2023/06/29

Study suggests that most of evolutionary trees could be wrong - The theory of Evolution is just a big unreliable mess


https://www.bath.ac.uk/announcements/study-suggests-that-most-of-our-evolutionary-trees-could-be-wrong/

Excerpt: "New research led by scientists at the Milner Centre for Evolution at the University of Bath suggests that determining evolutionary trees of organisms by comparing anatomy rather than gene sequences is misleading. The study, published in Communications Biology, shows that we often need to overturn centuries of scholarly work that classified living things according to how they look.

Since Darwin and his contemporaries in the 19th Century, biologists have been trying to reconstruct the “family trees” of animals by carefully examining differences in their anatomy and structure (morphology).

However, with the development of rapid genetic sequencing techniques, biologists are now able to use genetic (molecular) data to help piece together evolutionary relationships for species very quickly and cheaply, often proving that organisms we once thought were closely related actually belong in completely different branches of the tree.

For the first time, scientists at Bath compared evolutionary trees based on morphology with those based on molecular data, and mapped them according to geographical location.

They found that the animals grouped together by molecular trees lived more closely together geographically than the animals grouped using the morphological trees.

Matthew Wills, Professor of Evolutionary Paleobiology at the Milner Centre for Evolution at the University of Bath, said: “It turns out that we’ve got lots of our evolutionary trees wrong.

“For over a hundred years, we’ve been classifying organisms according to how they look and are put together anatomically, but molecular data often tells us a rather different story.

“Our study proves statistically that if you build an evolutionary tree of animals based on their molecular data, it often fits much better with their geographical distribution.

“Where things live – their biogeography – is an important source of evolutionary evidence that was familiar to Darwin and his contemporaries.

“For example, tiny elephant shrews, aardvarks, elephants, golden moles and swimming manatees have all come from the same big branch of mammal evolution - despite the fact that they look completely different from one another (and live in very different ways).

“Molecular trees have put them all together in a group called Afrotheria, so-called because they all come from the African continent, so the group matches the biogeography.”

The study found that convergent evolution – when a characteristic evolves separately in two genetically unrelated groups of organisms – is much more common than biologists previously thought.

Professor Wills said: “We already have lots of famous examples of convergent evolution, such as flight evolving separately in birds, bats and insects, or complex camera eyes evolving separately in squid and humans.

Source: https://www.eurekalert.org/multimedia/800610
“But now with molecular data, we can see that convergent evolution happens all the time – things we thought were closely related often turn out to be far apart on the tree of life.

“People who make a living as lookalikes aren’t usually related to the celebrity they’re impersonating, and individuals within a family don’t always look similar - it’s the same with evolutionary trees too.

“It proves that evolution just keeps on re-inventing things, coming up with a similar solution each time the problem is encountered in a different branch of the evolutionary tree.

“It means that convergent evolution has been fooling us - even the cleverest evolutionary biologists and anatomists - for over 100 years!”

Dr Jack Oyston, Research Associate and first author of the paper, said: “The idea that biogeography can reflect evolutionary history was a large part of what prompted Darwin to develop his theory of evolution through natural selection, so it's pretty surprising that it hadn't really been considered directly as a way of testing the accuracy of evolutionary trees in this way before now.

“What's most exciting is that we find strong statistical proof of molecular trees fitting better not just in groups like Afrotheria, but across the tree of life in birds, reptiles, insects and plants too.
“It being such a widespread pattern makes it much more potentially useful as a general test of different evolutionary trees, but it also shows just how pervasive convergent evolution has been when it comes to misleading us.”"

Summary and conclusions:
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2023/06/21

DNA doesn't dictate organismal traits or characteristics - RNAs in sperm affect offspring phenotype

DNA doesn't dictate organismal traits or characteristics - RNAs in sperm affect offspring phenotype


https://www.chop.edu/news/research-finds-rnas-sperm-influence-offspring-phenotype

Excerpt: "During fertilization, a sperm and egg cells unite to combine genetic information provided by both parents. For years, researchers have assumed fertilizing the egg was the primary role of sperm. But sperm do more than transmit paternal genes: They deliver a complex payload of RNA molecules that can modulate inherited characteristics of offspring.

In the last 10 to 15 years, researchers have learned that the paternal environment—including diet and stress—causes changes in small RNAs carried by the sperm and impacts offspring traits like metabolism and behaviors.

This forms the foundation of research for Colin Conine, PhD, an investigator with Children’s Hospital of Philadelphia’s Division of Neonatology. For his research in this area, Dr. Conine was named a 2021 Pew Scholar in the Biomedical Sciences. With four years of funding from Pew, Dr. Conine will elucidate the mechanisms behind this form of epigenetic inheritance in more detail than ever before.

Although historically RNAs have been thought of as intermediaries that help translate information from the DNA in our genes into functional proteins in our bodies, it is now also understood that RNA can play a regulatory role, helping to turn genes on or off. This often occurs via small, noncoding regulatory RNAs. When it comes to sperm, prior studies have shown that the paternal environment can regulate these small regulatory RNAs in sperm, with changes in diet leading to changes in transfer RNA (tRNA) fragments, whereas stress influences microRNAs.


However, there are millions of RNAs in sperm, many of which have not been identified and characterized. That’s where Dr. Conine’s research comes in. Dr. Conine’s research has already demonstrated that sperm RNAs can regulate embryonic gene expression after fertilization and that this regulation is important for embryo implantation and development.

With the help of the Pew Award, researchers in his lab are using state-of-the-art techniques in reproductive biology, molecular biology, genomics, biochemistry, and genetics to characterize all RNAs in sperm across multiple species. Once he and his team provide a comprehensive overview of all the RNAs in sperm, they plan to test what impact those RNAs have on the next generation, learning what various RNAs regulate and how they impact offspring.

This work will provide insights into the inheritance and predisposition of disease and potentially lead to novel treatments for male fertility and developmental disorders.

Research in Focus

Dr. Conine’s lab is particularly interested in how RNAs present in sperm are capable of transmitting non-genetic information to their progeny, influencing offspring phenotype. This includes:
  • How small RNAs regulate gene expression in the male germline to support spermatogenesis and fertility
  • How small RNAs are packaged into mature sperm
  • How RNAs transmitted during fertilization are able to regulate early embryonic gene expression and development
  • How this regulation can alter developmental programs to produce a non-genetically inherited phenotype

“The fact that this happens specifically from the male side is particularly interesting,” says Conine. “For years, it’s been thought that sperm only contribute the genome. But this work— it’s background and our current research—makes people really reconsider how we think about fertilization and the role of sperm in early development.”"

Summary and conclusions:
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2023/06/20

Volvox algae - the favorite child of evolutionists proves that evolution does not happen

Volvox algae - the favorite child of evolutionists proves that evolution does not happen


When evolutionists are asked how multicellularity could have evolved, they quite often use Volvox algae as an example. It is considered a model example of evolution because it represents a type of simple multicellular organism. It is worth investigating a little more closely what the multicellularity of Volvox means and whether it proves that evolution has taken place.

Here's the phylogenetic tree of the Volvox algae:























Pay attention to Chlamydomonas reinhardtii, a very interesting organism. It is able to switch between being unicellular and multicellular. However, it is not a true multicellular organism because it lacks many mechanisms that a true multicellular organism needs. These are, for example, genes that code for proteins involved in an extracellular matrix (ECM), cell-to-cell communication, cellular differentiation and specialization, cellular cohesion and genes which alter the reproductive cycle. However, Chlamydomonas reinhardtii is able to efficiently adapt to changing environment and switch between unicellularity and (pseudo)multicellularity. Most commonly, it becomes multicellular when it is threatened by predators. Switching from a  unicellular to a multicellular state does not take long, only a few hundred generations. It's obvious that Chlamydomonas reinhardtii has built-in epigenetic mechanisms by which it is able to rapidly adapt to changing conditions and be protected from predators. Switching from unicellularity to multicellularity has nothing to do with random mutations or imaginary selection.

But there's more to come. Next we should focus on Volvox carteri, which is the favorite child for evolution believers. The phylogenetic tree above presents that it has descended from Chlamydomonas reinhardtii. There are 6 'speciation steps' between these two organisms. Interesting is, that Volvox carteri has lost the ability to switch back to a unicellular state. It has experienced a serious loss of genes due to epigenetic adaptations and speciation. This is not evolution, this proves that genetic entropy is a biological fact. The more adaptation, the more information loss. Evolution has no mechanism.

Summary and conclusions:
  • Chlamydomonas reinhardtii has built-in epigenetic mechanisms by which it is able to switch between unicellular and multicellular modes.
  • Volvox carteri belongs to the same group of organisms (same kind) as Chlamydomonas reinhardtii. It has experienced ecological adaptation and variation.
  • Switching between unicellularity and multicellularity doesn't take millions of years, but only weeks or months.
  • Adaptation of Volvox carteri has resulted in loss and corruption of biological information. This is why Volvox carteri has lost the ability to switch back to unicellular state.
  • Volvox algae confirm my previous observations; the more adaptation, the more information loss.
  • Evolution has no mechanism.
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2023/06/19

Natural selection is not able to weed out harmful mutations - Scientists have to select them by using modern technology

Natural selection is not able to weed out harmful mutations - Scientists have to select them by using modern technology


https://www.azolifesciences.com/news/20210608/Harmful-DNA-mutations-play-a-key-role-in-the-conservation-of-threatened-species.aspx

Excerpts: "Researchers in Lund, Copenhagen, and Norwich have demonstrated that detrimental mutations in DNA play a vital—but often overlooked—role in vulnerable species translocation and conservation initiatives."

"The researchers studied whether individuals would be most suited for translocation to other populations in a recent study published in the Science journal. Until now, conservation geneticists have chosen the most genetically diverse individuals.

The authors believe, however, that it is critical to evaluate what sort of genetic variation is being moved about. They used computer simulations and demonstrated that detrimental mutations in the genomes of translocated humans might create difficulties in future generations.

This so-called “mutation load” might endanger the viability of the new population in the long term, leading to extinction.

The ideal option, according to Hansson and van Oosterhout, a geneticist from the University of East Anglia in Norwich who conducted the study, is to remove people with numerous detrimental mutations while also choosing individuals from numerous diverse source populations."

"Active translocation of animals between localities is sometimes the last option available to conservation biologists. By carefully selecting individuals based on their low mutation load, we can minimize the loss of fitness that is normally associated with inbreeding in small populations.” 
Bengt Hansson, Biologist, Lund University
"Massive progress has been achieved in DNA sequencing technology, and individuals’ whole genomes may now be sequenced at comparatively low costs. This brings up new avenues for improving threatened species conservation management."

"For many species of mammals and birds, we now know which mutations are harmful. Similar mutations are also found in humans, so we understand what they do, and hence, we know what to look out for when analyzing the sequence data of those species. The advantage of using DNA sequencing is that we can see these mutations in the genome, even if an individual carries just a single copy of the mutant gene.” 
Van Oosterhout, Geneticist, University of East Anglia, Norwich 
“This means we can select against those bad mutations even before they cause a problem. Our computer model shows that at least theoretically, this ensures the best probability for population survival. This could help conservation managers in picking the optimal individuals of a threatened species for translocation into a new habitat,” concluded Oosterhout.

Summary and conclusions:

  • Mutation load is an inevitable phenomenon and because there is no junk-DNA, this genetic load results in corruption of biological information.
  • Natural selection is an imaginary force that is not able to weed out these harmful genetic errors.
  • Mutation load affects all kind of organisms in the wild. It affects also human beings.
  • Genetic diversity is not necessarily a good thing regarding survival of populations.
  • Scientists need to use modern technology, such as Crispr DNA editing techniques in order to select harmful mutations out of endangered species.
  • Evolution is not happening. Devolution wins.

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2023/06/17

Mutation load destroys the theory of Evolution

Mutation load destroys the theory of Evolution


https://www.uh.edu/news-events/stories/2017/july/07142017Graur-functional-genome.php

Excerpts: "In work published online in Genome Biology and Evolution, Dan Graur reports the functional portion of the human genome probably falls between 10 percent and 15 percent, with an upper limit of 25 percent. The rest is so-called junk DNA, or useless but harmless DNA.

Graur, Moores Professor of Biology and Biochemistry at UH, took a deceptively simple approach to determining how much of the genome is functional, using the deleterious mutation rate – that is, the rate at which harmful mutations occur – and the replacement fertility rate."
"Both genome size and the rate of deleterious mutations in functional parts of the genome have previously been determined, and historical data documents human population levels. With that information, Graur developed a model to calculate the decrease in reproductive success induced by harmful mutations, known as the “mutational load,” in relation to the portion of the genome that is functional."

"If 80 percent of the genome were functional, unrealistically high birth rates would be required to sustain the population even if the deleterious mutation rate were at the low end of estimates, Graur found.

“For 80 percent of the human genome to be functional, each couple in the world would have to beget on average 15 children and all but two would have to die or fail to reproduce,” he wrote. “If we use the upper bound for the deleterious mutation rate (2 × 10−8 mutations per nucleotide per generation), then … the number of children that each couple would have to have to maintain a constant population size would exceed the number of stars in the visible universe by ten orders of magnitude.”"

Mutation load? What does it mean?

Mutation load or genetic load is the reduction in the fitness of a population caused by recurrent deleterious mutations, genetic drift, recombination affecting epistatically favourable gene combinations, or other genetic processes. An example: Human mutation load can be measured by a mutation rate. Nature study: Every time human DNA is passed from one generation to the next it accumulates 100–200 new mutations, according to a DNA-sequencing analysis of the Y chromosome. Genetic load is a biological fact that occurs within all kind of organisms.


Evolution needs junk-DNA

Because of the inevitable mutation load, there has to be a protective buffer against deleterious mutations, in order for evolution to occur. This is why evolutionary biologists have believed that the maximum proportion of functional genome can't be higher than 25%. If it exceeds that, then evolution becomes a destructive process, as Dan Graur states.

Today, there is no junk-DNA

Serious scientific research has confirmed, that the theory of junk-DNA has seriously failed:

"In addition, there has been an explosion of research addressing possible functional roles for the other 98% of the human genome that does not encode proteins. In fact, >90% of the human genome is likely to be transcribed yielding a complex network of overlapping transcripts that include tens of thousands of long RNAs with little or no protein forming capacity; they are collectively called non-coding RNA."

Summary and conclusions:
  • Mutation load (genetic load) is an inevitable phenomenon occurring all over nature.
  • In order for evolution to occur, the functional share of genomes can't be larger than 25%.
  • According to modern science there is no junk-DNA. At least 90% of human genome is read for transcription and for the rest 10%, it's been found important regulatory tasks.
  • The theory of so called neutral mutations is based on the existence of junk-DNA.
  • There are at least 2 million harmful mutations in human genome worldwide but the number of random, fully beneficial mutations is 0.
  • Mutation load destroys the theory of evolution.
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2023/06/03

Genetic diseases are more common than previously thought - Evidence for Genetic Entropy

Genetic diseases are more common than previously thought - Evidence for Genetic Entropy


https://medicalxpress.com/news/2023-05-rare-diseases-previously-thought.html

Excerpt: "Rare diseases are often caused by defects in genetic material. If children inherit a defective gene from only one parent, they often are asymptomatic "carriers"—or at least that was the previous assumption. However, a research team from the University of Basel and the University Hospital Basel is now reporting that such carriers can also suffer from life-threatening diseases—and that rare hereditary diseases are therefore probably more common than previously thought.

Every child receives one set of chromosomes from their mother and one from their father. So for the majority of all genes, every human being has two copies—known as "alleles." A lot of rare hereditary diseases only emerge if both alleles of a gene carry a defect. This is also referred to as a "recessive" hereditary disease. If only one allele is affected, the other can compensate and no symptoms will occur.

Novel missense variant within the catalytic core of LIG4.
Recessive hereditary diseases include a large number of immunological disorders that are based on mutations in one of the estimated 2,500 to 5,000 genes that are relevant to the immune system. These diseases are characterized by susceptibility to infection or autoimmunity, in which the body launches an immune attack against itself.

Researchers led by Professor Mike Recher from the University of Basel and University Hospital Basel are now using the example of a recessive hereditary disease to show that the defect poses the risk of a restriction in immune system function even when it is present in only one allele.

"These kinds of cases have been far too frequently ignored in the past, based on the assumption that defects are only problematic if they are present in both alleles," Recher explains. "However, carriers can actually suffer from life-threatening diseases too, often as adults and with symptoms that can sometimes be uncommon."

The study, which also involved researchers led by Dr. Hiroyuki Yamamoto from the National Institute of Infectious Diseases (NIID) in Tokyo, Japan, has been published in the Journal of Allergy and Clinical Immunology.

Not enough enzyme for full function

In the study, the researchers report on mutations in the blueprint for an enzyme that is crucial for the diversity of antibodies and T-cells. Mutations in both alleles of this LIG4 gene lead to a major disruption of the body's immune response, and therefore to an increased risk of severe infections from an early age.

Previously, carriers of just one defective LIG4 allele were considered asymptomatic. But Recher and his team at the Department of Biomedicine are now reporting multiple cases where individuals have nevertheless exhibited severe symptoms that are only partially reminiscent of the original inherited disease. "In the case of these individuals, only having one functioning LIG4 gene does not seem to be sufficient," says the immunologist.

Unrecognized risks

Among the thousands of genes that are involved in the human immune system, there are a lot of mutations in just one allele where not enough is yet known about their importance for an effective immune response over the course of a person's lifetime.

"Our and other recent findings are showing that these defects may be the cause of previously unexplained immune disorders much more frequently than previously thought."

"We suspect that many rare recessive diseases may actually have more common counterparts, partly yet to be described, associated with unusual symptoms, a tendency to occur later in life and with a different inheritance pattern," Recher explains. But there will continue to be healthy carriers. "In addition to genetics, environmental factors such as infections or epigenetics also play a role here."

According to Recher, it is important that these new findings be taken into account in diagnostics. "When you understand what the problem is at a molecular level, this can suddenly open up some very targeted treatment options that are often low in side effects, and that don't just fight the symptoms but also the cause."

Summary and conclusions:
  • Asymptomatic carriers of gene defects often suffer from life-threatening diseases.
  • Definition of recessive and dominant genes should be called into question.
  • Even one broken allele might cause severe problems to the immune system.
  • DNA is highly organized information and the cell uses passive DNA libraries in a multi-functional way: One DNA sequence may be used for several purposes and often for the immune system.
  • There are over 2 million genetic defects in human genome worldwide but the number of random, fully beneficial mutations is 0.
  • Evolution never happened.
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