Originally posted by tgidkp
reply to post by tauristercus
first, since youve taken so many hits, i will show you where you have gone right with your thinking:
at the very earliest stages of the protogenome, somehow somewhere functionality arose. but at this stage, a membrane-bound cell is not yet necessary.
so, to properly calculate the odds of the very first functional biomolecule you will need to consider 10^10 biomolecules per liter multiplied by
total liters of the global ocean multiplied by around 1 billion years.
Hmmm ... some very interesting values you've thrown around there.
10^10 biomolecules per liter ? How did you arrive at this exact value ? What is a biomolecule anyway ?
Why multiply the above value with "total liters of the global ocean" ? For that matter, just HOW BIG
was your primeval "global ocean" ? Was
it small, medium or large ?
Why further multiply the above by a time scale of 1 billion years ? Why not 0.5 billion ... or 1.5 billion years ?
Some pretty lose and highly inaccurate maths going on there, wouldn't you say ? Unlike my probability calculations which WERE
So how can you make the following statement
... to properly calculate the odds of the very first functional biomolecule ...
when you're using such sloppy estimations ?
also, keep in mind that "functionality" at this stage is a dubious concept. so nature really doesnt have to work all that hard to come up with
some type of functional unit. in fact, there were probably an abundance of such functional units.
"functionality" is NEVER
a dubious concept as far as nature is concerned.
Any random mutation that results in a nucleotide sequence that is non-lethal from the carrying organism point of view has "functionality", whether
"positive" because it's a beneficial mutation or "neutral" because it's non-lethal.
at this point we still have not established a causal relationship between DNA and proteins
Hmmmm ... unless I've really missed an important point somewhere, my understanding has always been that one of the primary reasons for DNA's
existence is to store and supply upon demand the necessary information leading to gene expression / protein synthesis.
If you have an alternative method for protein synthesis that does NOT rely on the presence of DNA, then please mention what it is so I can research it
and further educate myself. Thanks in advance !
now, i will show you exactly where you have gone wrong (mistakes underlined):
...These 153 nucleotides MUST be added by nature to the chromosome in the correct sequence for insulin to be the resulting
...if insertions (mutations) are NOT ...blahblahblah...there are times when insertions (mutations) are blahblahblah...
now, even though in the initial stages of development, spontaneous polymerization by the addition of random nucleotides was a plausible mechanism,
you must now abandon that thought completely!
above in the quotes, you have equated "insertion" with "mutation". abandon it!
Abandon insertion mutations ? Absolutely not !
Insertion of nucleotides within the genome IS
I'm really surprised that you need ME to point out the following examples of mutation pathways to YOU.
Taken from Evolution 101 - Berkely
you are totally 100% correct in stating that random insertion of nucleotides into our simple functional sequence from above will NEVER result in
anything useful. you have been very busy calculating odds. but i will just go ahead and say NEVER!
rather, you must now consider that mutations arise from random mistakes produced by already functional machinery. these are your new
dice (see previous quote from Asyntax). on the raw level, you are still working with A,T,C,G. but you are no longer working exclusively at the
raw level. there is now a new, higher level of processing. this higher level of processing is capable of making its own mistakes, and the mistakes
that it makes are far more interesting and far more useful than the mistakes at the lower level.
Whether you are working on the "raw or higher" levels, as you put it, is immaterial.
The simple reason is that you can NEVER
escape from, bypass or side-step the probabilistic mechanism generating random mutations that operates
Lets take a look at the "raw level" first:
In this case, we're looking at creating a functional protein from scratch ... in other words, NOT reusing or borrowing existing base sequences.
Now as I've pointed out so many times before, a simple 153 base protein such as insulin has odds of 10^92 against a successful creation ... taking
into account the 10^24 degenerate alternatives, still gives ultra-astronomical odds of 10^68 against.
Someone earlier tried to side-step these odds by saying that each additional base to be added to complete the sequence actually needs much smaller
odds for success, of only 1 in 4 ... however this was incorrect.
They were treating each new base addition as an isolated event completely independent of any previous or future base additions. But this line of
thinking was fallacious as each new base addition IS
entirely dependent on what's come before ... and what's to come after.
We are talking CUMULATIVE
probability even on the "raw level", resulting in those stupendous odds of 10^68 against creating that 153 base
You can dispute this conclusion all you want but the fact remains that creating the required 153 base sequence randomly from scratch is entirely
probabilistic and entirely controlled by the Laws of Probability.
Go look it up in any high school maths book !
Ok, now for your "higher level" approach ...
Here, I assume, you're talking about creating a new functional protein derived from base sequences that already exist within the genome somewhere ...
possibly as non-functioning sequences or as part of other protein sequences that are functional.
In this example, lets give nature a break by picking an easy task and assume that by some fluke, there exists a strand of base sequences
153 bases in length and that is ALMOST
90% identical in sequence (you can't say I'm not being generous) to our desired end
product sequence ... namely insulin.
This means that approximately 138 bases are in the correct location within this sequence and 15 are not.
So natures task is to "replace" the 15 incorrect bases with 15 correct bases ... and if successful, out pops an insulin protein.
Now we have 23 pairs of chromosomes with 3.1 billion base pairs distributed amongst them ... so on average
, each chromosome pair has 135
million base pairs. But this value of 135 million base pairs is based on today's genome estimate ... so again, lets help nature out even more by
going back in time to when the average chromosome had say, half these bases - let's go with 75 million base pairs, shall we ?
Therefore we have our starting 90% correct sequence located on a chromosome, somewhere
amongst those 75 million bases ... already a bit of a
needle in a haystack situation, wouldn't you say ?
But lets press on regardless.
Now we'll assume a mutation rate of say, 100 mutations along that chromosome and we'll only consider mutations that make a base replacement only ...
as opposed to the other kinds of mutations that could potentially alter the existing 90% of already valid bases along that sequence, consequently
reducing the 90% down to lower values and taking us further away from our goal of 153 correct sequential bases.
So, we have 100 base replacing mutations that are entirely RANDOM
and could happen ANYWHERE
along the 75 million base length of our
chromosome. This works out to an average of 1 mutation every 750,000 bases.
This means that there is a probability value of 1 in 4,900 that one of those 100 random mutations would happen somewhere
within the chromosome
location containing our 153 base sequence. So we are looking at odds of 4,900 to 1 against
any of those 100 random mutations even being in the
right 153 base neighbourhood !
Ok, 4,900 to 1 against ... not bad odds, you might say.
However those are just the odds of one of the 100 random mutations happening somewhere
within our target sequence. We have to bear in mind that
out of that 153 base target, 138 bases are already
correct and we do not
want them changed by a random mutation ... we only want one of
the remaining 15 incorrect bases to be randomly mutated, hopefully into the correct base for that particular location within the sequence.
But based on the above information, we see immediately that there is a far greater chance (almost 91%) that the random mutation (if it even happens)
will hit one of the 138 correct bases instead of one of the 15 incorrect bases that we DO
want to change.
So it's quite plainly obvious that a random mutation acting against an existing but only partially correct sequence of bases, has a substantially far
greater probability of causing degradation to the sequence then it would have of improving it.
But wait, it gets worse ...
We calculated above that there was only a 1 in 4,900 chance that the random mutation would target one of the 153 bases in the sequence ... and out of
that a further 9 to 1 chance against one of the 15 incorrect bases being the actual target ... significantly decreasing further the TOTAL
of an incorrect base being hit.
But lets say that nature got lucky and did indeed hit one of those 15 incorrect bases with a random mutation.
Now we find ourselves in the situation that the already bad odds get even worse.
Lets say that the incorrect base about to be mutated is say an A ... and we actually need it to be replaced/mutated into say, a C.
The odds against this happening are 3 to 1.
The existing A could be replaced with another A, or replaced with a G, or replaced with a T ... all of which are incorrect and do nothing to improve
the quality of the 153 base sequence but instead, degrades it further away from our goal of evolving an insulin gene.
Phew ... so after all that, what do we have ?
We have starting odds of 4,900 to 1 against
one of the 100 mutations actually targeting one of the 153 bases in our sequence of interest.
These odds against are further increased dramatically by a 91% chance that the mutation will still target the wrong base within the sequence.
These odds against are further increased significantly with only a 1 in 3 chance that even if one of the incorrect bases is successfully targeted and
mutated, that the replacement base will be a desirable one.
So in conclusion, it is very easy to show that even on a "higher level", as you put it, and using an incomplete sequence that we hope to use as a
template to "evolve" a different sequence (to produce a protein), random mutations applied to that incomplete template sequence have been shown to
almost certainly degrade
that template sequence.
i hope that is a little more clear to you now.
Clarity has never been an issue for ME regarding mutational rate probabilities ... however it does seem to be a major stumbling block for many
So based on my examples and explanations above
I hope that is a little more clear to you now.