One more important reason to be skeptic about Darwins Theory

I agree. I was not specific enough. Evidently, if mutations occur, they are either neutral , or harmful. In case its neutral selection that perpetuates, no evolution happens, and if the new trait is harmful, but selected, either de-volution takes place, or the organism dies. None shows that a positive trait was selected, and able to outcompete other variants , and differential reproduction, spreading in the population.

I don’t get WHAT EXACLY ? The experiment above with bacterial evolution would have to be able to demonstrate that differential reproduction is a real outcome of natural selection, and higher survival rate and reproduction is the case. The experiment has not shown this.

Artificial selection is NOT natural selection.

@Otangelo_Grasso1

So Now you are telling me you only believe in Natural Selection on negative traits…

Well… that’s a step in the right direction I suppose. Just don’t say you don’t think Natural Selection is testable. Because obviously it is Very testable, and there is a whole field of evolutionary mathematics that develop statistical forecasts for Natural Selection.

LoL.

Didn’t you just plead (above) to be shown that Natural Selection is testable? Testing requires man-made control of certain variables.

If you are going to start arguing that Testing Natural Selection is impossible … because the chromosomes will know the selection isn’t Natural … then I’m dropping this discussion right here and now.

You really should stop thinking Creationists know what they are talking about.

It’s difficult to understand what you’re arguing here. You’ve just been shown an example in which new beneficial mutations spread in a population. You say you agree, and then state that mutations are all either neutral or harmful. The problem isn’t that you aren’t specific: it’s that your statement is simply wrong. We see new beneficial mutations occur all the time, in the lab and in the wild.

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@Otangelo_Grasso1

What do you think is going on when a really tiny dot of bacteria suddenly bursts free of his cousins and penetrates more deeply into the poisonous frontier?

That, my good sir, is differential reproduction.

You need to keep these phrases separate - - they mean very different things:

Natural Selection (not really debateable);
Speciation (we debate it all the time),
Differential Reproduction (just one of the factors behind Natural Selection);

And so on…

If you are going to object to something … you need to know which thing to object to.
Differential Reproduction is not controversial or negotiable… Dog Breeders create this situation all the time when they change a small dog into a bigger dog and vice versa…

You do realize that existing variation is much more frequent than mutation, don’t you? If so, why are you pretending that populations are somehow waiting around for mutations?

Once more i agree. positive mutations occur. The question is : WHAT IS THE MECHANISM. Has it been shown that natural selection does the job, or do bacterias have inbuild , pre-programmed mechanisms, eventually epigenetic mechanisms, to adapt ?

yes, we know that. That are inbuild, pre-programmed mechanisms.

Artificial selection has nothing to do with natural selection. And artificial selection does not mean random mutations are responsible.

Who is “we,” Otangelo? And since you know that, why are you acting as though populations are evolutionary static until new mutations occur?

I have no idea what you mean here. Talvez escrever em portugues seja melhor.

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I never made that claim. Do you even read and understand what i post ?

An essential ingredient of Darwins theory is that " Individuals possessing traits well suited for the struggle for local resources will contribute more offspring to the next generation ". This means that individuals with a certain genotype for a given locus or gene have more reproductive success than individuals within the same population that have other genotypes for for that same gene. What determines whether a gene variant spreads or not depends on an incredibly complex web of factors - the species’ ecology, its physical and social environment and sexual behavior. A further factor adding complexity is is the fact that high social rank is associated with high levels of both copulatory behavior and the production of offspring which is widespread in the study of animal social behavior. As alpha males have on average higher reproducitve success than other males, since they outcompete weaker individuals, and get preference to copulate, if other ( weaker ) males gain beneficial mutations (or the alphas negative mutations) as the alphas can outperform and win the battle for reproduction, thus selection has an additional hurdle to overcome and spread the new variant in the population. This does not say anything about the fact that it would have to be determined what gene loci are responsible for sexual selection and behavior, and only mutations that influence sexual behavior would have influence in fitness and the struggle to contribute more offspring to the next generation. Science would need furthermore to have the knowledge what traits are favoured in which environment. adaptation rates and mutational diversity and other spatiotemporal parameters, including population density, mutation rate, and the relative expansion speed and spatial dimensions. It is in praxis impossible to isolate these factors and see which is of selective importance, quantify them, plug them in (usually in this context) to a mixed multivariate model, and see whats statistically significant, and get meaninful, real life results. The varying factors are too many, and non predictive.

What we observe is gene entropy.

  1. Random mutations deteriorate the genome.
    heavenforum.org
    In a new paper in Science,3Khan et al, working with Richard Lenski [Michigan State], leader of the longest-running experiment on evolution of E. coli, found a law of diminishing returns with beneficial mutations due to negative epistasis. The abstract said:
    Epistatic interactions between mutations play a prominent role in evolutionary theories. Many studies have found that epistasis is widespread, but they have rarely considered beneficial mutations. We analyzed theeffects of epistasis on fitness for the first five mutations to fix in an experimental population of Escherichia coli. Epistasis depended on the effects of the combined mutations—the larger the expected benefit, the more negative the epistatic effect. Epistasis thus tended to produce diminishing returnswith genotype fitness, although interactions involving one particular mutation had the opposite effect. These data support models in which negative epistasis contributes to declining rates of adaptation over time.

  2. Adaptation of organisms to the environment happens.
    WHAT DARWIN GOT WRONG JERRY FODOR and MASSIMO PIATTELLI-PALMARINI

Additional phenomena, such as developmental modules, entrenchment and robustness, further separate random mutations at the DNA level from expressed phenotypes at the level of organisms.
Entrenchment
The different components of a genome and/or of a developmental structure usually have different effects ‘downstream’, that is, on the characteristics of the fully developed adult, through the entire lifetime. The magnitude of these effects is measured by the ‘entrenchment’ of that structure. The entrenchment of a gene or a gene complex changes by degrees - it’s not an all-or-none property. From an evolutionary point of view, the entrenchment of a unit has multiple and deep consequences for its role in different groups of organisms and different species, notably affecting other units that depend on its functioning. Generative entrenchment is seen both as an ‘engine’ of development and evolutionary change, and as a constraint. This amounts to saying that crucial developmental factors (‘pivots’ in Wimsatt’s terms) may be highly conserved and be buffered against change, or may undergo minor heritable changes with major evolutionary consequences. Generative entrenchment, as the expression aptly suggests, is very probably linked to spontaneous and quite general collective form-generating processes, but it is (of course) also under the control of genes, gene complexes and developmental pathways. How these different sources of order and change (some generically physico-chemical and some specifically genetic) interact is still largely unknown.

Robustness
A trait is said to be robust with respect to a genetic or environmental variable if variation of the one is only weakly correlated with variations in the other. In other words, robustness is the persistence of a trait of an organism under perturbations, be they random developmental noise, environmental change or genetic change. In recent years, robustness has been shown to be of paramount importance in understanding evolution, because robustness permits hidden genetic variation to accumulate. Such hidden variation may serve as a source of new adaptations and evolutionary innovations. It is an open, empirical and highly substantive question how narrowly such endogenous effects constrain the phenotypic variations on which external selection operates. It will take a while to find out. But, until that question gets answered, it is unadvisable to take a neo-Darwinist account of evolution for granted.

Master genes are ‘masters’
Many different traits are indissociably genetically controlled by the same ‘master gene’. Any mutation affecting one master gene, if viable, has an impact on many traits at once. A wellstudied gene family, called Otx, masterminds the development of kidneys, cranio-facial structures (Suda et al., 2009), guts, gonads and the cerebral cortex (segmentation and cortical organization).

Developmental modules
Let’s start with a definition. A module is a unit that is highly integrated internally and relatively insensitive to context externally. Developmental modules exist at different levels of organization, from gene regulation to networks of interacting genes to organ primordia. They are relatively insensitive to the surrounding context and can thus behave invariantly, even when they are multiply realized in different tissues and in different developmental phases. Different combinations of developmental modules in each context, however, produce a difference in their functions in development. There is evidence of the integration of several interacting elements into a module when perturbation of one element results in perturbations of the other elements in that module, or in gene-gene interaction (epistasis) within the module, in such a way that the overall developmental input-output relation is altered. This is another signal case in which the conservation of genetic and developmental building blocks, together with their multiple recombinations in different tissues and organisms, explains the diversity of life forms as well as the invariance of basic body plans. The reverberation of the effects of gene mutations is usually multiple and only the viable overall result is then accessible to selection. This complex system of master signals regulates tissues as different as the central nervous system, pharynx, hair cells, odontoblasts, kidney, feathers, gut, lung, pancreas, hair and ciliated epidermal cells across many different vertebrate and invertebrate species. Every mutation in anyone of the genes involved will alter many organs and their functions - a far cry from ‘beanbag genetics’. The lesson here is that modularity gives a new complex picture of evolution, one in which internal constraints and internal dynamics filter what selection can act upon, and to what extent it can do so. Precisely because so much cannot change, other things can change at the (so to speak) genetic periphery of organisms. It is often (although not always) the case that when we witness gene duplications, a ubiquitous kind of genetic modification, the ‘original’ gene continues acting as it did in earlier forms of life, while the ‘copy’ can ‘explore’ new functions over evolutionary time (these metaphors are commonplace in the professional literature) .

Coordination
The Russian zoologist and evolutionist Ivan Ivanovich Schmalhausen (1884-1963) had rightly stressed that living organisms are not the mere atomic ‘adposition’ of separate parts, but rather highly ‘coordinated’ systems (for a historical and critical review, see Levit et al., 2006). Today justice is done to Schmalhausen by experimental evidence that some mutations in genes specifically affecting one part of the body carry with them suitable modifications in other related parts. When limbs are induced ectopically (that is, where they don’t belong), often sensory neurons, receptor organs, cartilage and blood vessels also develop as a consequence around them (see Kirschner and Gerhart, 2005 for stunning examples). A laboratory-induced and quantitatively controllable modification in two key proteinsll in chick and finch embryos early in development produces as the main result variable elongation

Yes. Nothing you’ve posted casts the slightest doubt on this fact.

All organisms also have built-in, pre-programmed mechanisms for responding to changing circumstances. That’s a different thing.

provide a paper that does not just infer ns based on evolution and adaptation, but can show with data that ns is the driving mechanism. then you have a go.

all i am trying to figure out is, ALL mechanisms that drive adaptation. I am not against acknolwledging ns, if there is hard data and evidence.

Benkirk thinks someone who doesn’t even see Natural Selection when that is all there is to see is going to know or care about even more subtle areas of theory.

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There are scads of such papers. Here is one. It describes mutations that cause malaria parasites to be resistant to the drug artemisinin. The mutant versions have been observed to be increasing rapidly in frequency in Southeast Asia and to be associated with drug resistance. The mutations themselves cause the resistance: take them away, and resistant parasites become sensitive, and vice versa.

“Adaptation” is often defined as the product of natural selection, so other things you’re looking for may go under the name “acclimatization” or “phenotypic plasticity”.

@Otangelo_Grasso1

I think you would do better to ask for the kind of evidence there is, rather than unload both barrels of your shotgun and proclaim to the scientists here that there is no evidence for natural selection.

Some of the objections you are reciting on these BioLogos boards are objections made and resolved decades ago.

It makes no sense to reject Natural Selection, when the real issue for the comments
you are making is whether there is Speciation or not.

It makes no sense to reject Differential Reproduction as untestable, when Differential Reproduction is actually the easy factor to measure and mathematically predict. D.R. is about offspring - - and that tends to be the most noticeable part of a creature’s life cycle. When a frog lays eggs, or a bison drops a foal, it usually doesn’t go unnoticed.

It makes no sense to reject Common Descent, (which you haven’t mentioned this round) when we have many Evangelicals who actually agree that animals released from the Ark explored brand new ecological niches, and through “hyper-speciation”, created the lines of common descent of multiple millions of terrestrial species we find on the Earth today. I may not agree with the Creationist scenario, but it doesn’t offer you much credibility if you, as a Creationist, don’t even know about them.

It makes no sense to reject Evolution as untestable when you aren’t sure which parts of the T.o.E. are even in doubt.