Malevolent Designer News - How Bowel Cancer Is Designed To Outwit Our Imune System

Example hematoxylin and eosin (H&E) staining for polypoid cancer

Kayhanian, H., Cross, W., van der Horst, S.E.M. et al. (2024)

Bowel cancer turns genetic switches on and off to outwit the immune system | UCL News - UCL – University College London

You're creationism's favourite invisible designer and you want to make people suffer and die from bowel cancer. So, you design a tumour that grows, spreads, and destroys essential tissues and systems. All good so far.

But there is a problem: when you designed humans you gave them an immune system to protect them from the parasites you had designed to make them sick, and this immune system can detect the bowel cancer cells and kill them!

What do you do?

Well, obviously, you design the cancer cells so they outwit the immune system you designed, and since you designed it, you know exactly what its weaknesses and vulnerabilities are.

Easy peesy! You just design the cancer cells so they switch the immune system off!

What can you tell me about the aetiology of bowel cancer in humans? The aetiology of bowel cancer, also known as colorectal cancer, involves a combination of genetic, environmental, and lifestyle factors. Here's a detailed overview:

Genetic Factors

1. Hereditary Syndromes:
   • Familial Adenomatous Polyposis (FAP): Caused by mutations in the APC gene, leading to the development of numerous polyps in the colon and rectum, which can turn into cancer if not managed.
   • Lynch Syndrome (Hereditary Nonpolyposis Colorectal Cancer, HNPCC): Caused by mutations in mismatch repair (MMR) genes (e.g., MLH1, MSH2), leading to a higher risk of colorectal cancer and other cancers.
2. Family History:
   • Individuals with a first-degree relative with colorectal cancer have a higher risk, suggesting a genetic predisposition even outside of known hereditary syndromes.
3. Genetic Mutations:
   • Sporadic mutations in genes such as KRAS, BRAF, and PIK3CA are common in colorectal cancer.
   • Microsatellite instability (MSI) and chromosomal instability (CIN) play roles in tumorigenesis.

Environmental and Lifestyle Factors

1. Diet:
   • High intake of red and processed meats has been associated with an increased risk.
   • Low fiber intake is also linked to higher incidence rates.
2. Physical Inactivity:
   • Sedentary lifestyle increases the risk, while regular physical activity is protective.
3. Obesity:
   • Increased body weight, particularly abdominal obesity, is a risk factor.
4. Alcohol Consumption:
   • High alcohol intake is associated with an increased risk of colorectal cancer.
5. Smoking:
   • Long-term tobacco use is a known risk factor.

Other Risk Factors

1. Age:
   • The risk increases with age, with most cases diagnosed in individuals over 50.
2. Inflammatory Bowel Disease (IBD):
   • Conditions like Crohn's disease and ulcerative colitis increase the risk of colorectal cancer due to chronic inflammation.
3. Diabetes:
   • Type 2 diabetes is associated with a higher risk of colorectal cancer.
4. Previous Cancer History:
   • Individuals with a history of colorectal cancer or adenomatous polyps are at increased risk for recurrence.

Molecular Pathways

1. Adenoma-Carcinoma Sequence:
   • Most colorectal cancers develop from adenomatous polyps through a series of genetic mutations and epigenetic changes.
2. Serrated Pathway:
   • Involves serrated polyps, which follow a different molecular pathway characterized by mutations in the BRAF gene and widespread DNA methylation (CIMP - CpG island methylator phenotype).
3. Microsatellite Instability (MSI):
   • A hallmark of Lynch syndrome and some sporadic cancers, involving defects in DNA mismatch repair.

Prevention and Early Detection

1. Screening:
   • Regular screening (e.g., colonoscopy, fecal occult blood test) can detect precancerous polyps and early-stage cancer, significantly reducing mortality.
2. Diet and Lifestyle:
   • A diet high in fruits, vegetables, and fiber, along with regular exercise, can reduce the risk.
   • Limiting alcohol consumption and avoiding smoking are also beneficial.

Understanding these factors is crucial for both prevention and early detection strategies, improving patient outcomes and reducing the burden of colorectal cancer.

Or that's what you would have to believe if you were an intelligent [sic] design creationist, because you believe there is only one designer capable of that degree of control over living organisms.

Yes, I know your guru, Michael J Behe tried to give you a work-around for the parasite/cancer problem by inventing the biologically nonsensical, but Bible-literalist consistent, notions of 'devolution' and 'genetic entropy', but anything which benefits the cells, in this case the cancer cells, can't be called 'devolutionary' nor the result of 'genetic entropy' from some initial perfection, because something better can't be less perfect than something worse.

So, what has this intelligent [sic] designer come up with to make its bowel cancer better at killing us in an especially nasty way?

Well, nothing actually, because what the researchers from University College London, UK (UCL) and the University Medical Centre, Utrecht, Holland, who investigated it found was that it had evolved naturally, with no evidence of magic or malevolent intent anywhere in the mindless, unplanned process.

What they found is the subject of an open access paper in Nature Genetics and a press release from UCL:

Bowel cancer turns genetic switches on and off to outwit the immune system

Bowel cancer cells have the ability to regulate their growth using a genetic on-off switch to maximise their chances of survival, a phenomenon that’s been observed for the first time by researchers at UCL and University Medical Center Utrecht.

The number of genetic mutations in a cancer cell was previously thought to be purely down to chance. But a new study, published in Nature Genetics, has provided insights into how cancers navigate an “evolutionary balancing act”.

The researchers found that mutations in DNA repair genes can be repeatedly created and repaired, acting as ‘genetic switches’ that take the brakes off a tumour’s growth or put the brakes back on, depending on what would be most beneficial for the cancer to develop.

Researchers say the findings could potentially be used in personalised cancer medicine to gauge how aggressive an individual’s cancer is so that they can be given the most effective treatment.

Cancer is a genetic disease caused by mutations in our DNA. DNA damage occurs throughout life, both naturally and due to environmental factors. To cope with this, cells have evolved strategies to protect the integrity of the genetic code, but if mutations accumulate in key genes linked to cancer, tumours can develop.

Bowel cancer is the fourth most common cancer in the UK, with around 42,900 cases a year. Though still predominantly a cancer that affects older people, cases among the under 50s have been increasing in recent decades.

Disruption of DNA repair mechanisms is a major cause of increased cancer risk. About 20% of bowel cancers, known as mismatch repair deficient (MMRd) cancers, are caused by mutations in DNA repair genes. But disrupting these repair mechanisms is not entirely beneficial to tumours. Though they do allow tumours to develop, each mutation increases the risk that the body’s immune system will be triggered to attack the tumour.

Cancer cells need to acquire certain mutations to circumvent mechanisms that preserve our genetic code. But if a cancer cell acquires too many mutations, it is more likely to attract the attention of the immune system, because it’s so different from a normal cell. We predicted that understanding how tumours exploit faulty DNA repair to drive tumour growth – whilst simultaneously avoiding immune detection – might help explain why the immune system sometimes fails to control cancer development.

Dr Marnix Jansen, senior author
UCL Cancer Institute
University College London, London, UK

In this study, researchers from UCL analysed whole genome sequences from 217 MMRd bowel cancer samples in the 100,000 Genomes Project database. They looked for links between the total number of mutations and genetic changes in key DNA repair genes.

The team identified a strong correlation between DNA repair mutations in the MSH3 and MSH6 genes, and an overall high volume of mutations.

The theory that these ‘flip-flop’ mutations in DNA repair genes might control cancer mutation rates was then validated in complex cell models, called organoids, grown in the lab from patient tumour samples.

Our study reveals that DNA repair mutations in the MSH3 and MSH6 genes act as a genetic switch that cancers exploit to navigate an evolutionary balancing act. On one hand, these tumours roll the dice by turning off DNA repair to escape the body’s defence mechanisms. While this unrestrained mutation rate kills many cancer cells, it also produces a few ‘winners’ that fuel tumour development.

The really interesting finding from our research is what happens afterwards. It seems the cancer turns the DNA repair switch back on to protect the parts of the genome that they too need to survive and to avoid attracting the attention of the immune system. This is the first time that we’ve seen a mutation that can be created and repaired over and over again, adding it or deleting it from the cancer’s genetic code as required.

Dr Suzanne E. M. van der Horst, co-author
University Medical Center Utrecht, Holland.

The DNA repair mutations in question occur in repetitive stretches of DNA found throughout the human genome, where one individual DNA letter (an A, T, C or G) is repeated many times. Cells often make small copying mistakes in these repetitive stretches during cell division, such as changing eight Cs into seven Cs, which disrupts gene function.

The degree of genetic disarray in a cancer was previously thought to be purely down to chance accumulation of mutations over many years. Our work shows that cancer cells covertly repurpose these repetitive tracts in our DNA as evolutionary switches to fine-tune how rapidly mutations accumulate in tumour cells.

Interestingly, this evolutionary mechanism had previously been found as a key driver of bacterial treatment resistance in patients treated with antibiotics. Like cancer cells, bacteria have evolved genetic switches which increase mutational fuel when rapid evolution is key, for example when confronted with antibiotics. Our work thus further emphasises similarities between evolution of ancient bacteria and human tumour cells, a major area of active cancer research.

Dr Hamzeh Kayhanian, first author
UCL Cancer Institute
University College London, London, UK

The researchers say that this knowledge could potentially be used to gauge the characteristics of a patient’s tumour, which may require more intense treatment if DNA repair has been switched off and there is potential for the tumour to adapt more quickly to evade treatment – particularly to immunotherapies, which are designed to target heavily mutated tumours.

A follow-up study is already underway to find out what happens to these DNA repair switches in patients who receive cancer treatment.

Overall our research shows that mutation rate is adaptable in tumours and facilitates their quest to obtain optimal evolutionary fitness. New drugs might look to disable this switch to drive effective immune recognition and, hopefully, produce better treatment outcomes for affected patients.

Dr Hugo J. G. Snippert, co-senior author
University Medical Center Utrecht, Holland.

This research was funded with grants from Cancer Research UK, the Rosetrees Trust, and Bowel Research UK.

Cancer’s evasion of immune system destruction is a key element of its ability to grow and spread. Understanding exactly how bowel cancers do this is crucial to optimising treatment for patients. Bowel Research UK are delighted that our funding has contributed to producing this exciting new data, and we look forward to seeing how these discoveries could change treatments for future patients.

Georgia Sturt
Research and Grants Manager at Bowel Research UK

Abstract
Mismatch repair (MMR)-deficient cancer evolves through the stepwise erosion of coding homopolymers in target genes. Curiously, the MMR genes MutS homolog 6 (MSH6) and MutS homolog 3 (MSH3) also contain coding homopolymers, and these are frequent mutational targets in MMR-deficient cancers. The impact of incremental MMR mutations on MMR-deficient cancer evolution is unknown. Here we show that microsatellite instability modulates DNA repair by toggling hypermutable mononucleotide homopolymer runs in MSH6 and MSH3 through stochastic frameshift switching. Spontaneous mutation and reversion modulate subclonal mutation rate, mutation bias and HLA and neoantigen diversity. Patient-derived organoids corroborate these observations and show that MMR homopolymer sequences drift back into reading frame in the absence of immune selection, suggesting a fitness cost of elevated mutation rates. Combined experimental and simulation studies demonstrate that subclonal immune selection favors incremental MMR mutations. Overall, our data demonstrate that MMR-deficient colorectal cancers fuel intratumor heterogeneity by adapting subclonal mutation rate and diversity to immune selection.

Main
In human cells, DNA mismatch repair (MMR) is performed by protein complexes consisting of MutL homolog 1 (MLH1) and PMS1 homolog 2 (PMS2), known as MutL_α, and MutS homolog 2 (MSH2) and MutS homolog 6 (MSH6), known as MutS_α¹. Alternatively, MSH2 can pair with MutS homolog 3 (MSH3) in a complex called MutS_β. MutS_α and MutS_β each function as DNA mismatch detection modules with partially overlapping specificities, whereas MutL_α (MLH1/PMS2) executes MMR. Although the mutagenic impact of isolated MSH6 or MSH3 loss is relatively mild, combined MSH6/MSH3 inactivation in model systems drives a robust hypermutator phenotype². Importantly, while MMR had previously been treated as a single linear pathway focused on postreplicative mismatch correction, recent studies indicate that MutSα and MutSβ also participate in the repair of endogenous mutational processes during interphase (for example, due to 5-methylcytosine deamination or oxidative damage) independent of MLH1 (refs. ^3,4,5; Fig. 1a,b). Overall, these studies suggest that MutS cooperates with MutL during canonical postreplicative repair of misincorporated bases, while MutS can liaise with other partners such as MBD4 in the interphase noncanonical repair of endogenous DNA damage.

Fig. 1: Subclonal MSH6^F1088fs and MSH3^K383fs homopolymer frameshift mutations drive increased mutation burden in the MMRd CRC GEL WGS cohort.

a, MS-instable CRC. b, The MMR system safeguards genomic integrity by detecting and repairing replication-associated mismatches (left, blue). Recent studies indicate that MutS also participates in the repair of endogenous mutational damage independent of MLH1 (right, pink). c, Volcano plot showing the relationship between MS frameshifts in individual genes and total mutation burden in multiple linear regression analysis. For each independent variable, the P value of a two-sided t-test is plotted as −log₁₀(P). Two-sided F statistic (accounting for multiple independent variables in the regression model) P = 4.2 × 10⁻⁷. d, Pie charts showing mutation categories for MSH3 (top) and MSH6 (bottom). e, Cases with MSH6^F1088fs and/or MSH3^K383fs homopolymer frameshifts (in red), and cases without such mutations (in blue) ranked by mutation burden (n = 217). Clonal alterations in MMR genes MLH1, PMS2, MSH2 and MSH6, as well as subclonal MSH6^F1088fs and MSH3^K383fs frameshift status, are indicated below. Insets show MSH6^F1088fs and MSH3^K383fs mutation variant allele fraction. Extended Data Fig. 1a–c shows analysis restricted to BRAFV600E tumors. f–h, Number of SNV (f), number of InDel (g) and total mutation burden (h) according to MSH6^F1088fs and MSH3^K383fs mutation status. Median values are represented by horizontal black lines.

Loss of MMR proficiency occurs in about 15% of colorectal cancers (CRCs) resulting in the accumulation of single-nucleotide mismatches and frameshift variants due to short insertion and deletion (InDel) mutations in repetitive homopolymer sequences⁶. In most cases, this is due to sporadic MLH1 hypermethylation. The relentless accumulation of somatic variants renders MMR-deficient (MMRd) tumors immunogenic and provokes extensive immunoediting⁷. While many of the genetic targets associated with immune escape (for example, HLA (human leukocyte antigen) complex and B2M (beta-2 microglobulin) mutations) have been characterized, the evolutionary trajectories MMRd tumors take to navigate their immune selection landscape remain unknown⁸.

Here we visualize the clonal architecture of evolving MMRd tumors to allow joint analysis of individual tumor subclones and the immune microenvironment at clonal resolution. We find that subclonal MMRd lineages harness hypermutable homopolymer sequences in MSH6 and MSH3 to adapt cellular mutation rate and mutation bias to subclonal immune selection. This strategy allows MMRd tumor subclones to engage in an evolutionary arms race with the evolving immune system and efficiently explore immune adaptation solutions while minimizing the deleterious impact of prolonged genomic hypermutation on cellular fitness.

Kayhanian, H., Cross, W., van der Horst, S.E.M. et al.
Homopolymer switches mediate adaptive mutability in mismatch repair-deficient colorectal cancer. Nat Genet (2024). https://doi.org/10.1038/s41588-024-01777-9

Copyright: © 2024 The authors.
Published by Springer Nature. Open access.
Reprinted under a Creative Commons Attribution 4.0 International license (CC BY 4.0)

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The Malevolent Designer: Why Nature's God is Not Good

This book presents the reader with multiple examples of why, even if we accept Creationism's putative intelligent designer, any such entity can only be regarded as malevolent, designing ever-more ingenious ways to make life difficult for living things, including humans, for no other reason than the sheer pleasure of doing so. This putative creator has also given other creatures much better things like immune systems, eyesight and ability to regenerate limbs that it could have given to all its creation, including humans, but chose not to. This book will leave creationists with the dilemma of explaining why evolution by natural selection is the only plausible explanation for so many nasty little parasites that doesn't leave their creator looking like an ingenious, sadistic, misanthropic, malevolence finding ever more ways to increase pain and suffering in the world, and not the omnibenevolent, maximally good god that Creationists of all Abrahamic religions believe created everything. As with a previous book by this author, "The Unintelligent Designer: Refuting the Intelligent Design Hoax", this book comprehensively refutes any notion of intelligent design by anything resembling a loving, intelligent and maximally good god. Such evil could not exist in a universe created by such a god. Evil exists, therefore a maximally good, all-knowing, all-loving god does not.

Illustrated by Catherine Webber-Hounslow.

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Refuting Creationism - What The Bible's Authors Forgot About

Aerial photograph of “funerary avenues” (foreground) and the Khaybar Oasis (background), facing south‐west.

© AAKSAK and the Royal Commission for AlUla

Location of the AlUla and Khaybar Counties, with details of the Khaybar Oasis and Volcano cores zones under the remit of RCU.

© AAKSAK and the Royal Commission for AlUla.

A struggling people languishing across barren lands? No, evidence shows life in ancient Saudi Arabia was complex and thriving

Living not a stone's throw from the Canaanite Hills where the authors of genesis made up their origin myths and filled the gaps in their knowledge and understanding with magical tales of invisible sky gods made of nothing creating things out of nothing with a few magic words, there was a thriving community of semi-nomadic farmers. These neolithic people traded extensively in the area and may even have been ancestral to the Middle Eastern pastoralists, or at least had a strong cultural influence on them.

Contrary to the Bible's authors' tales of a Universe consisting of a small, flat planet with a dome over it, being magicked up out of nothing between 6,000 and 10,000 years ago, and a global genocidal flood 4000 years ago, there were people building circular buildings in what is now North West Saudi Arabia between 6,500 and 8,000 years ago, and the remains of their dwellings show no signs of ever having been inundated.

That the Bible's authors, who had only oral traditions to go on, failed to acknowledge these near neighbours, speaks to their culturally chauvinistic parochialism and their intention to create the belief that they, and they alone, were the descendants of a magically-created first couple, created without ancestors, although they show some signs of awareness of other people in their tale of the sons of that first couple managing to find wives.

So, how do we know about these neolithic people from North West Arabia? From the artifacts and remains of buildings which would have been destroyed and swept away, or at least covered in a deep layer of fossil-bearing silt, by a global flood deep enough to cover the highest mountains in which almost every living thing perished, had it been a real event.

How these were discovered is the subject of an article in The Conversation by Jane McMahon, Research Associate, Discipline of Archaeology, University of Sydney, New South Wales, Australia. Her article is reprinted here under a Creative Commons license, reformatted for stylistic consistency:

Refuting Creationism - More On The Oldest Cave Art From 41,200 Years Before Creation Week

The oldest known cave art

Leang Karampuang in the Maros-Pangkep karst,
South Sulawesi, Indonesia

Found in a cave in Indonesia, we can now show the world’s oldest figurative art is 51,200 years old

Just a couple of days ago I wrote about the oldest known cave art, in Indonesia from 41,200 years before Creationists believe the Universe existed. As expected, this news has been completely ignored by creationists, presumably through fear of having to consider the terrifying prospect of being wrong and so not as important as they like to think they are.

Here then is an article about the discovery from The Conversation by four of the authors of the paper in Nature from Australian Universities - Adhi Oktaviana, PhD Candidate in Archaeology, Griffith University; Adam Brumm, Professor of Archaeology, Griffith University; Maxime Aubert, Professor of Archaeological Science, Griffith University and Renaud Joannes-Boyau, Professor in Geochronology and Geochemistry, Southern Cross University.

Their article is reprinted under a Creative Commons license, reformatted for stylistic consistency:

Refuting Creationism - The Swamp Monster from 300 Million BCE

Fossil Gaiasia jennyae skull and spine

Credit: C. Marsicano.

Gaiasia jennyae (artist's impression)

Credit: Gabriel Lio

Giant salamander-like creature was a top predator in the ice age before the dinosaurs - Field Museum

Way back in the 99.9975% of Earth's history that occurred before creationism's legendary 'Creation Week' with its small, flat planet with a dome over it that Creationists think was the entire universe, there was something nasty lurking in the southern swamps.

It was some 300 million years before 'Creation Week' to be approximately precise and had already made it to the apex predator of its time, strongly suggesting there were other edible things roaming the same ancient swamps.

The creature, known to science as Gaiasia jennyae was a giant amphibian, a descendant of amphibians that had been extinct for 40 million years from a phylum that was to give rise to the reptiles and eventually the dinosaurs some 40 million years later.

As an amphibian, it would have been tied to water for reproduction as its eggs were fertilised externally in water and its larval form would have lived in water, probably breathing with gills, like the tadpoles of frogs, newts, toads and salamanders of today.

It's modus operandum appears to have been a slow ambush predator, laying in a swamp with its huge mouth open ready to snap up anything that came within range with interlocking jaws and the front of its mouth bristling with large, sharp teeth that gave its prey little chance of surviving. It's skull alone was over 2 feet long and the whole creature was larger than an adult human being.

Gaiasia was a stem tetrapod, in other words it was close to creatures that had evolved from Tiktaalik, the lobe-finned fish that first crawled onto land and would later evolve into the terrestrial tetrapod vertebrates, amphibians, reptiles, birds and mammals that comprise the world's larger land animals and several aquatic species that have returned to the water.

Refuting Creationism - How A Common Bacterium Became A Dangerous Pathogen - By Evolution, Naturally

Pseudomonas aeruginosa

Pseudomonas aeruginosa

Scientists map how deadly bacteria evolved to become epidemic | University of Cambridge

Aficionados of creationism's putative intelligent designer will doubtless be thrilled to discover the imaginative lengths it's gone to to ensure as many people get sick as possible with its cleverly designed bacterium, Pseudomonas aeruginosa, which has gradually been modified over the last 200 years to make it more effective and more resistant to the antibiotics medical science has developed to protect us. There is even a strain specially 'designed' to infect children with cystic fibrosis, just to add to their suffering.

Since these modifications involve genetic mutations which improve the bacterium's ability to love and replicate, we can dismiss the scientific gibberish Michael J Behe invented to explain parasites away as 'devolutionary' and due to 'genetic entropy, since even Michael J Behe would be hard pressed to explain how an advantageous mutation can be less perfect that what went before it. Something better can't be less perfect than something less good, unless you invoke a private definition of 'perfect' that means something which can be bettered.

So, what are these changes in this dangerous pathogen that makes it a problem for people with other health conditions?

Good Riddance To Bad Rubbish - Why The 'Entitled' Sleazy Tories Lost

Kier Starmer enters No. 10 as UK Head of Government.

UK election: Tory downfall is democracy rectifying its mistakes

On July 4th 2024, the British people voted overwhelmingly to remove the Conservative Party from office after 14 years of Conservative and Conservative/Liberal Democrat coalition government. The country had had enough of the chaos, incompetence and self-serving greed, sleaze and corruption of a party of entitle rich people united only by the single slogan - "What's in it for me?"; a party that had always put self and party interest and factional infighting above the national interest, comprised of people who thought the rules were for ordinary people and shouldn't apply to them; people for whom compassion is for softies and morality is the size of the bottom line on the balance sheet.

Source: House of Commons Library

Dave, Boris and the entitled Bullingdon Boys at Oxford.

David "Call me Dave" Cameron's period in office had been a period of gratuitously cruel cuts in social services on the pretext of an internation banking collapse, while there was plenty of money to cut taxes to their rich backers. He and his Old Etonian and Oxford Bullingdon Boy pal, George Osborn, presided over a massive reduction in welfare spending which saw an increase in poverty for the first time since WWII and made food banks part of everyday life for working people and their families. As a distraction and to try to neuter the Euro-sceptic wing of his party, Cameron held a wholly unnecessary referendum on membership of the European Union which, after a spectacularly inept campaign, he lost while the referendum opened up the divisions in his party and deepened the splits, and promptly resigned to leave others to clean up the mess.

Theresa May - left to clear up Cameron's mess.

Cleaning up the mess was left to the hapless Theresa May who was handed the poison chalice of trying to negotiate a 'Brexit' agreement which included border controls, but which had no border controls between Northern Ireland and the Irish Republic in line with the Good Friday Agreement which had brought peace to Northern Ireland after 30 years of de facto civil war in the province. May also had to deliver the impossible promises made by the 'leave' faction led by another entitled Old Etonian and Bullingdon Boy, Boris Johnson, such as vast sums of additional money for the NHS that had been a major element in the 'leave’ factions campaign strategy of lies and disinformation, along with stoking up racism, Islamophobia and xenophobia against the free movement of labour within the EU.

Boris Johnson's notorious referendum bus lie.

May had emerged as the 'anyone but Boris' candidate and, despite inheriting a healthy majority from Cameron, decided to hold a general election two years before she needed to, then ran a campaign so inept that she came close to losing and ended up with needing to bribe Ulster Unionist MPs to give her a 'supply and confidence' agreement in which they agreed not to vote against her in a confidence motion or oppose the Finance Bill. Her weakness further empowered the euro-sceptic faction which had now coalesced around Boris Johnson, and which rejected any Brexit agreement which threatened to treat Northern Ireland differently to the rest of the UK, which made it impossible to reach an agreement which kept the Good Friday Agreement intact.

Refuting Creationism - Denisovans Survived In Tibet For 160,000 Years - 150,000 Of Them Before 'Creation Week'

Entrance to Baishiya Karst Cave.

Credit: Dongju Zhang’s group (Lanzhou University).

Excavations at Baishiya Karst Cave.

Credit: Dongju Zhang’s group (Lanzhou University).

Extinct humans survived on the Tibetan plateau for 160000 years - University of Reading

The problem with trying to cling to the daft notion that Earth is only 10,000 years old and that Homo sapiens didn't evolve but were magicked out of dirt without ancestors or biological relatives, is that science keeps on proving that idea wrong, by discovering other hominins and a history that occurred in that 99.9975% of Earth's history that happened before 10,000 years ago.

So, here is some more evidence for creationists to ignore, lie about or misrepresent. It concerns a population of archaic Eurasian hominin know to science as the Denisovans, which are yet to be given a definitive species name because too few remains have been discovered, other than their DNA.

Their DNA has been isolated from a finger bone discovered in the Denisova Cave in the Altai mountains of Siberia and it shows that they interbred both with Neanderthals and with early Homo sapiens as the latter spread across Asia into their range.

Refuting Creationism - Indonesian Cave Painting From 41,200 Years Before 'Creation Week' - Untouched By The 'Global Genocide'!

[left caption]

[right caption]

Oldest known picture story is a 51,000-year-old Indonesian cave painting | Archaeology | The Guardian

Another drop in the torrent of counter-evidence engulfing creationism came today with the news that a team of archaeologists led by experts from Griffith University, Australia have dated a painting found in a cave in the Indonesian island of Sulawesi, to be from at least 41,200 years before the legendary 'Creation Week'. This adds yet more data to the mountain of evidence showing the authors of Genesis didn't know what they were taking abut so just made stuff up.

To be fair to the story-tellers, how could they possibly have known about caves in Indonesia, let along what early humans had been doing in them? They thought the Universe was a small, flat place with a dome over it, centred on the Middle East.

Refuting Creationism - Now It's 60-Million-Year-Old Grape Seed Fossils!

Lithouva - the earliest fossil grape from the Western Hemisphere, ~60 million years old from Colombia. Top figure shows fossil accompanied with CT scan reconstruction. Bottom shows artist reconstruction.

Photos by Fabiany Herrera, art by Pollyanna von Knorring.

Sixty-million-year-old grape seeds reveal how the death of the dinosaurs may have paved the way for grapes to spread - Field Museum

If you're a creationist cult leader whose livelihood depends on fooling scientifically illiterate simpletons into thinking Earth is just 10,000 years old and the creation myth in the Bible is literal science and history, about the last thing you need is a bunch of paleontologists to find 60-million-year-old fossil grape seeds and publish their findings in a peer-reviewed science journal.

Actually, the publication is the least of your worries because your dupes will never read anything remotely scientific in case it makes them begin to wonder if they could be wrong, but what do you do about the 60-million-year date? You lie about the scientists, obviously.

You tell your dupes that scientists just make up dates to suit their 'anti-God' agenda because they are all part of a massive Satanic conspiracy, confident that the same thinking defect that causes creationism in an adult also causes conspiracism. So you can be sure they'll fall for it, no matter the absurdity of the idea that millions of biomedical scientists and their assistants, the managers of all the major universities and research establishment around the world, the editors of science journals and all their staff, are in on the conspiracy and never break ranks and blow the whistle on it.

Refuting Creationism - An Australian First Nation Ritual From Before 'Creation Week' and Through Creationism's Genocidal Flood

Professor Bruno David and Uncle Russell Mullett in Cloggs cave

Professor Bruno David (left) and Uncle Russell Mullett were part of a research team who excavated Cloggs Cave in Gunaikurnai Country.

Supplied: Gunaikurnai Land and Waters Aboriginal Corporation.

New archaeological find uncovers 12,000 year old First Nations ritual - Monash University

The problem with creationism's origin myths is that the people who made them up only knew of their small area around the Canaanite Hills, so they had no idea what was happening elsewhere or any history of life on Earth of other human cultures. Indeed, because they thought the entire Universe consisted of a small, flat planet with a dome over it, they didn't even suspect there might be inhabited land in a southern hemisphere of a spheroid planet.

So, news that the GunaiKurnai Land and Waters Aboriginal Corporation (GLaWAC) and Monash University researchers have unearthed evidence of rituals dating back 500 generations (i.e. 12,000 years, or 2,000 years before the Bible's authors imagined the Universe was created) and that the ritual is till used today, having survived the legendary global genocidal flood that the Bible's authors imagined, along with this archaeological evidence in a cave that would have been flooded by any such global flood, had it really happened.

Unintelligent Design - Why Do Males Have Useless Nipples? - It's Evolution, Naturally!

New mathematical model sheds light on the absence of breastfeeding in male mammals - News and events, University of York

Ask an intelligent [sic] design creationists why males have nipples, and you'll get lots of evasion and avoidance but no answer beyond mutterings about an 'ineffable god', and 'not knowing the minds of the creator', betraying the religious underpinning of creationism.

So, why exactly do males have nipples?

The answer is, of course, evolution.

Refuting Creationism - More Evidence of Endosybiosis in Progress

A group of diatoms with their fluorescently-labeled symbionts.

© Max Planck Institute for Marine Microbiology Bremen/Mertcan Esti

The rhizobial nitrogen fixing symbionts (fluorescently-labeled in orange and green using genetic probes) residing inside diatoms collected from the tropical North Atlantic. The nucleus of the diatom is shown in bright blue.

© Max Planck Institute for Marine Microbiology Bremen/Mertcan Esti

Long-standing marine mystery solved: How algae get nitrogen to grow

Readers my remeber my article about how a team of scientists have discovered a new cell organelle in the process of transforming from a free-living nitrogen-fixing bacterium to becoming an endosymbiont of a marine alga, in much the same way that cyanobacteria became the chloroplasts of plant cells and rickettsia bacteria became the mitochondria of all eukaryote cells.

Now a different team, from the Max Planck Institute for Marine Microbiology, the Alfred Wegener Institute and the University of Vienna, have reported on a similar phenomenon in the form of a bacterium closely related to the Rhizobia that form a symbiotic association with leguminous plants such as peas and bean, which has teamed up with a marine diatom. This symbiotic relationship involves the bacterium living within the single cell of the diatom, unlike the relationship between Rhizobia and legumes in which the bacteria live in special nodes on the roots of the plants, but not inside the plant cells as such.

What is the chemical pathway by which nitrogen-fixing bacteria convert atmospheric nitrogen into ammonia and nitrates? Nitrogen-fixing bacteria play a crucial role in the nitrogen cycle by converting atmospheric nitrogen (N₂) into ammonia (NH₃), which can be further converted into nitrates (NO₃⁻) by other microorganisms. The chemical pathway for nitrogen fixation primarily involves the enzyme nitrogenase, which catalyzes the reduction of atmospheric nitrogen to ammonia. Here is an overview of the pathway:

1. Nitrogen Fixation
   Nitrogenase Enzyme Complex:
   • Components: The nitrogenase complex consists of two main proteins: the iron (Fe) protein and the molybdenum-iron (MoFe) protein.
   • Reaction:
     \[ \begin{equation*} \begin{aligned} \text{N}_2 + 8H^+ + 8e^- + 16ATP & \\ \rightarrow 2NH_3 + H_2 + 16ADP + 16Pi & \end{aligned} \end{equation*} \]
   • Steps:
     1. Electron Donation: Electrons are donated from ferredoxin or flavodoxin to the Fe protein.
     2. ATP Hydrolysis: ATP binds to the Fe protein and is hydrolyzed, providing energy for the transfer of electrons.
     3. Electron Transfer: Electrons are transferred from the Fe protein to the MoFe protein.
     4. Nitrogen Reduction: The MoFe protein reduces atmospheric nitrogen (N₂) to ammonia (NH₃) in a series of steps involving the binding and reduction of N₂.
2. Ammonia Assimilation
   Once ammonia is produced, it can be assimilated into organic compounds or further processed into other nitrogenous compounds.
   
   Conversion to Nitrates
   The conversion of ammonia to nitrates occurs in two steps involving nitrifying bacteria:
   
   
   Step 1: Ammonia to Nitrite
   Bacteria Involved: Ammonia-oxidizing bacteria (AOB), such as Nitrosomonas. \[ \text{NH}_3 + \text{O}_2 \rightarrow \text{NO}_2^- + 3H^+ + 2e^- \] Step 2: Nitrite to Nitrate
   Bacteria Involved: Nitrite-oxidizing bacteria (NOB), such as Nitrobacter. \[ \text{NO}_2^- + \frac{1}{2}\text{O}_2 \rightarrow \text{NO}_3^- \]

Summary of Pathway

1. Nitrogen Fixation: Atmospheric nitrogen (N₂) is converted to ammonia (NH₃) by nitrogenase enzyme complex in nitrogen-fixing bacteria.
2. Ammonia Assimilation: Ammonia can be incorporated into organic molecules or further processed.
3. Nitrification: Ammonia is first oxidized to nitrite (NO₂⁻) by AOB and then nitrite is oxidized to nitrate (NO₃⁻) by NOB.

This pathway is essential for making atmospheric nitrogen available to plants and other organisms in a usable form, thereby sustaining the nitrogen cycle in ecosystems.

This association in the oceans accounts for the supply of fixed nitrogen in the seas which is then available for plant and ultimately animal life.

Of course, any intelligent designer would have given the diatoms the necessary genes to fix nitrogen themselves, just as it would have given legumes the same ability, but evolution, in its haphazard, unplanned and unintelligent way often produces sub-optimal, overly complex solutions to problems simply because that solution was better than what went before; there is no intelligence to think about using processes designed earlier or of the elegance of the solution.

The discovery is the subject of an open access paper in Nature and a press release from Vienna University (Universität Wien):

Long-standing marine mystery solved: How algae get nitrogen to grow

Newly discovered symbiosis between Rhizobia and diatoms could also open new avenues for agriculture

In a new study, scientists from the Max Planck Institute for Marine Microbiology, the Alfred Wegener Institute and the University of Vienna shed light on an unexpected partnership: A marine diatom and a bacterium that can account for a large share of nitrogen fixation in vast regions of the ocean. This symbiosis likely plays a key role for global marine nitrogen fixation and productivity, and thus uptake of carbon dioxide. The newly-discovered bacterial symbiont is closely related to the nitrogen-fixing Rhizobia which live in partnership with many crop plants and may also open up new avenues for engineering nitrogen-fixing plants. The results were published in the current print edition of the renowned journal Nature.

Nitrogen is an essential component of all living organisms. It is also the key element controlling the growth of crops on land, as well as the microscopic oceanic plants that produce half the oxygen on our planet. Atmospheric nitrogen gas is by far the largest pool of nitrogen, but plants cannot transform it into a usable form. Instead, some crop plants like soybeans, peas and alfalfa (collectively known as legumes) have acquired Rhizobial bacterial partners that "fix" atmospheric nitrogen into ammonium, which can be used by plants. This partnership makes legumes one of the most important sources of proteins in food production.

Yet, how marine plants obtain the nitrogen they need to grow has not yet been fully clarified. Scientists from the Max Planck Institute for Marine Microbiology, the Alfred Wegener Institute and the University of Vienna now report that Rhizobia can also form similar partnerships with tiny marine plants called diatoms – a discovery that solves a long-standing marine mystery and which has potentially far-reaching agricultural applications.

An enigmatic marine nitrogen fixer hiding within a diatom

For many years it was assumed that most nitrogen fixation in the oceans was carried out by photosynthetic organisms called cyanobacteria. However, in vast regions of the ocean there are not enough cyanobacteria to account for measured nitrogen fixation. Thus, many scientists hypothesized that non-cyanobacterial microorganisms must be responsible for the "missing" nitrogen fixation.

For years, we have been finding gene fragments encoding the nitrogen-fixing nitrogenase enzyme, which appeared to belong to one particular non-cyanobacterial nitrogen fixer but, we couldn’t work out precisely who the enigmatic organism was and therefore had no idea whether it was important for nitrogen fixation.

Marcel M. M. Kuypers, lead author
Max Planck Institute for Marine Microbiology, Bremen, Germany

In 2020, the scientists travelled from Bremen to the tropical North Atlantic to join an expedition involving two German research vessels. They collected hundreds of liters of seawater from the region, in which a large part of global marine nitrogen fixation takes place, hoping to both identify and quantify the importance of the mysterious nitrogen fixer. It took them the next three years to finally puzzle together its genome.

It was a long and painstaking piece of detective work but ultimately, the genome solved many mysteries.

Bernhard Tschitschko, first author
Max Planck Institute for Marine Microbiology, Bremen, Germany Now: Department of Microbiology
University of Innsbruck, Innsbruck, Austria.

Based on the nitrogenase gene fragment we had seen in many marine samples before, one would have expected to find this gene in a Vibrio-related organism, but by carefully piecing together the genetic information it turned out that instead, it belonged to a genome closely related to known Rhizobia, which typically live in symbiosis with legume plants.

Daan R. Speth, co-author
Max Planck Institute for Marine Microbiology, Bremen, Germany Now: Centre for Microbiology and Environmental Systems Science
Division of Microbial Ecology
University of Vienna, Vienna, Austria,

Together with its surprisingly small genome, this raised the possibility that the marine Rhizobia might be a symbiont.

The first known symbiosis of this kind

Spurred on by these discoveries, the authors developed a genetic probe which could be used to fluorescently label the Rhizobia.

This allowed us to visualize the Rhizobia directly in their native habitat - the complex environmental samples collected in the Atlantic.

Katharina Kitzinger, co-author
Max Planck Institute for Marine Microbiology, Bremen, Germany
Now: Centre for Microbiology and Environmental Systems Science
Division of Microbial Ecology
University of Vienna, Vienna, Austria.

Indeed, their suspicions about it being a symbiont were quickly confirmed.

We were finding sets of four Rhizobia, always sitting in the same spot inside the diatoms. It was very exciting as this is the first known symbiosis between a diatom and a non-cyanobacterial nitrogen fixer.

Marcel M. M. Kuypers.

The scientists named the newly discovered symbiont Candidatus Tectiglobus diatomicola. Having finally worked out the identity of the missing nitrogen fixer, they focused their attention on working out how the bacteria and diatom live in partnership. Using a technology called nanoSIMS, they could show that the Rhizobia exchanges fixed nitrogen with the diatom in return for carbon. And it puts a lot of effort into it:

In order to support the diatom’s growth, the bacterium fixes 100-fold more nitrogen than it needs for itself.

Wiebke Mohr, co-author
Max Planck Institute for Marine Microbiology, Bremen, Germany

A crucial role in sustaining marine productivity

Next the team turned back to the oceans to discover how widespread the new symbiosis might be in the environment. It quickly turned out that the newly discovered partnership is found throughout the world’s oceans, especially in regions where cyanobacterial nitrogen fixers are rare. Thus, these tiny organisms are likely major players in total oceanic nitrogen fixation, and therefore play a crucial role in sustaining marine productivity and the global oceanic uptake of carbon dioxide.

A key candidate for agricultural engineering?

Aside from its importance to nitrogen fixation in the oceans, the discovery of the symbiosis hints at other exciting opportunities in the future. Kuypers is particularly excited about what the discovery means from an evolutionary perspective.

The evolutionary adaptations of Ca. T. diatomicola are very similar to the endosymbiotic cyanobacterium UCYN-A, which functions as an early-stage nitrogen-fixing organelle. Therefore, it’s really tempting to speculate that Ca. T. diatomicola and its diatom host might also be in the early stages of becoming a single organism.

Marcel M. M. Kuypers.

Tschitschko agrees that the identity and organelle like nature of the symbiont is particularly intriguing.

So far, such organelles have only been shown to originate from the cyanobacteria, but the implications of finding them amongst the Rhizobiales are very exciting, considering that these bacteria are incredibly important for agriculture. The small size and organelle-like nature of the marine Rhizobiales means that it might be a key candidate to engineer nitrogen-fixing plants someday.

Bernhard Tschitschko

The scientists will now continue to study the newly discovered symbiosis and see if more like it also exist in the oceans.

Original publication:
Bernhard Tschitschko, Mertcan Esti, Miriam Philippi, Abiel T. Kidane, Sten Littmann, Katharina Kitzinger, Daan R. Speth, Shengjie Li, Alexandra Kraberg, Daniela Tienken, Hannah K. Marchant, Boran Kartal, Jana Milucka, Wiebke Mohr, Marcel M. M. Kuypers (2024): Rhizobia-diatom symbiosis fixes missing nitrogen in the ocean. Nature (2024) DOI: 10.1038/s41586-024-07495-w

Participating institutions:

• Max Planck Institute for Marine Microbiology, Bremen, Germany
• Alfred Wegener Institute - Helmholtz-Centre for Polar and Marine Research, Bremerhaven, Germany
• University of Vienna, Vienna, Austria

Abstract
Nitrogen (N₂) fixation in oligotrophic surface waters is the main source of new nitrogen to the ocean¹ and has a key role in fuelling the biological carbon pump². Oceanic N₂ fixation has been attributed almost exclusively to cyanobacteria, even though genes encoding nitrogenase, the enzyme that fixes N₂ into ammonia, are widespread among marine bacteria and archaea^3,4,5. Little is known about these non-cyanobacterial N₂ fixers, and direct proof that they can fix nitrogen in the ocean has so far been lacking. Here we report the discovery of a non-cyanobacterial N₂-fixing symbiont, ‘Candidatus Tectiglobus diatomicola’, which provides its diatom host with fixed nitrogen in return for photosynthetic carbon. The N₂-fixing symbiont belongs to the order Rhizobiales and its association with a unicellular diatom expands the known hosts for this order beyond the well-known N₂-fixing rhizobia–legume symbioses on land⁶. Our results show that the rhizobia–diatom symbioses can contribute as much fixed nitrogen as can cyanobacterial N₂ fixers in the tropical North Atlantic, and that they might be responsible for N₂ fixation in the vast regions of the ocean in which cyanobacteria are too rare to account for the measured rates.

Main
Nitrogen is an essential component of all living organisms and limits life in the ocean. Atmospheric N₂ gas is the largest reservoir of freely accessible nitrogen, but it is biologically available only to microorganisms that carry the nitrogenase metalloenzyme and thus can fix N₂ into ammonia⁷. Even though a wide diversity of marine bacteria and archaea encode nitrogenase, the bulk of nitrogen fixation in the ocean has been attributed to cyanobacteria (ref. ⁴ and references therein). These phototrophs are capable of both free-living and symbiotic lifestyles, and can directly or indirectly contribute to carbon fixation and export production in the regions where they are abundant, such as oligotrophic coastal waters and margins of subtropical gyres⁸. Notably, in vast regions of the ocean, such as the centres of subtropical gyres, cyanobacterial N₂ fixers are too rare to account for the measured rates of N₂ fixation. Instead, a role of non-cyanobacterial N₂ fixers has been invoked, on the basis of the abundance of nitrogenase-encoding gene sequences (nifH), most of which belong to uncultured proteobacteria (for example, refs. ^3,5,9,10,11). So far, the most frequently detected non-cyanobacterial N₂ fixer is the so-called gamma-A, named after its nifH gene phylogeny that clusters within the Gammaproteobacteria¹². This enigmatic microorganism has been shown to be distributed in most world oceans, and its potential activity has been inferred from in situ nifH transcription^13,14. To date, however, there is no proof that gamma-A fixes N₂ in situ, and essentially all aspects of its physiology remain unknown.

An N₂-fixing rhizobial diatom endophyte We investigated the role of non-cyanobacterial N₂ fixation in the tropical North Atlantic during an expedition in January–February 2020. This region is responsible for around 20% of oceanic N₂ fixation⁸, and cyanobacteria can only explain approximately half of the rates measured in the region¹⁰. We detected high N₂ fixation rates of up to 40 nmol N l⁻¹ d⁻¹ in the surface waters (Extended Data Table 1), and the presence of both cyanobacterial and heterotrophic N₂ fixers—specifically, gamma-A—was confirmed by metagenomic sequencing (Extended Data Fig. 1a). Gamma-A nifH sequences were retrieved only from the large size fraction (greater than 3 µm) suggesting particle attachment or an association with a host organism (Extended Data Fig. 1a). We recovered a near-complete metagenome-assembled genome (MAG; 1.7 Mb, 37.8% GC, 98% completion with 0% redundancy) containing the gamma-A nifH gene, as well as a complete cluster of rRNA genes (Supplementary Table 1). Although the retrieved nifH sequence clustered within the Gammaproteobacteria as previously reported^3,14,15 (Extended Data Fig. 2), both 16S-rRNA-gene-based and whole-genome-based taxonomy¹⁶ firmly placed this MAG within the alphaproteobacterial family Hyphomicrobiaceae (Fig. 1a). This family belongs to the order Rhizobiales, which comprises the prominent rhizobial symbionts of nodule-forming terrestrial legumes^6,17,18. In addition to nifH, most other genes of the nif regulon are of gammaproteobacterial origin, including nifD and nifK, which encode the catalytic component of the nitrogenase; nifE, nifN and nifB, which encode the iron-molybdenum cofactor assembly proteins; and nifS, which is involved in metallocluster biosynthesis (Extended Data Fig. 2a). Almost all other genes in the gamma-A MAG are of alphaproteobacterial origin (Supplementary Table 1). On the basis of these results, we conclude that the gamma-A N₂ fixer is, in fact, an alphaproteobacterium that has acquired its nitrogenase genes through horizontal gene transfer from a gammaproteobacterial donor. Besides gamma-A, several other bacteria, including members of the order Rhizobiales, obtained their nitrogenase genes through horizontal gene transfer from a gammaproteobacterial donor (Extended Data Fig. 2b). Such horizontal gene transfer across classes, resulting in the acquisition of nitrogenase genes, has been reported previously for other N₂ fixers^19,20.

Fig. 1: Phylogeny and visualization of Candidatus Tectiglobus diatomicola and its diatom host.

a, Maximum likelihood phylogenetic tree of concatenated bacterial marker genes from the order Rhizobiales, showing the placement of Ca. T. diatomicola within the Hyphomicrobiaceae family (see Methods). The novel genus Ca. Tectiglobus, comprising Ca. T. diatomicola and its closest relative Ca. T. profundi, is highlighted in pink. Families within the Rhizobiales that contain known N₂-fixing legume symbionts and their exemplary host plants are shown. The order Parvibaculales was used as an outgroup. Black dots indicate more than 95% bootstrap support. Scale bar indicates amino acid substitutions per site. Plant icons were designed by Freepik (Neptunia oleracea) or created with BioRender.com. b,c, False coloured scanning electron microscopy (SEM) image (b) and confocal laser scanning microscopy image (c) of a Haslea diatom. Four Ca. T. diatomicola cells (pink, overlay of Hypho1147 and Hypho734 fluorescence in situ hybridization (FISH) probes; Extended Data Table 2) were detected next to the host nucleus (white; stained with DAPI). Scale bars, 5 µm.

We name the newly discovered species ‘Candidatus Tectiglobus diatomicola’ within a novel genus ‘Candidatus Tectiglobus’ (see Methods for etymology). One other marine MAG from the North Pacific, which we now name ‘Candidatus Tectiglobus profundi’, is affiliated with this novel genus, with 72% average amino acid identity with Ca. T. diatomicola (Supplementary Methods). Compared with their closest relative, a MAG from the Mediterranean Sea, both Ca. Tectiglobus species have a substantially reduced genome size (around 1.7 Mb versus around 5 Mb) and a strongly decreased GC content (around 38% versus around 54%) (Extended Data Fig. 3), which are features typical of endosymbionts²¹. Notably, a similar reduction in genome size and GC content is observed for the N₂-fixing cyanobacterial endosymbiont Candidatus Atelocyanobacterium thalassa, or UCYN-A, which lives in symbiosis with a haptophyte alga^22,23. Thus, the genome properties of Ca. T. diatomicola, together with its presence in the large size fraction, strongly indicate a host-associated lifestyle.

A couple of points here for creationists to ignore or lie about:

• The authors show no doubts that this is an evolutionary process and show no evidence of adopting creationist superstition as a better explanation.
• The endosymbionts have a much reduced genome compared to their free-living relatives, showing that their evolution has involved a loss of genetic information typical of both endosymbionts and endo-parasites, despite the creationist assertion that a loss of genetic information is either fatal or 'devolutionary' [sic]
• This process illustrates the processes involved in the earlier evolution of biodiversity which produced eukaryote cells from associations of prokaryotes, which itself illustrates how 'selfish' genes form co-operative alliances with other 'selfish' genes, despite creationists assertions that selfish genes can only produce selfish individuals.