Wednesday, 20 July 2022

Malevolent Designer News - Why Creationism's Divine Malevolence Gave Us Junk DNA

‘Junk’ DNA could lead to cancer by stopping copying of DNA - The Institute of Cancer Research, London

Creationists hate junk DNA because no intelligent designer would have included lots of DNA that does nothing apart from being replicated endlessly in every cell and passed on to each new generation. They also hate it because it contains 'fossil' relics from our remote ancestors and we share much of it with our close relatives, so it is very compelling evidence for evolution and common descent. The third reason they hate it is because it is available to mutate and occasionally give rise to new genetic 'information' when Creationist dogma says that no new genetic information can arise because of the Second Law of Thermodynamics' [sic].

So, creationist frauds put a great deal of effort into trying to debunk the idea that junk DNA really does do nothing. For that reason they should welcome this piece of research that shows that, far from doing nothing, junk DNA may actually cause cancer.

Yep! You read that right. Creationists such as Michael J. Behe will often use examples that, if they were intelligently designed, would portray the designer as a malevolent sadist who invents way to make his creation suffer.

For example, Behe has used both the flagellum of the bacteria Escherichia coli (E. coli) which better equips it for causing food poisoning, and the resistance of the Plasmodium parasites that cause malaria to the drugs used to prevent it, as examples of 'irreducible complexity' which he claims must have been designed, so Creationists are used to portraying their putative creator as an evil sadist. The fact that, if we subscribe to their superstition and apply their logic we have here an example of their god deliberately causing cancers, should come as no surprise.

This is because the Discovery Institute was founded as a fundamentally anti-science cult, rather than a pro-Christian cult. It has just parasitised evangelical Christianity as a vehicle for its anti-science propaganda because there is a target audience full of fearful, superstition and scientifically illiterate dupes who believe in magic and like to think they have a close personal relationship with the creator of the Universe who made it all just for them. It has always been more important to the Deception Institute to rubbish science and spread anti-science propaganda than to promote a god. Their primary objective is to destroy public confidence in science rather than to promote Christianity, as was shown in their strategic plan – the Wedge.


Further reading:
The Wedge (PDF). The Strategy document of the Discovery Insitute, to destroy American public confidence in science and replace it with Christian fundamentalism as a prelude to establishing a fundamentalist theocracy in the USA.


What the scientists at the Chester Beatty Laboratories, London, have discovered that should thrill creationists, is that Junk DNA may interfere with DNA replication in cells, so giving rise to cancer cells. Basically, because multicellular organisms such as humans, use the same method of cell replication as was used by remote single-celled organisms, the entire genome is replicated in every one of something like 17 trillion cells that make up the adult human body, even though only a fraction of it is going to be needed in the specialised cells of a multi-cellular organism, so the probability of something going wrong and producing a cancer is already very high.

As the ICR news release explains (incidentally, that the Institute for Cancer Research, not the Institute for Creation Research, which doesn't actually do any research and has no laboratories):
Scientists have found that non-coding ‘junk’ DNA, far from being harmless and inert, could potentially contribute to the development of cancer.

Their study has shown how non-coding DNA can get in the way of the replication and repair of our genome, potentially allowing mutations to accumulate.

It has been previously found that non-coding or repetitive patterns of DNA – which make up around half of our genome – could disrupt the replication of the genome.

But until now scientists have not understood the underlying mechanism, or how it could contribute to cancer’s development.

Reconstituting DNA replication in a test tube

In the new study, scientists at The Institute of Cancer Research, London, reconstituted the entire process of DNA replication in a test tube in order to understand it more completely.

The researchers were able to describe how repetitive patterns of DNA are copied during replication and how they are able to stall replication entirely – increasing the risk of errors that can be an early driver of cancer. This vital knowledge may eventually lead to better drugs and treatments.

The researchers believe the work could also help to improve the diagnosis and monitoring of some cancers, such as bowel cancer, where common errors in copying the repetitive sequences of DNA indicate whether cancer is progressing.

The study, published in Nature Communications, was funded by Wellcome and the Royal Society, with additional support from The Institute of Cancer Research (ICR) itself.

DNA replication errors trigger damage response

Scientists at the ICR – a charity and research institute – found that when the DNA replication machinery encountered repetitive DNA, it was able to unwind the DNA strands, but it sometimes failed to copy the opposite DNA strand. This error could cause replication to stall, resulting in collapse of the replication machinery in a manner similar to that induced by DNA damage.

The findings lead scientists to believe that repetitive DNA sequences could trigger a damage response signal indicating that errors in DNA replication have occurred and require repair.

DNA damage and ensuing genome instability are known to promote cancer formation and progression, so the research strengthens the link between junk DNA and cancer.

It was scientists at the ICR who, in the 1960s, provided the first conclusive evidence that DNA damage is the fundamental cause of cancer. In the early 2000s, ICR researchers then showed that drugs called PARP inhibitors could be genetically targeted against cancers with DNA repair mutations.

Our researchers now hope that improved understanding of DNA replication, and how it can go wrong, might lead to new ways of treating the disease.

Junk DNA plays an important role

Study leader Dr Gideon Coster, Team Leader in Genome Replication at The Institute of Cancer Research, London, said:

We wanted to understand why it seems more difficult for cells to copy repetitive DNA sequences than other parts of the genome. Our study suggests that so-called junk DNA is actually playing an important and potentially damaging role in cells, by blocking DNA replication and potentially opening the door to cancerous mutations.

We now believe that repetitive DNA sequences trigger a response that is very similar to the one induced by DNA damage, which we know can lead to cancer. Our study therefore fundamentally advances our understanding of cancer, and I’m hopeful it will help us come up with new treatments in the future.

Exploiting fundamental weaknesses in cancer

Professor Kristian Helin, Chief Executive of The Institute of Cancer Research, London, said:

This study helps to unravel the puzzle of junk DNA – showing how these repetitive sequences can block DNA replication and repair. It’s possible that this mechanism could play a role in the development of cancer as a cause of genetic instability – especially as cancer cells start dividing more quickly and so place the process of DNA replication under more stress.

Understanding the mechanisms underlying genetic mutation and instability is critical if we are to find innovative new ways to treat cancer that exploit fundamental weaknesses in cancer cells.

Copyright: © 2022 The authors.
Published by Springer Nature Ltd. Open access. (CC BY 4.0)
The ICR team's paper is published, open access, in the journal, Nature Communications. In the abstract the scientists say:
Abstract

Accurate chromosomal DNA replication is essential to maintain genomic stability. Genetic evidence suggests that certain repetitive sequences impair replication, yet the underlying mechanism is poorly defined. Replication could be directly inhibited by the DNA template or indirectly, for example by DNA-bound proteins. Here, we reconstitute replication of mono-, di- and trinucleotide repeats in vitro using eukaryotic replisomes assembled from purified proteins. We find that structure-prone repeats are sufficient to impair replication. Whilst template unwinding is unaffected, leading strand synthesis is inhibited, leading to fork uncoupling. Synthesis through hairpin-forming repeats is rescued by replisome-intrinsic mechanisms, whereas synthesis of quadruplex-forming repeats requires an extrinsic accessory helicase. DNA-induced fork stalling is mechanistically similar to that induced by leading strand DNA lesions, highlighting structure-prone repeats as an important potential source of replication stress. Thus, we propose that our understanding of the cellular response to replication stress may also be applied to DNA-induced replication stalling.

Of course, these sorts of problems are the consequence of a utilitarian 'design' process which has no plan and no ultimate purpose in mind. This particular problem is a direct consequence of the fact that, as living organisms evolved from single-celled to multicellular organisms, they retained exactly the same mechanism for cell replication, which includes replicating the entire genome in every cell, and a consequence of the fact that, over many million years and trillions of iterations of the cycle of reproduction and filtering through the sieve of selection, there is no mechanism for correcting the errors in replication that give rise to duplication of whole chunks of DNA which are then free to mutate without loss of function, and so accumulate as non-coding regions, or 'junk' DNA.

Nor is there a reliable mechanism for removing the remnants of ancient retrovirus DNA that has become included in the genome and accumulated over time as 'junk'. The fact is that DNA replication is not a perfect system, hence we have mutations on which natural selection can operate to give evolution. None of this would be the case if living organisms were the design of an omniscient creator, unless that creator intentionally included the mechanisms for causing cancer in its designs.

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