Why do you think

[Sheldon]

@Tin-Man

Being an atheist and having to always defend my belief in non-belief can be overwhelming sometimes.

Have you considered asking Jesus for help?

@Tin-Man

I never would have converted to this stupid non-belief religion.

Yeah, you need to reject Satan.

[Calilasseia]

Was anyone else’s suspicions aroused, when taking a peek at that paper Quim linked to?

The full citation for which is, wait for it:

Mutation Bias Reflects Natural Selection In Arabidopsis thaliana by J. Grey Monroe, Thanvi Srikant, Pablo Carbonell-Bejerano, Claude Becker, Mariele Lensink, Moises Exposito-Alonso, Marie Klein, Julia Hildebrandt, Manuela Neumann, Daniel Kliebenstein, Mao-Lun Weng, Eric Imbert, Jon Ågren, Matthew T. Rutter, Charles B. Fenster & Detlef Weigel, Nature, 602: 101-105 (2022)

Let’s highlight that title again, shall we? Namely:

Mutation Bias Reflects Natural Selection In Arabidopsis thaliana

Now I wonder why the authors chose that title?

Second, this:

@Quim

Finally, we find that genes subject to stronger purifying selection have a lower mutation rate.

shows that far from I and others here not understanding evolution, Quim doesn’t understand evolution. Because he obviously doesn’t understand what purifying selection is. Purifying selection occurs when a gene is critical for metabolic function, and mutations disrupting that function are lethal. As a corollary, genes falling into this category have a habit of being highly conserved, and it’s no surprise that post hoc mutation rates for these genes will be observed to be lower, simply because the lethal variants have been rapidly eliminated. As a corollary, the following:

@Quim

We conclude that epigenome-associated mutation bias[2] reduces the occurrence of deleterious mutations in Arabidopsis

First of all, the term “epigenome associated mutation bias” is defined nowhere in the paper by the authors. I’m not surprised at this, because there’s a lot of waffle spouted on this subject even by actual biologists, let alone pedlars of dupicitous apologetics. But it’s interesting that no mechanism is presented in this paper to back up this term, as should happen in any proper, rigorous submission.

Indeed, the authors of this paper seem to have trouble keeping track of propter hoc versus post hoc mutations throughout the paper, and end up presenting clains therein that are little more than blind assertions as a result. If I have been a peer reviewer for this paper, I’d have sent it back to the jounral editor with a substantial list of reasons for rejection.

Second, Quim obviously doesn’t understand the proper use of the word “random” in scientific circles, and as a corollary, ends up resurrecting Canard #10 from my grand list of creationist canards. From said exposition, I’ll reiterate what scientists actually mean when they use the word “random”, viz:

When a scientist uses the word “random”, said usage involves a wealth of rigorous meaning underpinning the word. In scientific circles, the word “random” is used frequently as a shorthand for “we know multiple testable natural processes can produce this outcome, but we lack the audit trail of data telling us which of the possibilities actually occurred”. Under such circumstances, scientists model the system using a random variable, which is an entity that has a precise meaning in the realm of mathematical statistics.

Within that discipline, a random variable is a variable whose values conform to a probability distribution. Said conformity to a probability distribution can be the outcome of deterministic processes, courtesy of the fact that once again, multiple testable natural processes can generate the outcome in question. What happens in rigorous scientific circles, is that where possible, experiments are conducted under controlled conditions, to determine how often each relevant testable natural process contributes to the outcome, and a probability distribution is constructed on the basis of that experimental data.

Furthermore, in precise work, a random variable is modelled using what is known as a Markov chain process. Once probabilities are assigned to the different testable natural processes contributing to a given outcome, a tree diagram is constructed, in which each of the processes, and their experimentally determined probabilities, are linked together. The point here being that each of the inputs to a given node in a Markov chain process is itself a deterministic testable natural process. The probability aspect arises from how frequently each of the processes involved contributes to the outcome.

So not only did Quim choose an extremely bad paper for his apologetics, but also peddled a well-known creationist canard into the bargain.

[skriten]

@Tin-Man

I never should have climbed out from under that sentient rock.

Dumbass (muttering to self) Uh, wtf Tin? You had a nice secure spot and you just had to take it for granite…

Edit (my driveway is talking to me)

[Sheldon]

@Calilasseia

Quim doesn’t understand evolution

You’re confused, he’s a genius who knows better than 99% (his number) of biologists.

@Calilasseia

there’s a lot of waffle spouted on this subject even by actual biologists

Well there you go, according to @Quim 99% of them.

@Calilasseia

But it’s interesting that no mechanism is presented in this paper to back up this term, as should happen in any proper, rigorous submission.

I am sure @Quim will address this in his Nobel acceptance speech.

@Calilasseia

Second, Quim obviously doesn’t understand the proper use of the word “random” in scientific circles,

Geniuses are mavericks, they needn’t and don’t play by the rules.

@Calilasseia

not only did Quim choose an extremely bad paper for his apologetics, but also peddled a well-known creationist canard into the bargain.

You’re posting your way right out of @Quim’s memoirs, thas’all I’m saying.

[Sheldon]

Ok I was saving this, but now it seems like the right time.

Quim
noun

VULGAR SLANG•BRITISH
a woman’s genitals.

I recognised it right off obviously.

[Calilasseia]

Meanwhile, dealing with this latest floater in the toilet bowl of discourse:

@WhoAreYou

Sheldon,

Please explain why flood stories around the world share things such as;

Just because mythologies contain the requisite assertions, doesn’t mean that those assertions constitute fact. Are you ever going to learn this elementary lesson?

Furthermore, it’s no surprise that pre-scientific humans with limited imaginations, living alongisde water bodies with a habit of inundating surrounding land on a regular or semi-regular basis, will concoct mythologies with recurring themes. You seem to think that some sort of fantastic magic process is needed for this: no it isn’t.

Then there’s the little matter of there being NO EVIDENCE that the fantasy “global flood” ever happened. Indeed, I’ve already presented to you, in detail, the cogent reasons why the fantasy “global flood” never happened on two separate occasions in this very thread, namely in post #572 and post #1217. Yet here you are again, ignoring that presentation of evidence, none of which you even attempted to acknowledge the existence of on each occasion I presented it.

Instead of addressing those issues, you pretend that they never existed or were never presented to you, and resort to irrelevant and fatuous ex recto apologetic fabrication to try and prop up this diseased mythological fantasy, and moreover, try do do so by reference to yet more blind mythological assertions.

When are you going to learn, ONCE AND FOR ALL, that BLIND MYTHOLOGICAL ASSERTIONS DO NOT CONSTITUTE FACT? Step out of your complacent and duplicitous Christian Nationalist bubble once and for all, and start learning how REALITY works, instead of wasting time spooning up whatever lies on the subject you’re being fed by your “pastor” while he’s banking his “tithes” in an offshore slush fund.

Learn once and for all that your mythology inspired fantasies are garbage, and bear no relation to how reality operates. REALITY pisses on your infantile creationist fantasies from such a great height, that the piss is travelling at close to the speed of light when it lands. Indeed, I’ve already mentioned in post #744, the little matter than in order for your fantasies to be correct, basic trigonometry has to be wrong, and my response to this is “good luck with that”. Indeed, I presented in full, the paper in question via a Google Docs document here, demonstrating this.

Your sad little Jeebus fantasies don’t even rise to the level of competence to be worthy of a point of view, and the only reason we’re bothering with them, is because you’re providing us with practically the canonical pedagogical tool, with which to demonstrate that in order to be a creationist, you have to lie to everyone including yourself. Far from being an advertisement for your shitty little religion, you’re providing us with the very ammunition we need to destroy it. But I’ve noticed that creationists have a habit of being too stupid to realise this.

[skriten]

@Calilasseia

Was anyone else’s suspicions aroused, when taking a peek at that paper Quim linked to?

Yes, despite the limits of my education, my posted response: (edited for brevity)

“The paper does not support the claim.
The research, which is ongoing, indicates a possible “protective mechanism” for essential genes, altering the percentage of truly random mutations. The conclusions of the paper you cited do not make the bald claim that mutations are not random. While this is clearly a headline-grabbing claim, even if eventually supported by additional research, it indicates an additional aspect of mutation, not a completely new explanation as you so vociferously implied.
Full disclosure, I also am not an evolutionary biologist, but I can and do read, and your declarations of superiority over the entire scientific field would have to improve dramatically to reach the level of batshittery.”

While I do not possess the educational background to understand all of the research data, I do my best and can certainly ascertain misrepresentations and mischaracterizations when I see them.
I welcome any clarifying analyses your expertise can provide. 🫤

[skriten]

@Sheldon

I recognised it right off obviously.

Yeah, me too…I figured it was more in your face smugness…

[Calilasseia]

@skriten:

Ah, this takes us into the wonderful (but at times, sadly non-rigorous) world of epigenetics.

First we need a definition. Epigenetics covers the emergence of stable (and indeed, heritable) changes in an organism that do not arise from changes in a germline DNA sequence. So far, so good. But of course, the question naturally arises in the astute mind, what mechanisms underpin and facilitate said changes?.

Now on the Wikipedia page, the following factors are cited as being implicated in epigenetic change:

[1] Development (either in utero or during early childhood, or in corresponding stages in other organisms);
[2] Environmental chemicals;
[3] Pharmacoactive compounds;
[4] Aging;
[5] Diet.

However, there’s a little problem. While some well-understood mechanisms are proposed for some of these changes, others are, shall we say, left dangling in the wind a little. Furthermore, a deeper dive into some of the proposed mechanisms just cited, reveals that genetics is still underpinning said mechanisms.

Take development, for example, during which the selective silencing and activation of certain genes in certain embryonic cells, leads to the cells in question differentiating into various organs or tissues. A famous and tragic example of the disruption of this process is provided by Thalidomide, which in humans, results in gross interference with the operation of Hox genes (the genes responsible for the basic human bauplan), and generates the malformations that became a major public health scandal in the 1960s. However, I’m not aware of any literature that points to the resulting changes being heritable, and it should be obvious that questionable ethical boundaries would have to be crossed in order to determine this.

Furthermore, much of the literature on epigenetics covers, wait for it, DNA damage, which I would have thought, by definition, involved sequence changes.

One example that was presented to me some time ago as being ‘epigenetics’, was the differentiation of bee larval fates (referred to in the literature as "diphenic caste production), depending upon whether the larvae were fed “bee bread” (a mixture of pollen and other substances provided by worker adults) or “royal jelly” (a nutrient produced exclusively by queen bees). Rapamycin and FK506 pharmacology studies, along with RNAi knockdown, led to the discovery of a specific gene implicated in this process, which is selectively activated by the difference in diet. I’ll provide the relevant literature now, starting with:

The Making Of A Queen: TOR Pathway Is A Key Player In Diphenic Caste Development by Avani Patel, M. Kim Fondrk, Osman Kaftanoglu, Christine Emore, Greg Hunt, Katy Frederick, Gro V. Amdam, PLoS One, 6: e509 (June 2007), doi:10.1371/journal.pone.0000509

I quote from the paper thus:

@Patel et al (2007)

Background. Honey bees (Apis mellifera) provide a principal example of diphenic development. Excess feeding of female larvae results in queens (large reproductives). Moderate diet yields workers (small helpers). The signaling pathway that links provisioning to female developmental fate is not understood, yet we reasoned that it could include TOR (target of rapamycin), a nutrient- and energy-sensing kinase that controls organismal growth. Methodology/Principal Findings. Here, the role of Apis mellifera TOR (amTOR) in caste determination is examined by rapamycin/FK506 pharmacology and RNA interference (RNAi) gene knockdown. We show that in queen-destined larvae, the TOR inhibitor rapamycin induces the development of worker characters that are blocked by the antagonist FK506. Further, queen fate is associated with elevated activity of the Apis mellifera TOR encoding gene, amTOR, and amTOR gene knockdown blocks queen fate and results in individuals with worker morphology. Conclusions/Significance. A much-studied insect dimorphism, thereby, can be governed by the TOR pathway. Our results present the first evidence for a role of TOR in diphenic development, and suggest that adoption of this ancestral nutrient-sensing cascade is one evolutionary pathway for morphological caste differentiation in social insects.

What the authors did was to test the hypothesis that the kinase enzyme coded for by the TOR gene (in this case, the amTOR variant present in Apis mellifera) influenced development based upon environmental conditions.

Honey bee larvae are fed with a special substance known as ‘royal jelly’ for the first 48 hours of life. Those larvae destined to become workers (the majority) are then fed after this initial period with a food comprising pollen and other ingredients (nicknamed “bee bread”), and the amount of royal jelly that they receive is reduced significantly. A larva that is destined to become a queen, however, is fed royal jelly throughout its larval live in quantity. A special “queen cell” is constructed to receive the egg, the egg is laid therein, and the cell is stocked with a surplus of royal jelly (continually renewed so that the larva always has more royal jelly present than it can eat at one sitting).

Now, it turns out that the TOR pathway involves a nutrient sensitive kinase enzyme, and this has been found to be of influence in other insects in particular. That staple of genetics research, Drosophila melanogaster, was subject to TOR pathway investigation as cited by the above paper:

@Patel et al (2007)

INTRODUCTION

TOR is the central component of a conserved eukaryotic signaling pathway that regulates cell and organismal growth in response to nutrient status [1,2]. Growth rate correlates with ribosome number and metabolism, and TOR-dependent growth control in yeast and Drosophila involves transcriptional regulation of ribosomal and metabolic genes [3,4]. Suppression of the Drosophila TOR pathway results in prolonged pre-adult development and reduces larval and adult body sizes [2].

So, the authors considered it likely that the TOR pathway played at least some role in the differential development of bee larvae as described above.

@Patel et al (2007)

In sum, these signatures of experimental variation in TOR signaling strikingly resemble the naturally occurring diphenism of the highly eusocial honey bee, where two alternative female phenotypes – the reproductive queen caste and the facultatively sterile worker caste – differentiate through social manipulation of larval nutrient status [5]. Queen-destined individuals, which receive a rich diet of royal jelly as larvae, are from the 3rd instar characterized by accelerated larval growth, upregulation of larval ribosomal and metabolic gene expression, rapid pre-adult development and large body sizes [5–7]. Worker-destined larvae, which receive a moderate diet of less nutritious jelly [5], are characterized by the opposite of all of these. Moreover, honey bee queens and workers diverge in morphological characters, other than organismal size, that involve the differential growth of body parts ([5], see below).

This pattern led us to hypothesize that the evolution of caste diphenism in honey bees involved adoption of TOR signaling as an ancestral mechanism for regulation of phenotypic plasticity in response to variation in nutrient status. Consequently, honey bee caste determination was predicted to be amTOR-dependent, and queen vs. worker development to be conditional on high vs. low amTOR signaling in larvae, respectively.

So, how was this investigated?

Well, it turns out that the TOR enzyme, the nutrient sensitive kinase, is blocked by an antibiotic called rapamycin. Indeed, this property led to the TOR pathway being thus named - Target Of Rapamycin. So, one way of investigating whether or not the TOR pathway is involved in diphenic caste development is to feed queen-destined larvae with rapamycin, and see if the inhibition of the TOR pathway by rapamycin leads to worker characteristics in the adult insect. Which is exactly what happened when subject to experimental test.

@Patel et al (2007)

Here, we first use pharmacology to implicate amTOR in the differentiation of female honey bees into queens and workers. Thereafter, we establish that amTOR is expressed at higher levels in queen-destined females. Finally, we make use of amTOR RNAi combined with double RNAi controls; i) exposure to GFP double stranded RNA and ii) knockdown of the honey bee vitellogenin gene; to demonstrate that queen-fate is blocked and workers develop when amTOR activity is reduced during development. This new insight represents the first evidence for a central role of TOR in a naturally occurring diphenism.

However, the tests to implicate the TOR pathway in diphenic caste development were somewhat more sophisticated than mere rapamycin inhibition, as is described above. First, rapamycin inhibition is used to demonstrate that queen-destined larvae become workers when the TOR pathway is inhibited. Second, another antibiotic, FK506, competitively inhibits rapamycin, and leads to the restoration of the TOR pathway even in the presence of rapamycin. Therefore use of the two antibiotics can be used to provide a robust first-stage test of the connection between the TOR pathway and diphenic caste development.

@Patel et al (2007)

[b]RESULTS

The TOR inhibitor rapamycin induces worker characters in queen-destined individuals[/b]

We first exposed colony-reared queen- and worker-destined 4–5th instar larvae to treatments with rapamycin, FK506 and vehicle control (2% ethanol). Pharmacological effects in younger stages could not be examined, as treated 1–3rd instar larvae were rejected by colonies. Rapamycin and FK506 are structural analogues that compete for binding to the highly conserved FK binding protein-12 (FKBP-12). The rapamycin-FKBP-12 complex, but not the FK506-FKBP-12 complex, inhibits TOR activity and, thus, rapamycin-mediated interference with TOR signaling can be antagonized (competitively inhibited) by FK506. This approach has been used with high specificity to study TOR in insects [8]. In queen-destined individuals, rapamycin prolonged pre-adult development (ANOVA: F_2,22 = 66.0, P < 0.0001, Fig. 1a), reduced wet-weight (size) at adult emergence (ANOVA: F_2,20 = 5.75.0, P < 0.01, Fig. 1b), and caused appearance of corbicula (pollen basket), a worker-specific morphological trait, while ovarian morphology remained queen-like (ANOVA: F_2,20 = 0.17.0, P = 0.84, Fig. 1c–d; queens have much larger ovaries than workers). Nutritional manipulation of 4–5th instar larvae, e.g., by transferring queen larvae into worker diet and vice versa, leads to similar intercastes with some traits characteristic of workers and some characteristic of queens (see [9] and refs. therein). Honey bee caste differentiation is a sequential process, with ovary size determined during the 3rd larval instar, and corbicula during the 4–5th larval instars [9]. In queen-destined larvae, the TOR inhibitor rapamycin caused developmental changes toward worker characters; predictably excluding a trait determined prior to the experiment (ovary size) and including a trait determined concomitant with rapamycin treatment (corbicula).

Worker-destined individuals were not affected by rapamycin/ FK506 pharmacology (ANOVA developmental time: F_2,117 =0.51, P = 0.51; wet-weight: F_2,41 = 0.64, P = 0.53, ovariole number: F_2,43 = 1.68, P = 0.20, Fig. 1e–g), consistent with the prediction that worker determination occurs when amTOR signaling is low in larvae.

So, having established that queen fate is associated with the TOR pathway, and that the kinase enzyme is somehow responsible for determining downstream signalling of other developmental aspects of a queen adult dependent upon royal jelly nutrient levels (details of this will doubtless be the subject of future papers), the next step was to establish that queen fate was due to elevated activity of the gene in question:

@Patel et al (2007)

Queen fate is associated with elevated activity of the Apis mellifera TOR encoding gene, amTOR

Several mechanisms can influence TOR signaling [1,2]; one is the transcript level of TOR mRNA [10]. As a next step, we explored if the critical decision-point of caste determination (3rd larval instar) was characterized by variation in amTOR expression that correlated with developmental fate. Using larvae reared as queens and workers by colonies, we found that 3rd instar queen-destined females had approximately two-fold higher amTOR mRNA levels than 3rd instar worker-destined larvae (ANOVA: F_1,12 = 9.46, P < 0.01, Fig. 2a). Moreover, after larval feeding and growth were completed (spinning 5th instar), this difference in amTOR expression was no longer present (ANOVA: F_1,11 = 1.55, P = 0.24, Fig. 2b). Relative amTOR levels in larvae, therefore, are consistent with general patterns of growth [5] that characterize queen- and worker-destined individuals. Also, high vs. low amTOR activity in the 3rd instar correlate with queen vs. worker developmental fate, respectively – in agreement with the role we propose for amTOR signaling in honey bee caste determination.

So, the scientists established that elevated expression of the gene was notable in queens, and that the signalling corresponded to the results from the pharmacology manipulation experiments.

As a second test, the scientists then used gene knockdown techniques to examine the effects of eliminating the expression of the gene altogether. To ensure that this was robust, another gene knockdown was used to ensure that the intended gene knockdown technique did not influence the TOR pathway as an artifact of using RNAi knockdown, but was specific to the gene in question.

@Patel et al (2007)

amTOR gene knockdown blocks queen fate and results in workers

To test the effect of amTOR on caste development, we combined in vitro rearing of 1–5th instar larvae (i.e., removed from the colony setting) with suppression of amTOR activity by RNAi. Larvae were given a diet made primarily of royal jelly that yields up to 50% queens. Due to methodological challenges [11], in vitro rearing typically does not yield a higher proportion of queens. The amount of amTOR double-stranded RNA (dsRNA) delivered to larvae was adjusted to yield a transient two-fold reduction of amTOR levels (Fig. 2c–d, 3rd instar ANOVA: F_1,21 =32.06, P < 0.00001, Fig. 2c, vs. spinning 5th instar F_1,14 = 0.11, P < 0.75, Fig. 2d), thereby mimicking the relative expression pattern observed in colonies (Fig. 2a–b).

Initially, the same amount of dsRNA derived from green fluorescent protein (GFP) sequence was used as control. We found that suppression of amTOR activity reduced the growth of the developing larvae (ANOVA: F_1,28 = 99.29, P < 0.00001, Fig. 3a), prolonged pre-adult development (ANOVA: F_1,19 = 48.00, P < 0.00001, Fig. 3b–c), reduced wet-weight (size) at adult emergence (ANOVA: F_1,19 = 68.28, P < 0.00001, Fig. 3d), and ultimately caused all amTOR knockdowns (n = 10) to emerge with fully developed worker morphology (Fig. 3e). In the control group, the proportion of females with queen morphology was 55% (n = 11), as expected from diet alone. Remaining controls were intercastes (e.g., Fig. 3f–g), a result common with in vitro rearing [11]. Thus, in a nutritional environment that encouraged queen differentiation, a physiologically relevant suppression of amTOR activity was sufficient to silence queen development. Instead, individuals emerged with a worker morphotype.

The specificity of the effect of amTOR was tested in a control experiment where the gene vitellogenin was suppressed by RNAi. vitellogenin is transcribed in male and female honey bee larvae, and the protein is present in low amounts during larval development [12]. In adults, vitellogenin is a major yolk precursor with pleiotropic effects [13,14]. Putative roles in larvae remain unclear, but previous experiments show that vitellogenin knockdown does not obstruct normal development [15,16], suggesting that vitellogenin could serve as a valid RNAi control. Also, we verified that although amTOR RNAi reduces vitellogenin mRNA levels (ANOVA: F_1,26 = 6.07, P < 0.02, Fig. 4a) vitellogenin RNAi does not affect amTOR (for vitellogenin ANOVA: F_1,15 = 5.25 P < 0.04, Fig. 4b, vs. for amTOR F_1,41 = 0.36, P = 0.55, Fig. 4c). This information is consistent with a positive effect of TOR on vitellogenin transcription described in mosquito [8], and further shows that vitellogenin RNAi is not confounded by effects on amTOR.

In comparison to vitellogenin RNAi, amTOR RNAi reduced larval growth (ANOVA: F_1,34 = 299.20, P < 0.0001, Fig. 4d); delayed development (ANOVA: F_1,8 = 87.48, P < 0.0005, Fig. 4e), and reduced final adult size (ANOVA: F_1,8 = 28.67, P < 0.001). As observed for GFP dsRNA control (Fig. 3), vitellogenin knockdowns emerged with queen morphology; amTOR knockdowns emerged as workers (Fig. 4f–g). Thus, the blocking of queen fate that occurs after amTOR knockdown is not an artifact of RNAi.

So, what we have here is evidence that there is a genetic basis for phenotypic plasticity in Apis mellifera, leading to diphenic caste development depending upon the nutrient environment that the larva is reared in, and consequently evidence for the existence of at least one differential developmental process, based upon a specific gene, that can lead to two manifestly different outcomes in an organism on the basis of the effect of environmental influence upon that gene-driven developmental pathway. It is likely that similar interactions are going to be apposite in other developmental pathways (and in other organisms), and that it may transpire that epigenetic phenomena rest upon developmental pathways with built-in environmental cue sensitivity. Indeed, it was the investigation of the effect of the TOR pathway on Drosophila and other organisms in the first place that led to the investigation of the TOR pathway as a suitable control for diphenic caste development.

The above should prove informative with respect to some of the assertions surrounding epigenetics

[skriten]

Thanks for the response, and yes it is informative.

Edit (I’m not worthy )

[AtheistChMG]

@WhoAreYou here, have fun.

And here is an in depth explanation why we know that Genesis story has one origin and it is not even from the first hand experience. It’s just a retold story.

Irving Finkel | The Ark Before Noah: A Great Adventure

Do you think that magic is real?

[Sheldon]

Since @WhoAreYou has ignored my questions for many weeks now, I will be answering anything he posts, by repeating those questions:

So @WhoAreYou

1. How does the human genome evidence a deity, as you claimed?
2. Why is atheism almost universal among elite biologists, if as you claimed, there is evidence for a deity in their field of expertise?
3. Why do you keep claiming the Noah myth has any validity, when the geological record demonstrates unequivocally no global flood has ever occurred? (see the video posted above by @AtheistChMG.

Since he has been relentlessly dishonest in evading these responses to his claims, these questions are all he will get from now on, until he makes some effort to offer a candid answer, that does not involve deflection or whataboutism, or outright evasion. Or an admission that he has no credible or rational answer, and some acknowledgement that these claims are not just unevidenced subjective beliefs he holds, but that they are actually falsified by objective evidence.

[Calilasseia]

@Sheldon:

Of course, another tactic to watch out for, is the one I refer to as “the creationist reboot”. This particular piece of duplicity arises, whenever a body of evidence refuting a creationist assertion is presented. What then happens is that [1] the creationist refuses even to acknowledge the existence of said presentation of refuting evidence, followed by [2] the creationist waiting until he/she thinks said presentation has been forgotten by the audience, followed by the resurrection of the previously refuted assertion as if it had never been addressed.

This tactic has been on display several times here already.

[Quim]

@Tin-Man

I’m still trying my damnedest to figure out how Harley Quim thinks debunking Evolution is going to change our disbelief in any god(s).

Why are you attributing words to me that I have never spoken? You know, atheists can be just as intellectually dishonest as extremists of any religion.

@Sheldon

• Evolution is SCIENCE. are you with me so far?
• Evolution is wrong, the cheque is in the post on this one, but let’s just run with it for now.
• Evolution is science, I know, but I was worried that wasn’t sinking in, so I repeated it.
• Since evolution is wrong, and he is definitely going to show this at some point, so you might as well just accept it now. This means science is wrong.
• So anything science says that contradicts any part of religion, or just because it doesn’t evidnece any deity, doesn’t mater, because SCIENCE CAN BE WRONG SEE?
• So you’re wrong to not believe in god. Wrong wrong wrong…

No, my point is that a theory, even when tested with repeated evidence and appearing rational, may still be incorrect. This does not prove the existence of God. Rather, it demonstrates that human knowledge is more flawed and imaginative than we would prefer to acknowledge. That is the extent of it.

[Quim]

@Calilasseia

shows that far from I and others here not understanding evolution, Quim doesn’t understand evolution.

First and foremost, I want to emphasize that I am not a creationist. I want to make it clear, once again (and possibly for the fifth time), that my ideas about religion, mythology, or sentience are entirely separate from what I am currently discussing. This is merely an example highlighting how science can potentially believe in a mechanism that is flawed. The evidence lies in the fact that the simulation you provided is not generating the level of complexity that some of my simulations have achieved.

For instance, my simulations have successfully generated starfish, worms, fungi, spheres, and other naturally occurring organizational forms. What’s interesting is that this outcome was unexpected and emerged as a byproduct of employing a significantly different approach from yours.

Moreover, my simulations have been deliberately constrained to prevent excessive complexity that could overload the computer, produce an abundance of junk DNA, and occasionally duplicate the entire DNA sequence. They also demonstrate convergent evolution and neutral mutations that contribute to it. In fact, these simulations exhibit many of the phenomena observed in nature. On the other hand, your simulation is incapable of producing even a fraction of these results.

And NO… I’M NOT A GENIUS. I’m just an ordinary person who asked the right question.

Therefore, it is important to acknowledge that your model of evolution is incapable of producing the anticipated outcome when simulated.

@Calilasseia

Quim doesn’t understand evolution. Because he obviously doesn’t understand what purifying selection is. Purifying selection occurs when a gene is critical for metabolic function, and mutations disrupting that function are lethal. As a corollary, genes falling into this category have a habit of being highly conserved, and it’s no surprise that post hoc mutation rates for these genes will be observed to be lower, simply because the lethal variants have been rapidly eliminated. As a corollary, the following:

In short, the organism has the ability to control the mutation rates in different sections of the genetic code. This opens the door to a wide range of consequences that can essentially be summarized as “mutations are not entirely random.”

@Calilasseia

If I have been a peer reviewer for this paper, I’d have sent it back to the jounral editor with a substantial list of reasons for rejection.

This is a perfect example of censorship in science being used to sustain a fundamentally flawed mechanism. I kindly request that you conduct a simulation yourself to demonstrate your understanding of the functionality of evolution.

Thank you.

[Sheldon]

@Quim

@Tin-Man

I’m still trying my damnedest to figure out how Harley Quim thinks debunking Evolution is going to change our disbelief in any god(s).

Why are you attributing words to me that I have never spoken?

Liar, you claimed that evolution was incompatible with an atheistic worldview. You also claimed that core aspects of evolution were wrong, and that you knew better than “99%” of biologists, and were going to prove this, nothing on the news yet of course, quelle surprise.

@Quim

No, my point is that a theory, even when tested with repeated evidence and appearing rational, may still be incorrect.

So a straw man that no one has ever disputed. However this is also mendacious, since you claimed evolution is incorrect, and you claimed to know this, and claimed “99%” of biologists were wrong, and that you would prove it. So using the phrase “may still be incorrect” is doubly dishonest here. Why you think you can lie to us with impunity like this isn’t clear, but all anyone need do is read through your posts.

@Quim

This does not prove the existence of God.

Gerraway…

@Quim

Rather, it demonstrates that human knowledge is more flawed and imaginative than we would prefer to acknowledge.

Science and its methods are demonstrably more successful at understanding reality than the kind of unevidenced superstition you’re peddling. In fact science is demonstrably our best method by any objective margin.

@Quim

That is the extent of it.

No it wasn’t, you’re lying again.

[Cognostic]

@Quim

No, my point is that a theory, even when tested with repeated evidence and appearing rational, may still be incorrect.

So, YOu are admitting you are wrong?

[MrDawn]

@Quim

No, my point is that a theory, even when tested with repeated evidence and appearing rational, may still be incorrect.

[Whitefire13]

@Quim

No, my point is that a theory, even when tested with repeated evidence and appearing rational, may still be incorrect.

Are you using theory as in capital T, Theory, or hypothesis/papers?

This does not prove the existence of God.

Agreed

Rather, it demonstrates that human knowledge is more flawed and imaginative than we would prefer to acknowledge. That is the extent of it.

Human individuals can (and do) hold some flawed and imaginative ideas. In groups, these ideas can be re-enforced. However, the scientific method weeds and addresses many of these known flawed/biased pitfalls. That’s why it’s so rigorous

Hmmm I guess I still have to write here to post. (Flawed stupid forum techies )

[Cognostic]

@Whitefire13

Hmmm I guess I still have to write here to post. (Flawed stupid forum techies )

Essentially Quin is correct; however, he is attempting to reduce ‘theory’ to something akin to ‘common knowledge.’ Even when theories are incorrect, they rarely lose their utility. Euclidian Geometry and Non-Euclidian Geometry, Newtonian Gravity and Einstein Gravity, for examples. Any new theory must do a better job of explaining all the facts than the old theory. It is not that the theory is wrong, it is that we have found a new way to organize the facts. A way to see them differently and more encompassing. A theory is the height of scientific understanding. It is the very best we can do with our current knowledge. It is what is accepted by the best and brightest on our planet. Quin’s ‘poo-poo’ of the idea of scientific theory is not worth the page it is written on. The idea that ‘Theories change,’ or may be incorrect, is built on pure ignorance of the scientific method.

What are your degrees in Quin?