Let’s suppose there was a first Last Universal Common Ancestor (LUCA) or a small population of it. How did it overcome deleterious harmful mutations, in order not to go extinct?
M.LYNCH (2003): Although uncertainties remain with respect to the form of the mutational-effect distribution, a great deal of evidence from several sources strongly suggests that the overall effects of mutations are to reduce fitness. Indirect evidence comes from asymmetrical responses to artificial selection on life history traits, suggesting that variance for these traits is maintained by downwardly skewed distributions of mutational effects. More direct evidence comes from spontaneous mutation accumulation (MA) experiments in Drosophila, Caenorhabditis elegans, wheat, yeast, Escherichia coli, and different mutation accumulation (MA) experiments in Arabidopsis. All of these experiments detected downward trends in mutation accumulation (MA) line population mean fitness relative to control populations as generations accrued. As far as we know, there is no case of even a single MA line maintained by bottlenecking that showed significantly higher fitness than its contemporary control populations. 2
M.C. Whitlock (2004): The overall effect of mutation on a population is strongly dependent on the population size. A large population has many new mutations in each generation, and therefore the probability is high that it will obtain new favorable mutations. This large population also has effective selection against the bad mutations that occur; deleterious mutations in a large population are kept at a low frequency within a balance between the forces of selection and those of mutation. A population with relatively fewer individuals, however, will have lower fitness on average, not only because fewer beneficial mutations arise, but also because deleterious mutations are more likely to reach high frequencies through random genetic drift. This shift in the balance between fixation of beneficial and deleterious mutations can result in a decline in the fitness of individuals in a small population and, ultimately, may lead to the extinction of that population. As such, a change in population size may determine the ultimate fate of a species affected by anthropogenic change.3
J.C.Sandord (2022): Genetic Entropy is the genetic degeneration of living things. Genetic entropy is the systematic breakdown of the internal biological information systems that make life alive. Genetic entropy results from genetic mutations, which are typographical errors in the programming of life (life’s instruction manuals). Mutations systematically erode the information that encodes life’s many essential functions. Biological information consists of a large set of specifications, and random mutations systematically scramble these specifications – gradually but relentlessly destroying the programming instructions essential to life. Genetic entropy is most easily understood on a personal level. In our bodies there are roughly 3 new mutations (word-processing errors), every cell division. Our cells become more mutant, and more divergent from each other every day. By the time we are old, each of our cells has accumulated tens of thousands of mutations. Mutation accumulation is the primary reason we grow old and die. This level of genetic entropy is easy to understand. There is another level of genetic entropy that affects us as a population. Because mutations arise in all of our cells, including our reproductive cells, we pass many of our new mutations to our children. So mutations continuously accumulate in the population – with each generation being more mutant than the last. So not only do we undergo genetic degeneration personally, we also are undergoing genetic degeneration as a population. This is essentially evolution going the wrong way. Natural selection can slow down, but cannot stop, genetic entropy on the population level.
Apart from intelligence, information and information systems always degenerate. This is obviously true in the human realm, but is equally true in the biological realm (contrary to what evolutionists claim). The more technical definition of entropy, as used by engineers and physicists, is simply a measure of disorder. Technically, apart from any external intervention, all functional systems degenerate, consistently moving from order to disorder (because entropy always increases in any closed system). For the biologist it is more useful to employ the more general use of the word entropy, which conveys that since physical entropy is ever-increasing (disorder is always increasing), therefore there is universal tendency for all biological information systems to degenerate over time – apart from intelligent intervention.1
1. J.C.Sanford: Genetic entropy 2022
2. Michael Lynch: TOWARD A REALISTIC MODEL OF MUTATIONS AFFECTING FITNESS 2003 Mar
3. Michael C. Whitlock: Fixation of New Mutations in Small Populations 2004
Unfortunatelly for sweet LUCA nobody saw him/her/it therefore is just imagination. I mean if we want to talk about science then LUCA is just another fairytale like a multiverse or darwinian evolution.
as to the question of “How Would A Last Universal Common Ancestor Not Have Gone Extinct Because Of Mutations?”
This also reminds me of the ‘mutation protection paradox’,
Darwinian evolution depends on random ‘mutations/errors’ to DNA in order to give Darwinian evolution a semblance of feasibility. Yet there are multiple layers of error correction that are now found in the cell that protect against “random mutations” happening to DNA.
Some of the sophisticated and overlapping repair mechanisms found for DNA thus far include, (but are not limited to), the following:
Again, the dependency of Darwinian evolution on random mutations to DNA, and yet the existence of multiple layers of repair mechanisms that prevent random mutations from happening to DNA, has been termed the ‘mutation protection paradox’.
As the following article states, “The bottom line is that repair mechanisms are incompatible with Darwinism in principle. Since sophisticated repair mechanisms do exist in the cell after all, then the thing to discard in the dilemma to avoid the contradiction necessarily is the Darwinist dogma.”
Of supplemental note: the following articles give us a (small) glimpse into just how (very) sophisticated some of these repair mechanisms for DNA actually are,
Quote and Verse
Geneticist Dr. John Sanford and his 2018 presentation on genetic entropy
for National Institutes of Health.
During Q & A, he received the following question on living fossils:
https://youtu.be/2Mfn2upw-O8?t=3463
The answer might be – perhaps these species are not that old ? :))) or, these species get periodically fixed (like Dr. Sanford suggested, but he was sort of joking)
as to genetic entropy….
through the years, i debated lots of evolutionists.
I got schooled, repeatedly, that i don’t understand how evolution works – you know, how good mutations occur and these are selected and after long time of this process, here we (humans) are …
I asked them, to compare their list of known ‘good mutations’ with my list of known bad mutations.
Each time, it was a grotesque. Most of them couldn’t think of any good mutations. Some of them were parroting the sickle-cell mutation … and that was it.
So, Seversky, JVL, Chuck and Co., please let’s compare the list of good mutations with the following list of bad mutations
from Wikipedia:
“There are over 6,000 known genetic disorders in humans.”
https://en.wikipedia.org/wiki/List_of_genetic_disorders
Now, Seversky and Co, your list…. please ….
Functional coded information that is the foundation of life is incompatible with darwinism . If foundation is incompatible then everything that follows is incompatible:signalling,feedback loops,repair, adaptation to maintain homeostasis even the external environment is changing , etc…
I’ll be interested to see if any of the more well-known ID proponents pitch in to support Mr Grasso. I’m thinking of Behe, Meyer, Wells, Nelson and so on. That is a choice for them. My prediction is they will studiously fail to notice Mr Grasso’s contributions. Let’s wait and see if I’m right.
By all means continue the cheerleading in the meantime. It’s good for morale.
Sandy @5
the day Darwinists discovered DNA proofreading/repair mechanism(s), on that day Darwin’s theory of evolution felt apart.
Any repair has to be engineered. ANY.
In order to repair something, the following needs to be met:
1. one has to know that something is broken (DNA damage sensing)
2. one has to identify where exactly it is broken
3. one has to know when to repair it (e.g. you have to stop/or put on hold some other ongoing processes, in other words, you need to know lots of other things, you need to know the whole system, otherwise you make more damage…)
4. one has to know how to repair it (to use the right tools, materials, energy, etc, etc, etc )
5. and, eventually, you have to make sure that you fixed it OK. (this can be observed in DNA repair as well)
it is not surprising, that the theory of evolution was developed by natural science graduates who never made anything … these people are naive romantics … i don’t blame them for being naive … i blame them because in 21st century their theory is a direct attack on every engineer. This theory is as offensive as it gets …. and i can’t believe that this is still happening in 21st century …
Martin and Sandy, I think you will get kick out of the following findings which, fairly dramatically, underscores your point about needing to know what needs to be repaired, and knowing how to repair it,
Martin_r at 8,
“naive romantics”? Too much evidence is posted here that shows they – meaning the usual suspects – will promote evolution regardless of ANY claims to the contrary. Regardless of ANY facts to the contrary. A repair mechanism came about by chance, along with the necessary sensors to identify the problem and along with the necessary repair mechanism to fix the problem.
No, only a purpose-designed system can do this.
Since we are talking about paradoxes :
Peto’s paradox….
Marc Tollis (2017): In a multicellular organism, cells must go through a cell cycle that includes growth and division. Every time a human cell divides, it must copy its six billion base pairs of DNA, and it inevitably makes some mistakes. These mistakes are called somatic mutations (cells in the body other than sperm and egg cells). Some somatic mutations may occur in genetic pathways that control cell proliferation, DNA repair, apoptosis, telomere erosion, and growth of new blood vessels, disrupting the normal checks on carcinogenesis. If every cell division carries a certain chance that a cancer-causing somatic mutation could occur, then the risk of developing cancer should be a function of the number of cell divisions in an organism’s lifetime. Therefore, large-bodied and long-lived organisms should face a higher lifetime risk of cancer simply due to the fact that their bodies contain more cells and will undergo more cell divisions over the course of their lifespan. However, a 2015 study that compared cancer incidence from zoo necropsy data for 36 mammals found that a higher risk of cancer does not correlate with increased body mass or lifespan. In fact, the evidence suggested that larger long-lived mammals actually get less cancer. This has profound implications for our understanding of how the cancer problem is solved.
When individuals in populations are exposed to the selective pressure of cancer risk, the population must evolve cancer suppression as an adaptation or else suffer fitness costs and possibly extinction. Discovering the mechanisms underlying these solutions to Peto’s Paradox requires the tools of numerous subfields of biology including genomics, comparative methods, and experiments with cells. For instance, genomic analyses revealed that the African savannah elephant (Loxodonta africana) genome contains 20 copies, or 40 alleles, of the most famous tumor suppressor gene TP53. The human genome contains only one TP53 copy, and two functional TP53 alleles are required for proper checks on cancer progression. When cells become stressed and incur DNA damage, they can either try to repair the DNA or they can undergo apopotosis, or self-destruction. The protein produced by the TP53 gene is necessary to turn on this apoptotic pathway. Humans with one defective TP53 allele have Li Fraumeni syndrome and a ~90% lifetime risk of many cancers, because they cannot properly shut down cells with DNA damage. Meanwhile, experiments revealed that elephant cells exposed to ionizing radiation behave in a manner consistent with what you would expect with all those TP53 copies—they are much more likely to switch on the apoptotic pathway and therefore destroy cells rather than accumulate carcinogenic mutations.
https://bmcbiol.biomedcentral.com/articles/10.1186/s12915-017-0401-7
Comment: How does the author explain the origin of these protective mechanisms? He claims: “The solution to Peto’s Paradox is quite simple: evolution”. This is an ad-hoc assertion and raises the question: How could complex multicellular organisms have evolved if these cancer protection mechanisms were not implemented before the transition occurred, since, otherwise, these organisms would have gone extinct? This problem becomes even greater if considering, that animals with large body size supposedly evolved independently many times across the history of life, and, therefore, these mechanisms would have had to be recruited multiple times. The paradox is only solved, if we hypothesize that large animals were created independently by God, and right from the beginning equipped with tumor suppressor mechanisms from the get-go.
Any take by you, guys, on this one? When did cancer suppressor mechanisms originate? Before multicellularity arose?
A. B. Williams (2016): The loss of p53 is a major driver of cancer development mainly because, in the absence of this “guardian of the genome,” cells are no longer adequately protected from mutations and genomic aberrations. Intriguingly, the evolutionary occurrence of p53 homologs appears to be associated with multicellularity. With the advent of metazoans, genome maintenance became a specialized task with distinct requirements in germ cells and somatic tissues. With the central importance of p53 in controlling genome instability–driven cancer development, it might not be surprising that p53 controls DNA-damage checkpoints and impacts the activity of various DNA-repair systems. 64
B. J. Aubrey (2016): The fundamental biological importance of the Tp53 gene family is highlighted by its evolutionary conservation for more than one billion years dating back to the earliest multicellular organisms. The TP53 protein provides essential functions in the cellular response to diverse stresses and safeguards maintenance of genomic integrity, and this is manifest in its critical role in tumor suppression. The importance of Tp53 in tumor prevention is exemplified in human cancer where it is the most frequently detected genetic alteration. This is confirmed in animal models, in which a defective Tp53 gene leads inexorably to cancer development, whereas reinstatement of TP53 function results in regression of established tumors that had been initiated by loss of TP53.
TP53: Tumor Suppression and Transcriptional Regulation
Following activation, the TP53 protein functions predominantly as a transcription factor. The TP53 protein forms a homotetramer that binds to specific Tp53 response elements in genomic DNA to direct the transcription of a large number of protein-coding genes. The requirement for TP53 transcriptional activity in tumor suppression has been examined by systematically mutating the transactivation domains of the TP53 protein, rendering it either partially or wholly transcriptionally defective. Importantly, mutations resulting in complete loss of TP53 transcriptional activity ablate its ability to prevent tumor formation, supporting the concept that transcriptional regulation is central to the tumor-suppressor function. TP53-mediated tumor suppression is governed by transcriptional regulation.
TP53-mediated transcriptional regulation varies according to the type of stress stimulus and type of cell, so that appropriate corrective processes can be implemented. For example, minor DNA damage may institute cell-cycle arrest and activate DNA-repair mechanisms, whereas stronger TP53-activating signals induce senescence or apoptosis. Accordingly, the TP53 transcriptional response varies depending on the nature of the activating signal and the type of cell. The number of known or suspected TP53 target genes has increased into the thousands with dramatic differences in transcriptional responses observed among different cell types, different TP53-inducing stress stimuli, and varying time points following TP53 activation. These studies paint an increasingly complex picture of the modes by which TP53 can regulate gene expression. For example, before TP53 activation, a subset of target genes is transcriptionally repressed by the TP53 protein. More recently appreciated functions of the TP53 protein include widespread binding and modulation of enhancer regions throughout the genome and transcriptional activation of noncoding RNAs. Interestingly, the TP53-activated long noncoding RNA, lincRNA-p21, exerts widespread suppression of gene expression. The list of proposed TP53 target genes is vast and they are known to influence diverse cellular processes, including apoptosis, cell-cycle arrest, senescence, DNA-damage repair, metabolism, and global regulation of gene expression, each of which could potentially contribute to its tumor-suppressor function.
Todd Riley (2008): The p53 pathway responds to various cellular stress signals (the input) by activating p53 as a transcription factor (increasing its levels and protein modifications) and transcribing a programme of genes (the output) to accomplish a number of functions. Together, these functions prevent errors in the duplication process of a cell that is under stress, and as such the p53 pathway increases the fidelity of cell division and prevents cancers from arising. 63
K. D. Sullivan (2017): The p53 polypeptide contains several functional domains that work coordinately, in a context-dependent fashion, to achieve DNA binding and transactivation. (the increased rate of gene expression)
K. Kamagata (2020): Interactions between DNA and DNA-binding proteins play an important role in many essential cellular processes. A key function of the DNA-binding protein p53 is to search for and bind to target sites incorporated in genomic DNA, which triggers transcriptional regulation. How do p53 molecules achieve “rapid” and “accurate” target search in living cells? The genome encompasses DNA sequences that encode genes, and gene editing is the genetic engineering of a specific DNA sequence, including insertion, deletion, modification, and replacement. The main player in genome editing is a type of protein that can bind to DNA, known as DNA-binding proteins. DNA-binding proteins include enzymes, which can cut DNA or ligate two DNA molecules, and transcription factors, which can activate or deactivate gene expression. These proteins are classified into DNA sequence-specific and nonspecific binders.
The transcription factor p53 can induce multiple tumor suppression functions, such as cell cycle arrest, DNA repair, and apoptosis. p53 is presumed to solve the target search problem by utilizing 3D diffusion, 1D diffusion along DNA, and intersegmental transfer between two DNAs in the cell.
Comment: This transcription factor p53 actively searches targets in the genome to be expressed. This is a goal-oriented process implemented to activate processes that avoid the origination of cancer. Various players are required that work as a system. It is a team play. The p53 transcription factor has to be able to perform “rapid” and “accurate” target search, recognize it, and bind to the DNA sequence so it can be expressed, but most important, before it can act like a switch commanding “on”, the gene sequences to be expressed must be there, that is, the actors that are recruited to permit DNA repair, or apoptosis (cell death). It is an all-or-nothing business to convey the function to suppress the development and growth of tumors, and consequently, death. In other words, this is an irreducibly complex system where p53 would be functionless unless the actors to act upon were not there.
63. Brandon J. Aubrey: Tumor-Suppressor Functions of the TP53 Pathway 2016
64. A.B. Williams: p53 in the DNA-Damage-Repair Process 2016 May; 6
For all of these stages obviously the cell needs a Main Control Room from which to coordonate all the actions. Where is hidden this Control Room?
Outstanding. Lazarus.
Magnificent. TP53.
PS: After you hear these impressive findings and a darwinist come to preach about random mutations, random chemical reactions in cell ,and chance you start to think: Poor darwinist has bats in the belfry.The lights are on, but no one is home.
Junk DNA.? Most mutations will occur in non-functional regions where they do no harm?
Mutations are random only with respect to fitness.
If Sandford is correct about genetic entropy then how did life get started in the first place? If the rate of decay in the genome is such as to lead inevitably to catastrophic failure then how did complex multicellular organisms ever emerge?
As a YEC, he should also explain why his Creator should have designed life based on such a fatally flawed system.
And why are Lenski’s twelve tribes still going?
Sanford’s ideas always appeared to me as nonsense.
While there may be detrimental mutations, it only happens in a few and these entities will die off. Meanwhile millions of other entities do not have the mutation and they and their offspring should thrive.
Maybe I am wrong. But explain why a mutation that is deleterious would spread to all the members of a species.
Ba77,
A simpler example of adaptation is the sugar beet. Grown in ideal soil and ideal sunlight, it can yield up to 60% sugar. Grown in poor soil and with less light, it yields less.
A human being can become grossly obese which can increase the risk of health problems. If he loses the weight and goes on a healthy diet, he can avoid health problems.
Organisms are clearly adaptive. But one type of animal turning into another? Where does the new functional information come from? In a highly integrated system like the human body, any helpful mutation (if such a thing could happen) would have to occur in the right place and be correctly integrated into the system.
🙂 This darwinist mantra expired. I guess it’s time to learn new ones.
You didn’t pay attention how many processes anti-randomness take place in the cell and nobody will do that for you.
1. Lenski’s twelve tribes will be no more if they are let in natural environment to compete with uncoddled infidels .
2. Lenski’s twelve tribes of bacteria evolved into crippled bacteria (I guess some darwinists consider that crippled bacteria are more advanced/evolved than just bacteria ).
Not really. He is as crafty as a fox with 30 years experience in genetics but he doesn’t have God level “experience”. There are many things to be learned about cell but he is closer to the truth than others.
For example few more hidden/unknown error-repairing( or mapping ) processes that maintain the genome on the survival path would explain why we are not extinct.
@ Whistler
Whilst not the point of the LTEE, it nonetheless clearly demonstrates Sandford’s idea of “genetic entropy” is mistaken.
There’s no doubt obesity in humans can be life-threatening. Seems a bit of a non sequitur in this thread, though.
I’m sure it’s correct that, returned to an animal’s gut, the current twelve strains would be outcompeted to extinction by “wild” E coli. But what about the reverse.? What would happen if we were to see who would survive in Lenski’s sparse flask environment? Wild-type wipeout is my prediction. In fact, I bet it’s already been tested. Shall we check?