The subfossil jawbone of a polar bear that lived 115,000 to 130,000 years ago in Norway’s Svalbard archipelago. A genomic study includes an analysis of DNA extracted from a tooth attached to this jawbone, which is now housed at the Natural History Museum at the University of Oslo.
Credit: Photo by Karsten Sund, Natural History Museum (NHM), University of Oslo
A new study by scientists led by Charlotte Lindqvist at University at Buffalo (UB) in the U.S.; Luis Herrera-Estrella at the National Laboratory of Genomics for Biodiversity (LANGEBIO) in Mexico and Texas Tech University in the U.S.; and Kalle Leppälä at the University of Oulu in Finland has shown that the evolutionary divergence of brown bears, Ursus arctos, and polar bears, Ursus maritimus, into different species, was every bit as complex as that of hominins into the single extant species, Homo sapiens.
This illustrates how evolutionary divergence is often a far from straightforward process, with several periods of partial speciation, remixing and convergence and separation again until, as today, we can end up with two species that can still interbreed, indicating that barrier to hybridization have not yet fully evolved.
This, of course, is exactly what we would expect of a slow process over time, but not speciation events such as creationists wrongly believe scientists think is how evolution works. This is perhaps best illustrated with the simple analogy of one colour changes into another in a rainbow spectrum where it is impossible to say exactly where one colour ends and the next begins:
Where does the colour change?
The team used an expanded DNA dataset — including DNA from an ancient polar bear tooth — to tease out the details As the University at Buffalo news release explains:
This example of what creationists believe must have been designed by their allegedly omnibenevolent god takes some beating for its sheer ghoulish nastiness. It is the toadfly, Lucilia bufonivora, or to be precise, the parasitic larvae of the toadfly.
This little piece of divine malevolence (if you believe the intelligent [sic] design hoax) would have made it into my popular, illustrated book, The Malevolent Designer: Why Nature's God is not Good, had I been aware of it at the time. Maybe it will make it into a sequel one day.
This rather beautiful, metallic green fly, is a 'blow fly' of the Calliphoridae family, that are more familiar to most people as the blow flies such at the blue bottles and green bottles that lay eggs on dead animals and raw meat. It's the sort of thing in nature that creationists often point to and claim such an exquisite thing is evidence of design.
In a frankly astonishingly laissez faire response to the report into historical sexual abuses in member churches of the Southern Baptist Convention, North Carolina attorney and long-time committee member Joe Knott, warned against implementing the measures recommended to protect vulnerable children and women from sexually predatory pastors, youth workers and missionaries because it could lead to ruin.
I am terrified that we are breaching our long-standing position of being a voluntary association of independent churches, when we start telling churches that they should do this or do that to protect children or women.
UT Austin researchers confirmed that the genetic control region they discovered only controls the expression of a sodium channel gene in muscle and no other tissues. In this image, a green fluorescent protein lights up only in trunk muscle in a developing zebrafish embryo.
Image credit: Mary Swartz/Johann Eberhart/University of Texas at Austin.
Creationists might want to avoid reading this because it contains information, not only about evolution and how it forms the basis of scientific understanding of the facts, but also because it is about how new genetic information arose by gene duplication and subsequent repurposing of a duplicate gene to create a new organ - something that creationist frauds say can't happen because this is 'macroevolution' which requires a magic designer. The information comes from a research team from the University of Texas Austin and Michigan State University, led by Professor Harold Zakon of UT Austin, who have worked out how electric fish evolved their electric organs.
This is exciting because we can see how a small change in the gene can completely change where it’s expressed.
Professor Harold Zakon, corresponding author
Department of Neuroscience
And Department of Integrative Biology
The University of Texas, Austin, TX, USA.
Having duplicated a gene for producing the sodium pump in their cell membranes early on in their evolution, all fish carry this duplicate gene. The sodium pump is necessary for muscle cells to recover after contracting and so being available to contract again. The team has now shown that the African and South American electric fish have independently repurposed a 'spare' gene to create a new organ with unique abilities.
If they turned on the gene in both muscle and the electric organ, then all the new stuff that was happening to the sodium channels in the electric organ would also be occurring in the muscle, so, it was important to isolate the expression of the gene to the electric organ, where it could evolve without harming muscle.
Professor Harold Zakon
The researchers have discovered that just a short section of about 20 nucleotides in this repurposed gene controls whether it is expressed in any given cell. They found that this section is either altered or missing entirely in electric fish resulting in one of the two sodium pump genes being non-functional in these fish. This allowed the gene to be repurposed in the muscles of electric fish without harming the muscles, which still had the functional copy.
This research could have an application in human health by helping to understand how the variants of this gene work in conditions in which reduced sodium pump efficiency plays a part.
If you rewound the tape of life and hit play, would it play back the same way or would it find new ways forward? Would evolution work the same way over and over again? Electric fish let us try to answer that question because they have repeatedly evolved these incredible traits. We swung for the fences in this paper, trying to understand how these sodium channel genes have been repeatedly lost in electric fish. It really was a collaborative effort.
Jason R. Gallant, co-author
Department of Integrative Biology
And Ecology, Evolution, and Behavior Program
Michigan State University, East Lansing, MI, USA.
The UT Texas News release explains:
There are two groups of electric fish in the world—one in Africa and the other in South America. The researchers discovered that the electric fish in Africa had mutations in the control region, while electric fish in South America lost it entirely. Both groups arrived at the same solution for developing an electric organ—losing expression of a sodium channel gene in muscle—though from two different paths.
One of the next questions the researchers hope to answer is how the control region evolved to turn on sodium channels in the electric organ.
South American and African weakly electric fish independently evolved electric organs from muscle. In both groups, a voltage-gated sodium channel gene independently lost expression from muscle and gained it in the electric organ, allowing the channel to become specialized for generating electric signals. It is unknown how this voltage-gated sodium channel gene is targeted to muscle in any vertebrate. We describe an enhancer that selectively targets sodium channel expression to muscle. Next, we demonstrate how the loss of this enhancer, but not trans-activating factors, drove the loss of sodium channel gene expression from muscle in South American electric fish. While this enhancer is also altered in African electric fish, key transcription factor binding sites and enhancer activity are retained, suggesting that the convergent loss of sodium channel expression from muscle in these two electric fish lineages occurred via different processes.
Just to recap for any creationists who managed to stay the course and get through to the end: what this paper shows is not only that the authors regard the TOE as the foundation of their science, but also that new information can arise by gene doubling followed by mutation and environment-driven repurposing of redundant copies, but also that information can give rise to new structures with new functions, and all driven by natural selection from what is available to it, and with relatively few changes to the DNA. The advantages of this new organ can be seen from the fact that it evolved twice from the same starting point and converged on the same solution. And all without the assistance of magic.
Neanderthals may have had less prosocial behaviour than modern humans. They had smaller social groups and may have had a polygynous social structure with more male-male competition.
One of the more nonsensical creationist talking points you still hear occasionally, is that evolution can't account for altruism because survival of the fittest means the selfish survive at the expense of others less selfish. This is demonstrably untrue because the result of evolution show that cooperation at all levels of organisation, from intracellular organelles to social groups of multicellular organisms, is better than conflict, and human society especially demonstrates the truth of this where any tendency towards freeloading is moderated by social ethics and the affiliative needs of individuals.
Now this reasoning has been supported by research which shows that human evolution included improving the ability to empathize. Empathy, of course, is the basis for all human prosocial behaviour and is even acknowledged in the Judaeo-Christian holy books with the invocation to do unto others that which you would they do unto you - the 'golden rule', common to all human societies.
Modern human societies are characterised by comparatively high levels of prosocial behaviours such as intraspecies empathy, social tolerance, cooperation and altruism. Now, Constantina Theofanopoulou, as part of her doctoral thesis carried out under the co-supervision of Cedric Boeckx, ICREA researcher at the Institute of Complex Systems at the Universitat de Barcelona (UBICS) and Erich D. Jarvis, professor at Rockefeller University, has shown that this has an evolved genetic basis involving the genes that control oxytocin and vasotocin receptor in the brain. Oxytocin, also known as the 'love' hormone, is responsible for social bonding as well as sexual attraction and parent-child bonding.
By analysing the genomes of modern humans, Neanderthals and Denisovans as well as non-human primates, the common chimpanzees, bonobos and macaques, Theofanopoulou and her colleagues have shown that there are five sites in the oxytocin and vasotocin receptors where modern humans are unique in one of their two (or more) variants compared to archaic humans and non-human primates, and which are at the same time found in more than 70% of the modern human population.
The scientists have published their finding's, open access, in the journal, Comprehensive Psychoneuroendocrinology.
The Universitat de Barcelona news release gives more details:
Variants unique to modern humans in more than 70% of the population
Past studies that compared the entire modern human genome with the Neanderthal or the chimpanzee genomes have focused on changes that are fixed or nearly fixed in modern humans. This has led to them identifying sites where, for example, all Neanderthals had Adenine (one of the four nucleotides that with guanine, cytosine and thymine form the DNA) and nearly all modern humans (say, 98%) have Guanine. In this study, we searched for differences on locations where, by definition, not all modern humans share the same nucleotide, namely on polymorphic sites, where for example, 70% of the modern human population has Adenine and 30% Cytosine.
[the differences] might be relevant to the smaller social groups attributed to Neanderthals and Denisovans or to the decreased modern human androgenization. They might also be relevant to a different social structure, i.e., Neanderthals have been linked to a polygynous social structure and a higher level of male–male competition than most contemporary modern human populations.
The sites that are unique in both us and archaic humans versus non-human primates can elucidate the genetic underpinnings of the progressive social tolerance needed for the intensive cultural transmission of technological innovations (e.g., fire use) in the evolution of humankind, as well as for the reduced aggression indicated by several markers in early hominid evolution, such as the reduction of male canine size and the accelerated demographic success.
The convergent sites in modern humans and bonobos could be insightful for understanding the posited similarities in prosociality, social tolerance and cooperation between us and bonobos, and the differences of both compared to chimpanzees. For example, bonobos outperform chimpanzees on tasks relevant to social causality or theory of mind and are more attentive to the face and eyes, suggestive of higher empathic sensitivity.
Understanding developmental disorders through evolutionary lenses can aid into us achieving what we call an evo-devo (evolutionary and developmental biology) understanding of these disorders. If indeed “ontogeny recapitulates phylogeny”, then deciphering our evolutionary trajectory may shed light to new genetic spots for clinical research that might, in turn, lead to earlier disorder diagnosis.
Constantina Theofanopoulou, first author
PhD Candidate
Laboratory of Neurogenetics of Language
Rockefeller University, New York, USA
And Institute of Complex Systems
University of Barcelona
Catalonia, Spain
Considering the evidence on modern human prosociality and on the involvement of the oxytocin and vasotocin genes in social behaviours, the researchers hypothesized that the evolution of these genes might elucidate the genetic basis of the evolution of hominin prosociality. With this aim in mind, the study explored the differences between modern humans, archaic humans and non-human primates in polymorphic heterozygous sites in the human genome – locations where at least two alternative sequences are found in a population.
The study compared the available genomic sequences of these genes between modern humans, non-human primate species (e.g., chimpanzees, bonobos, and macaques) and, for the first time, archaic humans.
The researchers identified five sites in the oxytocin and vasotocin receptors where modern humans are unique in one of their two (or more) variants compared to archaic humans and non-human primates, and which are at the same time found in more than 70% of the modern human population. Next, they conducted functional and frequency analyses to establish whether the variants are relevant. They performed a range of analyses on the five sites and found that some of the variants are highly functional, indicating that they have an effect on the molecular function of the proteins activated by these genes.
The researchers also found that these sites are encountered in genome regions that are active in the brain, particularly in the cingulate gyrus, a brain region involved in social cognition-relevant pathways. Moreover, all these sites have been associated in other studies with a plethora of social behaviours or social deficits, such as autism, attention deficit hyperactivity disorder (ADHD), aggression, and so on.
These findings may help to explain some of the social differences between modern humans and what we presume to know about the social behaviours of Neanderthals and Denisovans.
Variants present only in modern and archaic humans
The study also found two sites on the oxytocin receptor under a positive selection in modern and archaic humans: that is to say, modern and archaic humans showed a variant that was not present in any other non-human primate. This means that these sites are found in very high percentages in the modern human population (in this case, more than 85%). These same sites have also been associated with a great many social behaviours or deficits, and one of them was predicted to be a highly functional site in their regulation analyses.
Convergent sites with bonobos
Lastly, the researchers found three sites where modern humans and bonobos, a primate species that shows convergence of prosocial behaviours with humans, have the same nucleotide.
All the sites identified in this study have also been independently associated with disorders that include social deficits, such as autism spectrum disorders (ASD).
Because the same sites were not found in the common chimpanzees, with whom we share common ancestry with bonobos, the team reasoned that the three sites which humans and bonobos have in common is most likely a case of convergent evolution. This emphasises the selective advantage in this mutation in bonobos, in which prosocial, empathetic behaviour is highly developed.
More detail is given in the abstract and highlight section to their paper:
We compared the oxytocin/vasotocin receptors in modern humans, archaic humans, and non-human primates.
We found 5 sites with modern human specific variation.
In these sites, the modern human allele is the major allele in the global population.
Several sites were predicted to be functional and with selection signatures in modern humans.
We also identified 3 sites of convergent evolution in modern humans and bonobos.
Abstract
Modern human lifestyle strongly depends on complex social traits like empathy, tolerance and cooperation. These diverse facets of social cognition have been associated with variation in the oxytocin receptor (OTR) and its sister genes, the vasotocin/vasopressin receptors (VTR1A/AVPR1A and AVPR1B/VTR1B). Here, we compared the available genomic sequences of these receptors between modern humans, archaic humans, and 12 non-human primate species, and identified sites that show heterozygous variation in modern humans and archaic humans distinct from variation in other primates, and for which we could find association studies with clinical implications. On these sites, we performed a range of analyses (variant clustering, pathogenicity prediction, regulation, linkage disequilibrium frequency), and reviewed the literature on selection data in different modern-human populations. We found five sites with modern human specific variation, where the modern human allele is the major allele in the global population (OTR: rs1042778, rs237885, rs6770632; VTR1A: rs10877969; VTR1B: rs33985287). Among them, variation in the OTR-rs6770632 site was predicted to be the most functional. Two alleles (OTR: rs59190448 and rs237888) present only in modern humans and archaic humans were putatively under positive selection in modern humans, with rs237888 predicted to be a highly functional site. Three sites showed convergent evolution between modern humans and bonobos (OTR: rs2228485 and rs237897; VTR1A: rs1042615), with OTR-rs2228485 ranking highly in terms of functionality and reported to be under balancing selection in modern humans (Schaschl, 2015) [1]. Our findings have implications for understanding hominid prosociality, as well as the similarities between modern human and bonobo social behavior.
It is entirely possible therefore that modern human groups were able to out-compete the archaic hominins because we were able to sustain larger cooperative groups, with reduced internal conflict stemming from male-male rivalry, than the archaic hominins could manage. This improved social cohesion gave us an evolutionary advantage, hence it came to predominate in the human gene pool, in a classic example of evolution by natural selection.
No doubt, despite evidence such as this to the contrary, we will still get creationists denying the common ancestry of humans and other apes and asserting that natural selection can't account for altruism and love because it would favour selfishness. Creationism requires its dupes to stay stoically ignorant of 'toxic' science. No doubt too that creationists will still make the increasingly forlorn claim that the TOE is a theory in crisis, despite the evidence such as that in this paper that it is fundamental to our understanding of biology and the only scientific theory that makes sense of the evidence without resorting to magical mysteries and childish fairy tales.
A new investigation into the evolution of Salmonella bacteria infecting Brazilian poultry shows that the introduction of a Salmonella vaccine, combined with increasing antibiotic usage by Brazilian farmers, has led to the rise of strains that are more antibiotic-resistant, but less likely to cause disease in humans. This is the conclusion by Andrea Micke Moreno of the University of São Paulo, Brazil, Alison Mather of Quadram Institute Bioscience, UK, and their colleagues, who conducted the investigation.
Their findings are published today the open access journal PLOS Genetics.
Information provided by PLOS ahead of publication explains:
A sure sign that a religion is losing its grip on the people is when public opinion differs markedly from its teachings. This is a manifestation of an increasing tension as social ethics progresses and leaves behind the fossilised ethics of religion from an earlier age. The local religions then have to change to keep up but in doing so, they alienate the traditionalists who tend to become an ever-diminishing minority, pushing it further out to the fringes, or leave the church in protest at its increasing abandonment of sacred principles.
The problem is a direct consequence of the control of public morals religions presume they have entitlement to and their claim of the divine authority of an omniscient god for so doing. This means they can adopt change only by abandoning their justification for their control and in effect, giving up the pretence that morals come from an omniscient deity who, by definition, is never wrong. The reality, of course, is that morals are a social construct that change and develop according to the developmental needs of society, and have no divine, objective basis save what goes to create a cooperative society that is pleasant to live in.
So the progressive forces in society produces a tension between them and the regressive, traditionalist forces of religion and the needs of religions to keep control of their people and so the livelihoods and power of the priesthood. A useful analogy is that of a rope by which religions try to hold back social progress until either the rope snaps and the people give up on that religion, or the religion is dragged, kicking and screaming into the modern age.
The Church of England (CofE) faces extinction within 40 years, according to the calculations of Dr John Hayward, a mathematician at the University of South Wales.
He arrived at this date by applying a technique normally used for assessing the increase or decrease in the spread of a pandemic such as COVID-19, which calculates at 'R' number. The 'R' number calculates how many people someone with the virus passes it on to on average. An 'R' number of one means the number of cases in the population remains constant; above 1 means it is increasing and below 1 means it is decreasing.
Interestingly, this view of religion and how it is spread is almost identical to the view expresed by Richard Dawkins in The Selfish Gene that religions behave like a parasitic virus in the human memepool.
The 'problem' the CofE and other Christian denominations face is that they are not infectious enough. Dr Hayward has calculated the CofE's 'R' number at 0.9, the same as that for the Catholic Church and an 'R' number that a COVID-19 epidemiologist would have welcomed at the height of the Pandemic. This means their congregations could disappear by 2062. The Methodists, with an 'R' number of about 0.85 could be extinct by 2040, lingering on little longer than the United Reformed Church with an 'R' number of about 0.8.
Other Christian denominations in the UK fare even worse and only a handful have 'R' numbers about 1 - the Elim Pentecostal Church and the Fellowship of Independent Evangelical Churches.
Several churches in Wales and Scotland face extinction before 2050 (i.e., within the next generation). They are the Welsh Presbyterians, the Church in Wales, the Welsh Independents, the Church of Scotland and the Scottish Episcopal Church.
The scale of the catastrophe facing the CofE can be seen from the change in membership since 1800, when 17% of the population were registered as members on the electoral role. That figure is now just 1.7%, i.e., a 99% decline in membership which fell below 1 million for the first time in 2019, at a time of population growth.
Given that rate of decline and the fact that the CofE now represents only a tiny minority of the population, the time is now well overdue for a review of its role in public life and especially its right to insert bishops into the UK's legislative upper chamber, the House of Lords.
The role of the monarch as titular head of this unrepresentative minority cult now needs to be abolished on the succession.
How human languages evolved is something of a mystery. I'm not talking about the neurological and anatomical development that made us able to vocalise and comprehend spoken communications because this is an obvious case of gene-meme co-evolution. What I'm talking about is the evolution of the various sounds into words and so into coded information that conveys a meaning.
This is an even bigger problem for creationists because, apart from the childishly implausible and contradictory accounts in their favourite textbook, the Bible, it offers nothing by way of a rational explanation. Firstly there is the tale that all the descendants of Noah spoke different languages, to account for the handful of Middle Eastern languages the authors were aware of (Genesis 10:1-5). Then we have the contradictory claim that the whole world spoke one language (Genesis 11:1) but God confounded their tongues so they all spoke languages incomprehensible to one another [sic] because he was afraid they would work together to build a tower up to Heaven - which in those days was just above the sky over the Middle East and accessible via a tall enough tower.
But nowhere does the Bible say anything about how we learned to combine different phonics into words. The assumption of the Bible's authors was that, right from start, language was fully formed as some sort of universal given. Even the talking animals (Genesis 3:1-5, Numbers 22:28-30) and plants (Judges 9:13) spoke with human language, using the recombination of human phonics to make the words they spoke, like humans do, even though they lack the neurological and physical means of doing so. Even when God spoke his first words (Genesis 1:3) he used a human combination of human phonics to make meaningful (to humans) words and sentences - in that case, in a language then spoken by no-one else, since there was no-one else to speak it - Ancient Hebrew.
It is of course, nonsensical. Our ability to cooperate in social groups and develop cultures in which agreed combinations of phonetics has agreed meanings, so we can construct new information by an agreed set of rules, is an evolved ability and one which we probably inherited from an ancestor we have in common with chimpanzees, as the work of scientists from the Institut des Sciences Cognitives Marc Jeannerod, Lyon, France, the Department of Neuropsychology, Max Planck Institute for Human Cognitive Sciences, Leipzig, Germany and the Taï Chimpanzee Project, Centre Suisse de Recherche Scientifique, Abidjan, Ivory Coast, shows.
The appointment by Pope Francis of Cardinal Matteo Maria Zuppi, Archbishop of Bologna, to the powerful post of President of the Italian Bishops' Conference, raises the delicious possibility of another major investigation into historical sex abuses by Catholic Priest in a devoutly Catholic Country, and of course the likely haemorrhage of membership from the church and loosening of the Church’s grip on national politics when the truth is revealed, as was seen in France, Spain, Ireland and elsewhere.
Zuppi is regarded as a liberal and was appointed by the Pope when Italian Bishops declined the Pope's invitation to be given the power to elect their president from amongst themselves. This gives him power in Italy second only to the Pope, who as Bishop of Rome is also Primate of Italy. He is believed to have strong links with the Sant’Egidio Community - a liberal-leaning, humanitarian community which describes itself as:
Sant’Egidio is a Christian community born in 1968, right after the second Vatican Council. An initiative of Andrea Riccardi, it was born in a secondary school in the centre of Rome. With the years, it has become a network of communities in more than 70 countries of the world. The Community pays attention to the periphery and peripheral people, gathering men and women of all ages and conditions, united by a fraternal tie through the listening of the Gospel and the voluntary and free commitment for the poor and peace.
Although it doesn't mention LGBTQ issues on its website, the Sant’Egidio Community is believed to support an inclusive approach to members of the LGBTQ community.
Italian bishops have long resisted calls for an enquiry into the sexual abuses of children by Catholic clerics but recently, they agreed to launch an enquiry into abuses over the past 10 years, having rejected one going back 50 years. Obviously, they know they have much to fear from such a long historical period going back to a time before the historical abuse scandals swamped the church and prompted actions to prevent them; a time when deference and a code of silence allowed abuses to go unreported and the abusers to continue their predation without let or hindrance. Similar enquiries in other countries have usually revealed thousands of victims of hundreds of priests, nuns and monks in most Catholic diocese and institutions, and a culture of tolerance, cover-up, facilitation and bullying of victims who dared to complain.
Zuppi's rise has been relatively rapid, having been ordained in 1981 and serving as an auxiliary bishop in Rome. He was appointed bishop of Villanova by Pope Benedict XVI in 2012 and Archbishop of Bologna by Pope Francis in 2015. He was made a cardinal by Pope Francis just 3 years ago, but he needs to tread carefully, as a too liberal approach with too much revelation of the murky world of Italian Catholicism, could alienate him from the powerful conservative wing of the Church which is especially strong in Italy, and that could scupper his chances of becoming the next Pope - a position for which he is currently regarded as a leading candidate.
Leaders of the Southern Baptist Convention in the USA have decided to release a formerly secret list of child abusers known to senior figures in the Convention. The list was originally started as a research project for an SBC committee in 2007 but was officially discontinued shortly after. However, a staffer continued to maintain it until 2022. It's existence was unknown until discovered by Guidepost Solutions, a firm employed as part of a multi-million dollar investigation into how the SBC handled abuse cases.
According to this report, the 205-page list contains details of cases involving "pastors, Sunday school teachers, camp counselors, music ministers, bus drivers and missionaries, with about 400 tied to SBC churches from Alaska to Alabama. In almost all of the cases, the abuse had led to arrests and jail time.". The compiler, whose name has been redacted from the released file, and who remains anonymous in the Guidepost Solutions report, has added the following disclaimer:
The precondition for Darwinian evolution is genetic difference between individuals in a population. This is the 'fuel' which drives evolution in an environment in which certain genetic variations are more advantageous than others, so the amount of this variation in any given population, is the main determinant of the rate of evolution.
In order to quantify the amount of this 'fuel of evolution', an international team led by Dr Timothée Bonnet from the Australian National University (ANU) spent three years trawling through reams of data, after which they were able to quantify how much species change occurred due to genetic changes caused by natural selection. It turned out to be about two to four times what was previously thought and evolution can go much faster than Darwin originally thought.
The Australian Nation University news release explains:
There are two types of plasmid integration into a host bacteria: Non-integrating plasmids replicate as with the top instance, whereas episomes, the lower example, can integrate into the host chromosome.
Horizontal gene transfer (HGT) plays an important role in the evolution of microorganisms like bacteria, but a lesser, though not unknown, role in multicellular organism. In bacteria, which freely share small bundles of DNA known as plasmids, even amongst unrelated species, HGT can be the means by which, in the right environment, a beneficial trait such as antibiotic resistance can spread rapidly through an entire microbiome. Plasmids are shed by bacteria into their environment where they can be picked up by other bacteria.
This was demonstrated recently by a study led by the researcher, Arthur Newbury, of the Environment and Sustainability Institute on Exeter University's Penryn Campus in Cornwall, UK. The significance of this finding is that it shows how antibiotic resistance can be spread by plasmids in waste water, for instance.
The third in a series looking at monkeypox and asking whether this is creationism's putative divine malevolence's latest attempt to increase the misery and suffering in the world with another of its nasty little creations.
If not, then creationists need to explain why it either didn't design this virus, or, if it did, why it didn't realise what it would do - and what else it was designed to do. Unlike the SARS-CoV-2 virus that is causing the ongoing COVID-19 pandemic, which is an RNA virus, the virus that causes monkeypox is a more complex, DNA virus that, again unlike the SARS-CoV-2, has the ability to repair mistakes in its DNA when it replicates, so mutations are much rarer.
Monkeypox viruses are from a subset of the Poxviridae family, known as Orthopoxvirus, which includes smallpox and cowpox (but not chickenpox).
An expert in the field explains what the monkeypox virus is, probably why why we are experiencing the current outbreak and what we can learn from the history of the closely-related smallpox virus.
This article is republished from The Conversation under a Creative Commons license. Read the original article. The Conversation is a charity set up to allow experts in the field to give expert insight into items of current public interest and to counter the deluge of lies and disinformation with which politically-motivated extremists are flooding the social media in the Trumpian/Putinesque so-called ‘post truth age’.
What is monkeypox? A microbiologist explains what’s known about this smallpox cousin
Monkeypox isn’t a new disease. The first confirmed human case was in 1970, when the virus was isolated from a child suspected of having smallpox in the Democratic Republic of Congo (DRC). Monkeypox is unlikely to cause another pandemic, but with COVID-19 top of mind, fear of another major outbreak is understandable. Though rare and usually mild, monkeypox can still potentially cause severe illness. Health officials are concerned that more cases will arise with increased travel.
I’m a researcher who has worked in public health and medical laboratories for over three decades, especially in the realm of diseases with animal origins. What exactly is happening in the current outbreak, and what does history tell us about monkeypox?
A cousin of smallpox
Monkeypox is caused by the monkeypox virus, which belongs to a subset of the Poxviridae family of viruses called Orthopoxvirus. This subset includes the smallpox, vaccinia and cowpox viruses. While an animal reservoir for monkeypox virus is unknown, African rodents are suspected to play a part in transmission. The monkeypox virus has only been isolated twice from an animal in nature. Diagnostic testing for monkeypox is currently only available at Laboratory Response Network labs in the U.S. and globally.
The name “monkeypox” comes from the first documented cases of the illness in animals in 1958, when two outbreaks occurred in monkeys kept for research. However, the virus did not jump from monkeys to humans, nor are monkeys major carriers of the disease.
Monkeypox belongs to the Poxviridae family of viruses, which includes smallpox.
Since the first reported human case, monkeypox has been found in several other central and western African countries, with the majority of infections in the DRC. Cases outside of Africa have been linked to international travel or imported animals, including in the U.S. and elsewhere.
Because monkeypox is closely related to smallpox, the smallpox vaccine can provide protection against infection from both viruses. Since smallpox was officially eradicated, however, routine smallpox vaccinations for the U.S. general population were stopped in 1972. Because of this, monkeypox has been appearing increasingly in unvaccinated people.
Indonesia began screening travelers after a monkeypox case was reported in Singapore in May 2019.
The virus can be transmitted through contact with an infected person or animal or contaminated surfaces. Typically, the virus enters the body through broken skin, inhalation or the mucous membranes in the eyes, nose or mouth. Researchers believe that human-to-human transmission is mostly through inhalation of large respiratory droplets rather than direct contact with bodily fluids or indirect contact through clothes. Human-to-human transmission rates for monkeypox have been limited.
Health officials are worried the virus may currently be spreading undetected through community transmission, possibly through a new mechanism or route. Where and how infections are occurring are still under investigation.
Signs and symptoms
After the virus enters the body, it starts to replicate and spread through the body via the bloodstream. Symptoms usually don’t appear until one to two weeks after infection.
Monkeypox produces smallpox-like skin lesions, but symptoms are usually milder than those of smallpox. Flu-like symptoms are common initially, ranging from fever and headache to shortness of breath. One to 10 days later, a rash can appear on the extremities, head or torso that eventually turns into blisters filled with pus. Overall, symptoms usually last for two to four weeks, while skin lesions usually scab over in 14 to 21 days.
While monkeypox is rare and usually non-fatal, one version of the disease kills around 10% of infected people. The form of the virus currently circulating is thought to be milder, with a fatality rate of less than 1%.
Vaccines and treatments
Treatment for monkeypox is primarily focused on relieving symptoms. According to the CDC, no treatments are available to cure monkeypox infection.
Because smallpox is closely related to monkeypox, the smallpox vaccine can protect against both diseases.
Evidence suggests that the smallpox vaccine can help prevent monkeypox infections and decrease the severity of the symptoms. One vaccine known as Imvamune or Imvanex is licensed in the U.S. to prevent monkeypox and smallpox.
Vaccination after exposure to the virus may also help decrease chances of severe illness. The CDC currently recommends smallpox vaccination only in people who have been or are likely to be exposed to monkeypox. Immunocompromised people are at high risk.
It seems that creationism’s putative designer saw an opportunity created by medical science when smallpox was eradicated altogether, so routine vaccinations against it were stopped as unnecessary, and repurposed a related virus to try to make up for what it had lost in terms of making people suffer with smallpox. At least, that's the conclusion if we assume for one moment that the childish notion of a magic designer of these things. For a creationist, the idea that this could be an evolutionary change which exploits the niche once occupied by a related species of virus with a common ancestry has to be ruled out by dogma. Inexplicably, it is thought more important that people regard their beloved creator god as a pestilential sadist rather than that they accept that evolution works and explains these things without the need for gods and magic.
The second in a series looking at the monkeypox outbreak and whether it is creationism's beloved pestilential malevolence's latest attempt to increase the suffering in the world.
The first in a series on monkeypox, reproduced from The Conversation, an open access online source aimed at providing trustworthy information by experts about subjects in the news.
How thrilled should creationists be that their divine malevolence appears to be having another go at spreading suffering and misery with another of its nasty little viruses?
The full report into partying at 10 Downing Street, under Boris Johnson's leadership, during the Covid-19 pandemic lockdown, when such gatherings were illegal. Johnson misled parliament when he stated that there were no such parties and that all the rules were followed at all times.
The full Sue Gray Report into illegal partying at 10 Downing Street.
This study provides more evidence that Covid vaccination is safe for both current and future pregnancies, and shows in a mouse model that immunization during the earliest stages of pregnancy provides antiviral antibodies to the fetus throughout the rest of pregnancy.
Two of the bogus antivaxxer claims with which the politically-motivated covidiot antivaxxer movement is trying to scare women into not getting vaccinated against COVID-19 are:
The vaccines cause birth defects if given during pregnancy.
The vaccines reduce fertility or cause sterility in women by producing antibodies against the protein syncytin-1, which in humans and related primates is involved in attaching the placenta during pregnancy.
Now both of these antivaxxer claims have been exposed as lies by Alice Lu-Culligan and her colleagues of the Yale School of Medicine, in a paper published open access today in PLOS Biology.
The second piece of disinformation was based on the fact that a small part of the SARS-CoV-2 spike protein that antibodies are produced against by the vaccines has a short sequence of amino acids that is also found in syncytin-1.
This is hardly surprising since syncytin-1 is the remnant of an ancient retrovirus that has been co-opted to aid in the attachment of the placenta in many primates. In fact, it's one of many pieces of evidence of common descent since it is present in all the old-world primates, but not in the new-world primates. The Wikipedia entry for syncytin-1 reads:
Syncytin-1 also known as enverin is a protein found in humans and other primates that is encoded by the ERVW-1gene (endogenous retrovirus group W envelope member 1). Syncytin-1 is a cell-cell fusion protein whose function is best characterized in placental development.[3][4] The placenta in turn aids in embryo attachment to the uterus and establishment of a nutrient supply.
The gene encoding this protein is an endogenous retroviral element that is the remnant of an ancient retroviral infection integrated into the primate germ line. In the case of syncytin-1 (which is found in humans, apes, and Old World but not New World monkeys), this integration likely occurred more than 25 million years ago.[5] Syncytin-1 is one of two known syncytin proteins expressed in catarrhini primates (the other being syncytin-2) and one of many viral genomes incorporated on multiple occasions over evolutionary time in diverse mammalian species.[6]
ERVW-1 is located within ERVWE1,[7][8] a full length provirus on chromosome 7 at locus 7q21.2 flanked by long terminal repeats (LTRs) and is preceded by ERVW1 gag (Group AntiGen) and pol (POLymerase) within the provirus, both of which contain nonsense mutations rendering them non-coding.[9][10]
Syncytin-1 is also implicated in a number of neurological pathologies, most notably, multiple sclerosis, as an immunogen.
According to information made available ahead of publication by PLOS, Lu-Culligan and her colleagues:
A new study by Lude Franke and colleagues of the University of Groningen, Netherlands has shown that some individuals were more affected than others by the COVID-19 pandemic, due to their genes.
Of course, any omniscient designer of those genes and of the SARS-CoV-2 virus, such as the one intelligent [sic] design creationists believe is the creator of everything, will have been fully aware of that fact when it created the virus, so can't escape the charge of deliberately targeting certain individuals because of their genetics.
The difference is to be found in how well or badly individuals coped not so much with infection by the virus, but with the overall social effect of the pandemic, including the measures to mitigate and control it.
Reconstructed view of the burial caves of the Xagħra Circle (Libby Mulqueeney after an original by Caroline Malone).
Source: Malone et al.2009. Mortuary Customs in Prehistoric Malta.Cambridge: McDonald, pp 375, 377. Malone, C., Stoddart, S., Trump, D. & Bonanno, A. (eds.). 2009. Mortuary Customs in prehistoric Malta. Excavations at the Brochtorff Circle at Xagħra (1987-1994). Cambridge: McDonald Institute.
A group of researchers from Trinity College, Dublin, Ireland, and their international colleagues, have shown how relative isolation on the small Mediterranean islands of Malta (and neighbouring Gozo) produced distinct genomes in the population, due to a combination of the 'founder effect' and a small population reduced at time to just a few hundred inbred individuals.
Contrary to current thinking, which sees oceans as highways at the time, allowing migration and mixing more easily than travel overland, this result suggests that over the period in question, the Mediterranean acted as a barrier to isolate the population of Malta, consequently they failed to acquire some of the genetic signatures that mark migration across the rest of Europe at the time.
Analysis of the genome of ancient (4500–5000-year-old) individuals from a cave burial at the Xagħra Circle on Gozo, compared to the genomes of individuals of the same age from burial sites around Europe, show evidence of a small population numbering in the hundreds and of inbreeding, which is to be expected of a small, isolated population. One of the individuals examined turned out to be the offspring of second-degree relatives.
Buck Scientist Uncovers Clues to Aging in Mitochondria
For the want of a better answer, Bible-literalist creationist will tell you that before Adam and Eve and 'The Fall' there was no death in the world and that death is the result of 'sin', not designed by their god at all, so their god can't be held responsible for all the lethal organisms that cause so much ill health, death and suffering in the world. They never manage to explain where the food Adam and Eve ate was alive during the whole of the eating, digestion and metabolism of it though, or whether their god made an exception in that case and allowed a little bit of death, just not human death.
Now, however, they have some more mental gymnastics to perform with the discovery that it is the mitochondria in all our cells that are responsible for aging - a process that leads ultimately to death unless illness of some sort intervenes. Scientists have known about this for some time, but a team of scientists from the Buck Institute for Research on Aging have worked out how it happens. Mitochondria, the powerhouses inside every eukaryote cell, are believed to be the descendants of a bacteria related to rickettsia which became incorporated with other organelles inside prokaryote cells.
The mitochondria in our cell still have their own DNA and replicate inside our cells, although much of their original genome has been incorporated into the cell nucleus. Because only the head of the sperm penetrates the egg at fertilisation and the head contains no mitochondria, we get all our mitochondria and so all our mitochondrial DNA from our mother and none from our father.
Basically, aging is caused by imperfect mitochondrial replication which is accumulated over the years until the mitochondria start to malfunction. Because they have given up some of the DNA into the cell nucleus, they need to reactivate some of it and import the products of it before they can replicate themselves, and this is where the process begins to go wrong, according to the Buck team.
The Buck News release explains what the team led by Buck Fellow Chuankai (Kai) Zhou, PhD, has discovered:
