evolved, for example -- but as we learned quite recently, feathers evolved (and were an evolutionary advantage) because dinosaurs needed to stay warm. Birds can fly because a feather which is efficient at capturing air and keeping a giant lizard warm also turns out to be very efficient at pushing air and keeping a proto-avian aloft.
[+] [-] aggie|10 years ago|reply
[+] [-] thescriptkiddie|10 years ago|reply
Genes which do not confer any advantage are just as likely to spread as ones that do. Evolution doesn't select for advantages, it selects against disadvantages. Evolution is just an emergent property of death.
[+] [-] epistasis|10 years ago|reply
This is not true, the question isn't whether neutral changes can spread, but simply what percentage of molecular changes that spread are neutral. In fact I think that molecular evidence has shown pretty convincingly that on the genome scale most changes are neutral, vindicating the Neutral theory of evolution:
https://en.wikipedia.org/wiki/Neutral_theory_of_molecular_ev...
[+] [-] x3n0ph3n3|10 years ago|reply
This is just false. Evolutionary theory requires no such thing and there's plenty evidence that each step towards the evolution of things like the eye provides marginal advantage to the organism even though it's not fully an eye.
[+] [-] kashyapc|10 years ago|reply
Allow me to quote [topic: 'The missing steps to complexity', page-45]:
"In The Origin of Species Darwin made the point that that natural selection actually predicts that intermediates should be lost. In that context, it is not terribly surprising that there are no surviving intermediates between bacteria and eukaryotes [e.g. plants, humans]. What is more surprising, though, is that the same traits do not keep on arising, time and time again -- like eyes.
We do not see the historical steps in the evolution of eyes, but we do see an ecological spectrum. From a rudimentary light-sensitive spot on some early worm-like creature, eyes have arisen independently on scores of occasions. That is exactly what natural selection predicts. Each small step offers a small advantage in one particular environment, with the precise advantage depending on the precise environment. Morphologically distinct types of eye evolve in different environments, as divergent as the compound eyes of flies and mirror eyes of scallops,or as convergent as the camera eyes that are so similar in humans and octopuses. Every conceivable intermediate from pinholes to accommodating lenses, is found in one species or another. We even see miniature eyes, replete with a 'lens' and a 'retina', in some single-celled protists [e.g. amoeba]."
[+] [-] fiatjaf|10 years ago|reply
What do you think of it? Is it serious enough? Because I think there is an obvious flaw in it, the question: why are these mutations linked?
[+] [-] redthrowaway|10 years ago|reply
[+] [-] xixixao|10 years ago|reply
[+] [-] mgkimsal|10 years ago|reply
I think it's more the case that things may spread if they don't have any disadvantage (like causing death).
[+] [-] pvg|10 years ago|reply
That doesn't sound right at all. Look at the some of discussion of the 'Irreducible Complexity' examples. https://en.wikipedia.org/wiki/Irreducible_complexity#Stated_...
[+] [-] digi_owl|10 years ago|reply
Best i can tell, all that is needed for something to be carried forward is for it to not be a hindrance.
Thus, a proto-wing could very well linger for generations without going anywhere simply because it does not hinder the lineage's survival.
Never mind that the planet has not been the shape we see it in for the entire time.
[+] [-] aaron695|10 years ago|reply
Google how the eye evolved, it didn't just mutate it was a series of slow gradual mutations.
What you are suggesting goes against evolution theory (which is ok with proper evidence)
It's a mutation theory which is hard to find a lot of info on and I can't find the proper name of.
But it is considered incorrect.
[+] [-] empressplay|10 years ago|reply
However, it didn't.
[+] [-] user_0001|10 years ago|reply
There is a common objection?
[+] [-] dnautics|10 years ago|reply
"Instead of working as enzymes (proteins that facilitate reactions inside the cell) the proteins were now what’s known as an interaction domain. They could communicate with and bind to other proteins, a useful skill for cells that have decided to trade the rugged individualist life for the collaboration of a group"
Enzymes switch between being enzymes and interaction domians across all taxa everywhere in the tree of life, so this is not the "money shot". Moreover, unicellular life do plenty of intracellular, collaborative communication (e.g. quorum sensing).
Reading the paper, the specific switch enabled the orientation of cell division to be communicated from one cell to another. This is interesting because this communication is not over an anisotropic chemical gradient, but encodes directional and spatial information.
[+] [-] ajross|10 years ago|reply
> A single mutation that repurposed a certain type of protein. Instead of working as enzymes (proteins that facilitate reactions inside the cell) the proteins were now what’s known as an interaction domain. They could communicate with and bind to other proteins, a useful skill for cells that have decided to trade the rugged individualist life for the collaboration of a group.
Which is total gibberish. Yet unsurprisingly the abstract to the actual paper (helpfully linked in the wapo article: http://elifesciences.org/content/5/e10147) is gibberish to me for different reasons.
Is anyone expert enough to attempt a "for technical dummies" reading?
[+] [-] gjm11|10 years ago|reply
Consider a growing multicellular organism. It grows by a process of cell division. Each division turns one cell into two adjacent cells. The structure it ends up with will depend on the orientation of those dividing cells (you'll tend to get growth "along the axis of division", so to speak).
A wide variety of multicellular organisms have a mechanism that orients cells according to features on the outside of neighbouring cells. (It "mediates spindle orientation in diverse animal taxa by linking microtubule motor proteins to a marker protein on the cell cortex localized by external cues", as the abstract puts it. The "mitotic spindle" is a structure involved in cell division, also called mitosis. It's mostly made out of long thin things called microtubules, and its job is to separate the chromosomes for the two new cells, which it does using "motor proteins". The cell cortex is the inner surface of the boundary of the cell.)
One part of this process is the way in which a protein involved in the mitotic spindle attaches itself to that thing on the cell cortex. The relevant bit of that protein is called the "guanylate kinase protein interaction domain" or GK_PID for short. A protein interaction domain is a bit of protein that interacts with other things; multiple different proteins can contain instances of the same interaction domain, just as multiple different programs can contain (say) the same code for computing SHA-256 checksums.
The paper reports evidence that a single mutation enabled the GK_PID to attach itself to the marker on the cell cortex. ("The complex was assembled through a series of molecular exploitation events, one of which – the evolution of GK_PID’s capacity to bind the cortical marker protein – can be recapitulated by reintroducing a single historical substitution into the reconstructed ancestral GK_PID."
So. This doesn't say that multicellularity was enabled by a single mutation. It says that one small but important part of a process that's necessary for complex multicellular organisms was enabled by a single mutation. Still pretty cool, but the journalistic science->hype conversion machine is clearly operating as usual here.
[+] [-] tokenadult|10 years ago|reply
[1] http://www.talkorigins.org/faqs/comdesc/
[+] [-] raz32dust|10 years ago|reply
[+] [-] gus_massa|10 years ago|reply
Read this comment of bmer about the original research article: https://news.ycombinator.com/item?id=10884255
[0] [Or to be more precise, IIRC the transition from bacteria to eucariota is more difficult. I'd worry about that step instead.]
[+] [-] dschiptsov|10 years ago|reply
[+] [-] osoba|10 years ago|reply
[+] [-] billiam|10 years ago|reply
[+] [-] dkural|10 years ago|reply
[+] [-] nickbauman|10 years ago|reply
https://en.wikipedia.org/wiki/Cambrian_explosion
[+] [-] JeffreyKaine|10 years ago|reply
[+] [-] x3n0ph3n3|10 years ago|reply
[+] [-] avaku|10 years ago|reply
[+] [-] unknown|10 years ago|reply
[deleted]
[+] [-] givan|10 years ago|reply
Where is this 600M years taken from? big claims based on assumptions, I don't like this kind of science, building on too many assumptions and you are going too far from the truth and this is the opposite of what science tries to achieve.
[+] [-] zbyte64|10 years ago|reply
That and the rise of multi-cellular life marks the beginning of the Cambrian explosion (542M years ago). That gives 60M years for the mutation to spread and specialize.
[+] [-] falsestprophet|10 years ago|reply
I didn't read the paper, but probably this technique: https://en.wikipedia.org/wiki/Molecular_clock
[+] [-] unknown|10 years ago|reply
[deleted]
[+] [-] once-in-a-while|10 years ago|reply
Are you folks aware that 1000 years is already a very long time? Any number bigger than, say 100.000 years is just the same as infinity, regarding to time.
This "infinity" problem simply requires too much faith, and will never have real evidence. Not very good attributes for a credible theory.
Maybe it's about time to get a better one, with less time involved? This way the faith required would be at a real human reachable level.
[+] [-] x3n0ph3n3|10 years ago|reply
Tell that to a geologist or an astrophysicist and you'll be laughed out of the room. There's plenty of evidence of timescales in the millions and billions of years.
[+] [-] ceejayoz|10 years ago|reply
Geologically? Not at all. It's 0.000022% of the age of the Earth.
[+] [-] buserror|10 years ago|reply