F Rosa Rubicondior: Epigenetics
Showing posts with label Epigenetics. Show all posts
Showing posts with label Epigenetics. Show all posts

Sunday 10 March 2024

Unintelligent Design - How Epigenetic Settings Are Passed To Daughter Cells - Even William Heath Robinson Would Be Impressed


Cracking Epigenetic Inheritance: HKU Biologists Discovered the Secrets of How Gene Traits are Passed on - Press Releases - Media - HKU

It all started when single-celled organisms started to form colonies of like-minded individuals. The easiest way to do it was for the two daughter cells of a dividing cell to stick together instead of going their own way. They in turn would have had more daughter cells until they formed large clump of cells, but, unless the cells began to perform distinct functions, there was no advantage to forming clumps like that instead of each cell going its own way and fending for itself. Fortunately, there were no large predators around, otherwise a clump of cells would have made a tasty snack and the whole idea would have been abandoned as too risky by half, and we would be stuck now with a world of single-celled organisms and nothing else.

However, with the trial and error which characterises biological development, some of the cells in the clump began to perform specialist functions. For example, as the clump got larger, specialist cells would have been needed to exchange gasses with the environment or the cells at the centre would have been deprived of oxygen and their waste in the form of carbon dioxide would have accumulated because diffusing across a large mass of cells would be too slow to keep up with production and the supply of oxygen would be too slow to keep up with the demand. The same thing applied to getting nutrients into the center of the clump.

So, the clumps which had specialist cells fared better in the competition for resources than those which were just undifferentiated clumps. In fact, the clumps with specialised cells would probably have eaten the undifferentiated clumps and become predators. And with predators there was pressure for increased specialisation for movement, ingestion and excretion, for more efficient respiration and for reproduction. And predation also produced pressure for more motility, for senses like sight and smell and maybe hearing and as the organisms became more complex so they needed nervous systems to coordinate their activities and process and respond to the stimuli their senses were receiving from their environment and some would have evolved defensive armour such as scales and spikes and hard shells and internal structures like cartilage and bone to give their bodies shape and form and to make their swimming apparatus stiffer and more powerful.

But what they never managed to do was find a different way to produce all the different specialist cells by a different method to that used by their single-celled ancestors, so every cell in their body had the full genome whether they needed it or not, and more often than not, they didn't need most of it. A bone cell doesn't need to do what a nerve cell does, and a nerve cell doesn't need to do what a muscle cell does, and neither muscle nor nerve cells need to make bone, and what else needs to make elbow skin other than an elbow skin cell, except perhaps a scrotum skin cell? Yet they all have the genes for doing everything any one cell needs to do.

So, cue creationism's intelligent [sic] designer who has been designing and modifying all these different clumps of specialised cells but who, for some reason, seems incapable of recognising that its designs are heading for disaster unless it can think up a way to make sure each specialised cell has only the genes it needs. For reasons which no creationist apologist has ever managed to explain, their putative designer always behaves as though it can't undo a bad design and start again but is compelled to try to make the best of what it has muddled through with so far. In every way, creationism’s 'intelligent [sic] designer' behaves just like a mindless process operating without a plan, handicapped by acute amnesia, and constantly surprising itself with a new problem it designed just yesterday.

Just like the eccentric British designer and cartoonist, William Heath Robinson, no solution to a problem can be too complex even if it creates a new problem for which another overly complex solution has to be found. Unlikely objects, designed for a completely different purpose, will be pressed into service; a stepladder will be balanced precariously on top of a piano and an umbrella will be used to push a button when prodded by a sink plunger swinging on a length of knotted string. A labour-saving device for peeling potatoes will take half a dozen, intense and serious-looking men to operate it and peeling the potatoes will take considerably longer than had each man been given a potato peeler and left to get on with it. Eggs will be fried in a frying pan held over a candle lit by a match rubbed against a matchbox which swings into action when released by a lever when the scuttle-full of coal, or the boulder suspended on knotted string, lands on it.
Every hot-air ballon will have had several leaks mended with patches in a different fabric as will every set of bellows used to blow out the candle at the right time or make the fire burn up when needed to make the hot air balloon rise, which will be held down by a coal-scuttle full of coal until a man with nothing else to do, cuts the string with a pair of scissors when prodded in the back by an umbrella operated by a wheel with broken spokes joined together with sticks tied on with more string or held together with bent nails.

And the whole 'irreducibly complex', 'intelligently designed' machine would fail if just one component was taken away or a piece of knotted string broke.
So, what did creationism's intelligent designer produce to solve the problem of too many genes for the specialised cells? It produced the overly complex solution of epigenetics of course! There was no going back and starting again for our intrepid, muddle through, mend and make do, near-enough-is-good-enough utilitarian designer. Going back and starting again would have been far too simple.

So complex is this system, that a team of researchers has only just worked out how cells pass on their epigenetic settings to their daughter cells.

Their findings are the subject of a paper in Nature and a news release from the University of Hong Kong:

Figure 2.The cryo-EM structure of the yeast replisome in complex with FACT and parental histones (A) and its atomic model (B).
Modified from Li et al, Nature (2004)
Figure 2. The cryo-EM structure of the yeast replisome in complex with FACT and parental histones (A) and its atomic model (B).
Modified from Li et al, Nature (2004)
A research team led by Professor Yuanliang ZHAI at the School of Biological Sciences, The University of Hong Kong (HKU) collaborating with Professor Ning GAO and Professor Qing LI from Peking University (PKU), as well as Professor Bik-Kwoon TYE from Cornell University, has recently made a significant breakthrough in understanding how the DNA copying machine helps pass on epigenetic information to maintain gene traits at each cell division. Understanding how this coupled mechanism could lead to new treatments for cancer and other epigenetic diseases by targeting specific changes in gene activity. Their findings have recently been published in Nature.

Background of the Research

Our bodies are composed of many differentiated cell types. Genetic information is stored within our DNA which serves as a blueprint guiding the functions and development of our cells. However, not all parts of our DNA are active at all times. In fact, every cell type in our body contains the same DNA, but only specific portions are active, leading to distinct cellular functions. For example, identical twins share nearly identical genetic material but exhibit variations in physical characteristics, behaviours and disease susceptibility due to the influence of epigenetics. Epigenetics functions as a set of molecular switches that can turn genes on or off without altering the DNA sequence. These switches are influenced by various environmental factors, such as nutrition, stress, lifestyle, and environmental exposures.

In our cells, DNA is organised into chromatin. The nucleosome forms a fundamental repeating unit of chromatin. Each nucleosome consists of approximately 147 base pairs of DNA wrapped around a histone octamer which is composed of two H2A-H2B dimers and one H3-H4 tetramer. During DNA replication, parental nucleosomes carrying the epigenetic tags, also known as histone modifications, are dismantled and recycled, ensuring the accurate transfer of epigenetic information to new cells during cell division. Errors in this process can alter the epigenetic landscape, gene expression and cell identity, with potential implications for cancer and ageing. Despite extensive research, the molecular mechanism by which epigenetic information is passed down through the DNA copying machine, called the replisome, remains unclear. This knowledge gap is primarily due to the absence of detailed structures that capture the replisome in action when transferring parental histones with epigenetic tags. Studying the process is challenging because of the fast-paced nature of chromatin replication, as it involves rapid disruption and restoration of nucleosomes to keep up with the swift DNA synthesis.

In previous studies, the research team made significant progress in understanding the DNA copying mechanism, including determining the structures of various replication complexes. These findings laid a solid foundation for the current research on the dynamic process of chromatin duplication.

Summary of Research Findings

This time, the team achieved another breakthrough by successfully capturing a key snapshot of parental histone transfer at the replication fork. They purified endogenous replisome complexes from early-S-phase yeast cells on a large scale and utilised cryo-electron microscopy (cryo-EM) for visualisation.

They found that a chaperone complex FACT (consisting of Spt16 and Pob3) interacts with parental histones at the front of the replisome during the replication process. Notably, they observed that Spt16, a component of FACT, captures the histones that have been completely stripped off the duplex DNA from the parental nucleosome. The evicted histones are preserved as a hexamer, with one H2A-H2B dimer missing. Another protein that involved in DNA replication, Mcm2, takes the place of the missing H2A-H2B dimer on the vacant site of the parental histones, placing the FACT-histone complex onto the front bumper of the replisome engine, called Tof1. This strategic positioning of histone hexamer on Tof1 by Mcm2 facilitates the subsequent transfer of parental histones to the newly synthesised DNA strands. These findings provide crucial insights into the mechanism that regulates parental histone recycling by the replisome to ensure the faithful propagation of epigenetic information at each cell division.

This study, led by Professor Zhai, involved a collaborative effort that spanned nearly eight years, starting at HKUST and concluding at HKU. He expressed his excitement about the findings, ‘It only took us less than four months from submission to Nature magazine to the acceptance of our manuscript. The results are incredibly beautiful. Our cryo-EM structures offer the first visual glimpse into how the DNA copying machine and FACT collaborate to transfer parental histone at the replication fork during DNA replication. This knowledge is crucial for elucidating how epigenetic information is faithfully maintained and passed on to subsequent generations. But, there is still much to learn. As we venture into uncharted territory, each new development in this field will represent a big step forward for the study of epigenetic inheritance.’

The implications of this research extend beyond understanding epigenetic inheritance. Scientists can now explore gene expression regulation, development, and disease with greater depth. Moreover, this breakthrough opens up possibilities for targeted therapeutic interventions and innovative strategies to modulate epigenetic modifications for cancer treatment. As the scientific community delves deeper into the world of epigenetics, this study represents a major step towards unravelling the complexities of replication-coupled histone recycling.

About the Research Team

Apart from Professor Yuanliang Zhai’s lab, the research team also includes Professor Xiang David Li from Department of Chemistry of HKU, Professor Yang Liu and Professor Keda Zhou from School of Biomedical Sciences of HKU, Professor Shangyu Dang from Division of Life Science of HKUST, and others. Learn more about Professor Yuanliang Zhai’s work and his research team: https://www.scifac.hku.hk/people/zhai-yuanliang or https://zhai95.wixsite.com/mysite-1

Co-authors include Mr Yuan Gao, Mr Jian Li, Dr Zhichun Xu from School of Biological Sciences (SBS) of HKU; Dr Ningning Li, Ms Yujie Zhang, Dr Jianxun Feng from School of Life Sciences of PKU, Dr Daqi Yu and Dr Jianwei Lin from Department of Chemistry of HKU, and Dr Yingyi ZHANG from Biological Cryo- EM Center of HKUST.

The journal paper can be accessed here: https://www.nature.com/articles/s41586-024-07152-2

Abstract

In eukaryotes, DNA compacts into chromatin through nucleosomes1,2. Replication of the eukaryotic genome must be coupled to the transmission of the epigenome encoded in the chromatin3,4. Here we report cryo-electron microscopy structures of yeast (Saccharomyces cerevisiae) replisomes associated with the FACT (facilitates chromatin transactions) complex (comprising Spt16 and Pob3) and an evicted histone hexamer. In these structures, FACT is positioned at the front end of the replisome by engaging with the parental DNA duplex to capture the histones through the middle domain and the acidic carboxyl-terminal domain of Spt16. The H2A–H2B dimer chaperoned by the carboxyl-terminal domain of Spt16 is stably tethered to the H3–H4 tetramer, while the vacant H2A–H2B site is occupied by the histone-binding domain of Mcm2. The Mcm2 histone-binding domain wraps around the DNA-binding surface of one H3–H4 dimer and extends across the tetramerization interface of the H3–H4 tetramer to the binding site of Spt16 middle domain before becoming disordered. This arrangement leaves the remaining DNA-binding surface of the other H3–H4 dimer exposed to additional interactions for further processing. The Mcm2 histone-binding domain and its downstream linker region are nested on top of Tof1, relocating the parental histones to the replisome front for transfer to the newly synthesized lagging-strand DNA. Our findings offer crucial structural insights into the mechanism of replication-coupled histone recycling for maintaining epigenetic inheritance.

This Heath-Robinson solution to a problem which no intelligent designer would design in the first place, is repeated in every one of your 17 trillion cells and in every cell of every multicellular organism on the planet. A hugely wasteful and error-prone, needlessly complex system of which any intelligent designer would be ashamed, but which creationist frauds fool their ignorant dupes into believing is evidence of intelligence. In reality of course, it's evidence of exactly the opposite.

It's not even humorous and entertaining like William Heath-Robinson's ridiculously complicated, irreducibly complex, machines.

Tuesday 6 February 2024

Unintelligent Design - How Scientists Are Learning to Do What Creationism's 'Intelligent' Designer Found Too Difficult - Or Didn't Want To Do!


The proteins needed to create limb progenitor cells are marked with different colors under a microscope.
Images: Yuji Atsuta/Tabin lab
The Surprisingly Simple Recipe for Starting to Grow a Limb | Harvard Medical School

Visit any site of a supposed Marian miracle, such as Lourdes, now selling 'miracle cures' that almost never work and those that do can be attributed to the medication the pilgrim was receiving prior to the visit, or to spontaneous regression, the placebo effect or a psychosomatic condition, and you may find lots of crutches supposedly left there as testament to the cure of mobility disorders, but what you will never find is the artificial limb discarded by someone who had a spontaneous regeneration of an amputated limb.

Or visit any of the lucrative travelling, carefully stage-managed 'faith healing circuses' where people appear to be 'cured' of all manner of ailments at the touch of a 'healer', who, for perhaps obvious reasons, never works in a hospital, and you will never witness the regeneration of a limb, or even part of a limb. Not even a finger or toe.

And before some-one cites, the 'Miracle of Calanda', this is such an obvious hoax that it's a miracle anyone believes it.

Despite having allegedly created a universe from nothing and all living things from dirt, creationism's god appears to be incapable, even with the help of his miracle-working mother, to be able to regrow a human limb.

The problem is one of the designer's own making (if you believe creationists) because it would involve the epigenetic resetting of the cells at the end of the stump, so they become stem cells again, capable of making all the different specialist cells in a limb, like bone, muscle, skin, nerves and blood vessels and growing to the right shape in the right place. That was a once-only ability in the developing embryo.

Epigenetics, as I have written about many times, is necessary because the cells of a multicellular organism replicate the same way our single-celled ancestors did - by replicating the entire genome every time in every daughter cell. But the benefit of multicellularity is that cells are specialised so only need a few genes, not the entire genome and having the wrong genes active in a specialist cell would be detrimental, so most of them need to be switched off by the epigenetic system. A problem which could have been avoided by any omniscient, omnipotent designer by just replicating those genes that were going to be needed by the specialist cells, but not something a mindless, natural process with no foresight, no reverse gear and no means of scrapping a bad design and starting again, could have avoided.

And yet medical scientists investigating the problem believe they have discovered the basic principles involved, which turn out to be "surprisingly simple", so well within the capabilities of even creationism's rather limited god.

The scientists, led by Harvard Medical School geneticists, have published their findings in an open access paper in a Cell Press journal, Developmental Cell and explain it in a Harvard Medical School news release by Stephanie Dutchen:

Saturday 3 February 2024

Unintelligent Design News - Why Women Are More Prone To Lupus Than Men - Evolution, Or Does Creationism's God Just Hate Women More?


The classic 'butterfly rash' of systemic lupus erythematosus (SLE)
Lupus and other autoimmune diseases strike far more women than men. Now there's a clue why

In my days as an operational paramedic, I once had to move a 26 your old women to hospital because lupus had made her so ill her blood pressure was below the safe level to maintain her renal function.

It was so low I couldn't even sit her up to carry her down stairs without her losing consciousness, so I had to run a couple of units of IV fluid into her to bring it up enough to make it safe to move her. She really was profoundly ill and at death's door. But such was the nature of the profession that, having delivered her safely to hospital and handed her over to the care of doctors and nurses, that was the end of my role in her care, so I never heard the outcome.

The autoimmune condition, lupus erythematosus, is caused by a malfunction of the immune system in which something triggers it to turn against the sufferer's own body instead of the invasive pathogens from which it has evolved to protect us. Although, of course, a creationist would hotly dispute the idea that a system like our immune system evolved at all, and would insist that it was intelligently [sic] designed by their favourite, evidence-free, supernatural deity without whom nothing can be created, presumably because they believe chemistry and physics don't know how to behave without a magic god telling them.

But an intelligently-designed immune system would only malfunction and turn against the person it is supposedly designed to protect if it were either incompetently designed or malevolently designed and is doing what it was designed to do - randomly increasing the suffering in the world. The evidence is that lupus is far more common in women than in men by a ratio of 9:1, which begs the question, does the designer just hate women more than men or was he more diligent when designing men's immune system then when designing women's?

The answer, as anyone who understands anatomy and physiology and particularly, evolution, will tell you, is that as an evolved system, we can expect compromises and a lack of perfection because evolution is a utilitarian process with no foresight and no reverse gear, so we are stuck with a sub-optimal immune system that evolved in an ancient ancestor, maybe even a pre-vertebrate ancestor. Certainly, all known vertebrates have one, and some, like that of bats, is far superior to ours.

Now a team of researchers at Stanford University School of Medicine, Stanford, CA, USA have worked out why lupus is far more common in women than men. Ther results are published, open access, in Cell and explained in a Stanford Medical news release. But first, a little AI background:

Sunday 28 January 2024

Unintelligent Design - How A Virus Saved The Unintelligent Designer's Blushes Early In Multicellular History


A virus that infected animals hundreds of millions of years ago has become essential for the development of the embryo

I've remarked before how similar biological systems are to the machines the late William Heath Robinson designed for solving simple, everyday problems. Simple solutions were eschewed for more complicated ones and unlikely items were used in ways they weren't intended for, such as a grandfather clock standing on a piano to support a platform balanced on top. Everything was held together by pieces of knotted string and labour-saving devices took far more people than would have been needed to do the job more simply.

And yet, the whole contraption worked, or at least looked as though it would if were ever made, but take any part away and the whole thing would fail, in an example of what creationists call 'irreducible complexity'.

So, let's pretend that creationism's, 'intelligent'[sic] designer really is behind the design of living organisms and see how closely Heath Robinson unwittingly parodied it:
Just such an example of a Heath Robinson machine in biology was revealed a few days ago in an open access paper published in Science Advances, explaining how a virus which became incorporated in the genome of an early multicellular organism provided a solution to a problem of the designer's own making. The problem it solves was how to overcome the problem created by choosing the same method of cell replication in multicellular organisms that single-celled organisms use, where the entire genome needs to be replicated at each division.

The entire 'point' of multicellularity, and what gave it its success over single-celled organisms is division of labour, in other words, specialisation, so the organisms can be divided into tissues and organs that perform a specialised task. This means that every cell has to have the potential to carry out every function, in the genes it inherits from its parent cell, yet only a few genes are need for its particular specialty.

The process by which this is achieved is the complicated epigenetic system which turns off unneeded genes as the cells differentiate into different cell lines in the developing embryo, and these settings can't normally be reversed.

However, the sperm and egg which then fused to form the zygote from which a new embryo develops, are themselves specialised cells with all the epigenetic settings of their parent cells with an additional few of their own, and these are inherited by the zygote, so to make cell differentiation possible again, the zygote is quickly (within minutes of fertilisation) reset to a state of totipotency.

So, to overcome the epigenetic settings problem that is a problem of the designer's own making, the zygote needs to be epigenetically reprogrammed and this happens in two stages: first to produce a 'totipotent' cell with the potential to produce all the different cells in the embryo as well as the placenta, umbilical cord, and amniotic sack in which the embryo will develop, and then, soon after cell division begins, 'pluripotent' cells from which the different stem cells for the required specialised cell lines will develop.

How this was helped by a virus is the subject of the paper by researchers from the Spanish National Cancer Research Centre (CNIO), Madrid, Spain. First, a little AI background:

Sunday 7 January 2024

Unintelligent Design - How Creationism's Incompetent Designer Tries To Fix It's Bad Design


New Study Reveals Crucial 'Housekeeping' Genetic Elements and Their Potent Role to Fight Cancer|THE INSTITUTE OF MEDICAL SCIENCE, THE UNIVERSITY OF TOKYO

The thing about Creationism's putative intelligent [sic] designer is that it isn't just your common or garden variety of jobbing designer; it is allegedly omniscient, omnipotent and perfect, so anything it designs should be perfectly designed to do exactly what it does, nothing more and nothing less. Creationists need to ignore that aspect of its designs when it comes to the problem of all the parasites that live on and in the animals and plants it supposedly created or they need to perform some double-think mental gymnastics and blame something else which, even though their putative intelligent designer is the only entity capable of designing anything living, also designs things.

Creationists also need to ignore the fact that good design is minimally complex and pretend it’s a hallmark of good design. But imagine a manufacturing process that is so badly designed that it needs whole layers of sub-processes to correct the mistakes, and then those sub-processes need more sub-processes to correct their mistakes!

Presumably, a creationist would look at that system with its vast array of monitoring and error corrections as evidence of intelligent design, regardless of the waste and inefficiency built into the system. In reality, of course, any competent process designer would get it right first time, or would scrap a bad design and start over, learning the lessons of earlier failures, so designing the perfect system with minimal complexity and minimal waste should not be beyond the wit of a perfect, omnipotent omniscient designer, should it?

Alas, what we see in nature is nothing like perfectly designed processes; instead, we see muddle, waste and inefficiency with layer upon layer of sub-processes simply to cope with the errors in the processes.

An example of just this situation inside the cells of our allegedly intelligently design bodies was discovered recently by a team of researchers from the Laboratory of Functional Analysis in silico (Nakai-lab) at The Institute of Medical Science, The University of Tokyo, Japan, led by Professor Kenta Nakai, head of the laboratory, and Dr. Martin Loza, Assistant Professor, in collaboration with Dr. Alexis Vandenbon, Associate Professor, from the Institute of Life and Medical Sciences, Kyoto University, Japan. Their work was published, open access, in Nucleic Acids Research on December 12, 2023.

The team found as many as 11,000 gene regulators, all needed for basic 'housekeeping' and error corrections within the cell. These are known as housekeeping cis-regulatory elements (HK-CREs). These elements are vital in maintaining cellular stability beyond conventional gene regulation, influencing diverse cellular functions across healthy cell types. Moreover, a subset of these housekeeping elements, particularly those related to zinc finger genes, was found to have reduced activity in diverse cancers, suggesting their role as potential housekeeping tumor suppressors.

These HK-CREs were believed to be simple on/off switches that regulated the activity of housekeeping genes, but that was far too simple for whatever designed this complex process, of course. The Japanese team found that these switches aren't only important for the enhancement of specific genes but are crucial for the basic functions that keep our cells healthy. In other words, they are needed to clean up and correct the mistakes in the basic cell functions.

Given the significant association between cancer and mutations in epigenetic components, every small insight we gain could be key in the ongoing battle against this disease, which has tragically claimed innumerable lives. Through extensive bioinformatics analyses, we aimed to emphasize HK-CREs profound impact on fundamental cellular processes, including their potential as essential housekeeping tumor suppressors.

Assistant professor Dr. Martin Loza, lead author
The Institute of Medical Science
The University of Tokyo, Japan
To summarise at this point then, the housekeeping genes (HKRs) are needed to clean up the errors and mess of a badly designed process, but then they need more genes (HK-CREs) to regulate their activity!

But it gets worse!

Thursday 28 December 2023

Malevolent Designer - How Creationism's Intelligent [Sic] Designer' Denied Us The Ability To Regenerate Limbs But Gave It To A Jellyfish


Cladonema pacificum
How jellyfish regenerate functional tentacles in days | The University of Tokyo.

Imagine for a moment that you're creationism's putative intelligent [sic] designer (the one on whom they've bestowed all the 'omnis' like omnipotence, omniscience and omnibenevolence) and you've created lots of creatures with the ability to regenerate body parts like limbs, tails and tentacles when they lose them, but you haven't given this ability to all of your creation, especially the one you supposedly love above all the others because its designed to be in your own image and you created all the other species to be at the disposal of your favourite.

What are some of the reasons you might have created them without the ability to regenerate missing body parts?
  • Incompetence? It can't be that because you're omnipotent, so nothing is impossible for you.
  • Amnesia? You just forgot to! It can't be that because you're omniscient, so know all things, past present and future so must remember creating the ability to regenerate limbs in salamanders, for example.
  • If it wasn't incompetence and it wasn't amnesia, it must have been deliberate. You chose not to because you didn't want your special creation to have this ability - even though you're allegedly omnibenevolent.

So creationists must be mistaken in at least one and possibly all of the qualities they've bestowed on you.

Or you've chosen to create humans and other animals, especially mammals, birds and most reptiles, less perfectly than you could have created them because you prefer to see them suffer when they have accidents.

And yet, according to recently published research by a Japanese research team, you gave that ability to a small jellyfish so it can regenerate its tentacles. Unless you prefer to see a human amputee struggle but not a jellyfish, why would you do that?

I'll leave that question for creationists to perform their usual intellectual gymnastic over, so they can continue to feel like the special creation of an omnipotent creator of the universe who loves them above the rest of its creation that it created just for them, like a narcissistic toddler, who thinks the world is just for him/her and someone must be making sure it stays that way.

Tuesday 9 May 2023

Creationism in Crisis - What We Can Learn About Evolution From a Single Individual's Genome

Slideshow code developed in collaboration with ChatGPT3 at https://chat.openai.com/

Comparing Genes of 240 Mammal Species—and One Famous Dog—Offers New Insights in Biology, Evolutionary History | HHMI

Still more evidence against creationism is being revealed by data provided by the Zonomia Consortium.

In a series of 11 papers published recently, is one by Professor Beth Shapiro, HHMI Professor at the University of California, Santa Cruz (UCSC) and director of evolutionary genomics at the UCSC Genomics Institute. In this work Professor Shapiro and her team analysed the genome of the famous sled dog, Balto, the hero of the 1925 'Serum run' to Nome, Alaska:

Friday 10 June 2022

Common Origins - How Modern Chromatin Shows the Common Ancestry of All Eukaryotes

Ancyromonas sigmoides, an understudied microbe that holds enormous promise for investigations into the origin of eukaryotes

Credit: Naoji Yubuki
Chromatin originated in ancient microbes one to two billion years ago | Centre for Genomic Regulation

For some bizarre reason, creationists often claim that the science of epigenetics somehow falsifies Darwinian evolution because, so they claim, it shows how genetic changes acquired after birth can be passed on to the next generation, although how that falsifies the observable fact that allele frequency in a population changes over time is never explained when the rehearsed talking points are regurgitated on cue.

It is ironic then, that, according to research by scientists at the Center for Genomic Regulation (CRG) at the Barcelona Institute of Science and Technology (BIST), Barcelona, Spain, a vital component of the epigenetic system, the chromatin, or histones, around which DNA is wrapped and which exerts a control over which genes are expressed in the specialised cells of multicellular organisms, had its origins in remote ancestral prokaryote organism some 1-2 billion years ago and so is evidence of common ancestry.

To make matters worse for creationists, the evidence suggests that histones probably evolved as defensive structures in response to selective environmental pressures by genetic parasites such as viruses, in classical Darwinian evolution by natural selection and the inevitable arms races.

As the CRG news release explains:

Thursday 18 March 2021

Evolution News - How Sperms Remember

New research shows how a father's experience can be passed on to his offspring.
How sperm remember | Newsroom - McGill University

This is the sort of paper that Creationist frauds can use to fool their scientifically illiterate dupes. It will be presented as 'proof' that Darwin was wrong all along and his 'rival' Jean-Baptiste Lamarck was right.

Lamarck, in his attempt to explain inheritance and evolution, had proposed that traits acquired after conception could be passed to children. He famously claimed a blacksmith, by developing string arms, would have sons who also had strong arms and be good blacksmiths. (In a sense, he was right but the mechanism, at least in sentient species, is via memes, not some assumed physical factor (genes were not know about then)). He was of course wrong about giraffes getting longer necks by stretching to reach higher leaves and passing on the stretched neck to their offspring. There is no way an acacia tree can stretch to avoid its leaves being eaten by giraffes, so Lamarckian inheritance can't explain arms races of that sort, even if it had some basis.

Darwin, on the other hand, argued that it was traits inherited from parents that were passed on and that these were fixed at conception (with occasional variations which could be 'favoured' by the environment in 'natural selection').

However, in recent years the science of epigenetics has thrown up a few challenges to the idea of a purely Darwinian inheritance . Basically, epigenetics is the study of how genes are deactivated in specialised cells so that the cell only performs the specific punction of its speciality. As I'll explain later, epigenetics, far from being the gift creationists have been praying for which is going to refute the hated Darwinian mechanism of evolution by natural selection, but it represents a major challenge to the neo-Creationist invention, intelligent [sic] design.

Creationist thinking is often simplistic and binary so, for example, if Lamarck was a little bit right, he was entirely right and Darwin was completely wrong. As this paper shows, and as always with biology, the truth is much more nuanced than that, which is partly why creationists have difficulty with the subject.

But first this piece of research by scientists at McGill University, Montreal, Canada, led by Sarah Kimmins, PhD, of McGill's Faculty of Medicine, Department of Pharmacology and Therapeutics. As the McGill news release explains:
Web Analytics