The watchtower Society's commentary on "Armaggedon."

What Is the Battle of Armageddon?

The Bible’s answer

The battle of Armageddon refers to the final war between human governments and God. These governments and their supporters oppose God even now by refusing to submit to his rulership. (Psalm 2:2) The battle of Armageddon will bring human rulership to an end.—Daniel 2:44.

The word “Armageddon” occurs only once in the Bible, at Revelation 16:16. Prophetically, Revelation shows that at “the place that is called in Hebrew Armageddon,” “the kings of the entire inhabited earth” will be gathered “together to the war of the great day of God the Almighty.”—Revelation 16:14.

Who will fight at Armageddon? Jesus Christ will lead a heavenly army to victory over God’s enemies. (Revelation 19:11-16, 19-21) These enemies include those who oppose God’s authority and who treat God with contempt.—Ezekiel 39:7.

Will Armageddon literally be fought in the Middle East? No. Rather than being restricted to one area, the battle of Armageddon will encompass the whole earth.—Jeremiah 25:32-34; Ezekiel 39:17-20.

Armageddon, sometimes rendered “Har–Magedon” (Hebrew Har Meghiddohn′), means “Mountain of Megiddo.” Megiddo was once a city in the territory of ancient Israel. History tells of decisive battles that were fought in its vicinity, including some that are recorded in the Bible. (Judges 5:19, 20; 2 Kings 9:27; 23:29) However, Armageddon cannot refer to the literal area near ancient Megiddo. There is no large mountain there, and even the entire adjoining Low Plain of Jezreel could not contain all those who will fight against God. Instead, Armageddon is the worldwide situation in which the nations assemble in their last stand against rule by God.

What will conditions be like during the battle of Armageddon? While we do not know how God will use his power, he will have at his disposal weapons such as those he has used in the past—hail, earthquake, flooding downpour, fire and sulfur, lightning, and disease. (Job 38:22, 23; Ezekiel 38:19, 22; Habakkuk 3:10, 11; Zechariah 14:12) In confusion, at least some of God’s enemies will kill each other, yet they will ultimately realize that it is God who is fighting against them.—Ezekiel 38:21, 23; Zechariah 14:13.

Will Armageddon be the end of the world? It will not be the end of our planet, since the earth is mankind’s eternal home. (Psalm 37:29; 96:10; Ecclesiastes 1:4) Rather than destroying humanity, Armageddon actually saves it, because “a great crowd” of God’s servants will survive.—Revelation 7:9, 14; Psalm 37:34.

Besides referring to the earth, though, the word “world” in the Bible sometimes refers to wicked human society opposed to God. (1 John 2:15-17) In this sense, Armageddon will bring “the end of the world.”—Matthew 24:3, King James Version.

When will Armageddon take place? When discussing the “great tribulation” that culminates in the battle of Armageddon, Jesus said: “Concerning that day and hour nobody knows, neither the angels of the heavens nor the Son, but only the Father.” (Matthew 24:21, 36) Nevertheless, the Bible does show that Armageddon takes place during Jesus’ invisible presence, which began in 1914.—Matthew 24:37-39.

A victory for religious liberty in France.

Highest Administrative Court in France Ends Discrimination

After our meeting together, I am happy and singing to myself. Your visit is comforting, and studying the Bible gives me purpose in life.

I just wanted to thank you for the legal, administrative, and spiritual measures you have taken to put this chaplaincy in place.

This provision is an answer to my prayers.

These comments from prison inmates in France express appreciation for the spiritual assistance provided by a minister of Jehovah’s Witnesses.

On October 16, 2013, France’s highest Administrative Court issued a decision that ended a period of discrimination against Jehovah’s Witnesses in France. The Court’s ruling allows ministers of Jehovah’s Witnesses to enter prisons as certified chaplains to offer spiritual counseling to inmates who request a visit. *

Witness Ministers Denied Chaplain Certificates

For many years, prison authorities allowed Witness ministers to visit prisons to offer spiritual guidance and counseling despite their not having a chaplain certificate that officially recognized them as ministers. This began to change in 1995 after a Parliamentary Commission released a controversial report containing a list of so-called dangerous sects that included Jehovah’s Witnesses. This negative classification did more than attack the Witnesses’ image—it sparked a wave of discrimination against them. One manifestation of this was seen in the prison system.

Although parliamentary reports are not legally binding, some prison administrations used the 1995 report as a basis to restrict Witness ministers’ access to inmates who requested spiritual assistance. A Witness minister could visit inmates under common law as a private citizen but not in his official capacity as a minister. He was no longer allowed to bring a Bible or any religious literature with him. All visits had to be conducted in a public visiting room in an atmosphere that was not conducive to a spiritual discussion. One Witness minister said that the atmosphere in the visiting room “was like that of a train concourse, with a similar noise level.” Some prison facilities required that inmates be strip-searched after a visit because it was not with a government-certified chaplain.

In an effort to obtain the same rights as certified ministers of other religions, ministers of Jehovah’s Witnesses began applying for chaplain certificates through the French penitentiary administration in 2003. All applications were categorically denied. The Witnesses appealed these arbitrary and discriminatory refusals to a higher administrative authority but were again denied. The official reason given by France’s Ministry of Justice for refusing to certify Witness ministers as chaplains was that Jehovah’s Witnesses were not on the list of religions that were authorized to enter prisons. The Ministry also expressed concern that granting a chaplain certificate to one of Jehovah’s Witnesses would only encourage other religious minorities to request chaplain certificates. After unsuccessful attempts to resolve the matter through the Ministry of Justice, the Witnesses had no other choice but to pursue this issue in court.

Government Refuses to End Discrimination

In 2006, Jehovah’s Witnesses initiated lawsuits to annul the refusals and to order the Ministry of Justice to grant chaplain certificates to Witness ministers. Every Administrative Court and Court of Appeals in the country that ruled on the matter declared that the government’s refusals were illegal. Moreover, in 2010, the French High Authority for the Fight Against Discrimination and for Equality denounced the government’s position and recommended that the Minister of Justice put an end to the discrimination.

The French government not only ignored this warning and the court decisions but also lodged appeals with the Council of State, France’s highest Administrative Court.

Historic Decision in Favor of Jehovah’s Witnesses

In 2013, the Witness cases eventually came before the Council of State, which joined nine similar cases for consideration. In its October 16, 2013, decision, the Court rejected the appeals submitted by the French government. It stated that in order to respect a prisoner’s rights, the Penitentiary Administration must, “as soon as the request is made, certify a sufficient number of religious ministers as chaplains, subject only to the safety and good order requirements of the facility.” Further, referring to the French Constitution and the European Convention on Human Rights, the Council of State declared that “freedom of opinion, conscience and religion of incarcerated individuals is guaranteed and that they may practice the religion of their choice.” As a result of this decision, to date, 105 chaplain certificates have been issued in France, including its overseas territories, making it possible for prison inmates to receive pastoral visits from Jehovah’s Witnesses.

In January 2014, the French Penitentiary Administration appointed one of Jehovah’s Witnesses, Jean-Marc Fourcault, as the national chaplain of Jehovah’s Witnesses. In this role, Mr. Fourcault has access to all prisons in France. He is also authorized to act as the representative of Jehovah’s Witnesses before the Penitentiary Administration. Mr. Fourcault states: “From now on, just like representatives from other authorized religions, Jehovah’s Witness chaplains will be able to meet with inmates privately and in dignified and appropriate locations, sometimes in their own cell.”

This decision is an important victory for freedom of religion in France. It reaffirms that detained individuals have the right to practice the religion of their choice and to be visited by a minister of their choice. Jehovah’s Witnesses are grateful that French courts ended this discrimination, marking another step forward in the recognition of Jehovah’s Witnesses as a religion in France.

The spectre of Lamarck looms.

Lamarck Rescued by RNA? New "Level of Organization" Found for Epigenetic Inheritance

Evolution News & Views February 5, 2015 4:20 AM |

 

 

 

Here's the bottom line from a new paper in PNAS: "To our knowledge, these results demonstrate for the first time that a somatic tissue of an animal can have transgenerational effects on a gene through the transport of double-stranded RNA to the germline." Whoa!

The triumphalist history of Darwinism shows Charles Darwin trouncing Lamarck's "inheritance of acquired characteristics" with the new theory of natural selection. The narrative is often given a decisive coup-de-grace with the retelling of experiments in 1891, when August Weismann cut off the tails of multiple generations of mice, proving that acquired characteristics are not inherited. If Lamarckism were true, bodybuilders would have muscular sons. That doesn't happen, so ha ha! Lamarck's theory is falsified and defunct. Long live Darwin!

What's usually left out of this narrative is that Lamarckism did not go out the exit so quietly. In fact, Darwin himself became more Lamarckian in subsequent editions of The Origin. There continue to be Lamarck fans (example at The Mermaid's Tale) and detractors (example at Real Clear Science). Scientific controversies are rarely decisive. Historians of science like to point out that some of the most clear-cut cases, like the demise of caloric theory and phlogiston theory, did not convince everyone due to one crucial experiment.

The new paper in PNAS is muddying the waters again. Since the word "epigenetics" entered the vocabulary, more old-school geneticists have had to backpedal from the Central Dogma (DNA makes RNA makes protein) to varying degrees. These days, it is common to see admissions of "epigenetic inheritance" and "lateral gene transfer" adding to the neo-Darwinist recipe. What's new about the PNAS paper is experimental verification of a mechanism for inheritance of acquired characteristics in certain cases. It may only apply to roundworms. It may be limited in what it can accomplish. But it happens; and rather than following Darwin's rule of random variations, it involves information transfer.

The germline is separated from the rest of the body, or soma, during early development in most animals, consistent with the suggestion that environmental effects on soma throughout the lifetime of an animal cannot influence inheritance through the germline. However, some environmental changes can cause effects that last for three or more generations, even in the apparent absence of changes in the genotype... These transgenerational epigenetic effects are presumably initiated either by direct changes within the ancestral germline or by the transfer of information from ancestral somatic cells to the ancestral germline.

The researchers found an agent of information transfer in the form of double-stranded RNA (dsRNA). Previous work showed that dsRNA from neurons can travel from one somatic cell to another, silencing genes. This is the first time this process is observed to affect the germline, at least in the lab roundworm Caenorhabditis elegans.

Here, we show that neuronal mobile RNAs can enter both somatic and germ cells to trigger gene silencing. Although silencing in somatic tissues is not detectably inherited despite multigenerational exposure to neuronal mobile RNAs, silencing in the germline is inherited for many generations after a single generation of exposure to neuronal mobile RNAs.

How many is many? "Inherited silencing due to the ancestral production of neuronal mobile RNAs persisted for >25 subsequent generations," they found. In short,

We found that neurons can transport forms of dsRNA into the germline to cause silencing that can last for many generations, and that such transgenerational silencing is restricted to the germline with distinct genetic requirements for initiation and maintenance.

Requirements? Maintenance? That doesn't sound like Darwin's "random variations." It almost sounds like a designed mechanism to help subsequent generations adapt to environmental changes. Watch out for that word information:

Mobile RNAs that enter the germline can provide an organism with the ability to transfer gene-specific regulatory information from somatic cells across generations and could be one mechanism by which the environment elicits transgenerational effects in animals. Although restricted to the germline, transgenerational silencing by mobile RNAs could underlie effects of the environment across generations in some cases. For example, expression of some genes within the germline can affect longevity, and transgenerational silencing of such genes might underlie the longevity that results from ancestral starvation in C. elegans. Thus, additional experiments are needed to determine the role of mobile RNAs, if any, in the transport of such experience-dependent information from somatic cells to subsequent generations in C. elegans.

That's fine for roundworms, but we can't expect higher organisms to act Lamarckian, can we? The authors consider the possibility that a similar import mechanism for dsRNA (SID-1) works in mammals, but realize that mammals have extra protections against germline changes:

The presence of a mammalian homolog of the dsRNA importer SID-1 that is also required for the uptake of dsRNAs into cells raises the possibility that dsRNA generated from distant somatic cells -- potentially in response to environmental influences -- may be imported through SID-1 into the mammalian germline to trigger transgenerational epigenetic changes. Consistent with this possibility, small RNAs have been found in circulation in mammals; dsRNAs have been detected in mammalian germ cells; and injection of RNAs into the early mouse embryo can trigger epigenetic silencing. However, even if RNAs from somatic cells are transported to the germline in mammals, they may not always initiate transgenerational inherited effects because they have to escape mechanisms that reprogram epigenetic information in each generation. Additional studies are required to determine whether specific mechanisms prevent environmental influences from triggering transmission of information in the form of mobile RNAs from somatic cells to the germline.

It's too early to tell, in other words, if this mechanism works for mammals. But consider these evidences that support the possibility: (1) Cases of epigenetic inheritance in humans are already known. (2) Mammals have a homologue of the SID-1 mechanism for importing dsRNA into germ cells. (3) Epigenetic information doesn't have to reside in the chromosomes; it can be transferred to the zygote via cytosolic proteins in the sperm or egg cells.

Before concluding that mammals need not apply, because they reset all the epigenetic codes each generation, more research will be needed. But if this mechanism for transferring environmental cues to the germline works for roundworms, why would it not work for other organisms? Why would a sophisticated system with "requirements" for "initiation" and "maintenance" be found only here in the animal kingdom?

A news item from the University of Maryland, where the research was conducted, does not restrict this mechanism to roundworms.

For more than a century, scientists have understood the basics of inheritance: if good genes help parents survive and reproduce [classic neo-Darwinism], the parents pass those genes along to their offspring. And yet, recent research has shown that reality is much more complex: genes can be switched off, or silenced, in response to the environment or other factors, and sometimes these changes can be passed from one generation to the next.

The phenomenon has been called epigenetic inheritance, but it is not well understood. Now, UMD geneticist Antony Jose and two of his graduate students are the first to figure out a specific mechanism by which a parent can pass silenced genes to its offspring. Importantly, the team found that this silencing could persist for multiple generations -- more than 25, in the case of this study.

They say that this finding "could transform our understanding of animal evolution." That's a euphemistic way of saying it could undermine it, turning it from chance to design. No more hoping for beneficial mutations by chance; look instead for organized systems for transferring information from the environment to the organism and its progeny, so that it can robustly adapt to change.

"For a long time, biologists have wanted to know how information from the environment sometimes gets transmitted to the next generation," said Jose, an assistant professor in the UMD Department of Cell Biology and Molecular Genetics. "This is the first mechanistic demonstration of how this could happen. It's a level of organization that we didn't know existed in animals before."

A new "level of organization" is design language, even if the researchers can't let go of the Darwin paradigm completely:

The team's biggest finding was that dsRNA can travel from body cells into germ cells and silence genes within the germ cells. Even more surprising, the silencing can stick around for more than 25 generations. If this same mechanism exists in other animals -- possibly including humans -- it could mean that there is a completely different way for a species to evolve in response to its environment.

"This mechanism gives an animal a tool to evolve much faster," Jose said. "We still need to figure out whether this tool is actually used in this way, but it is at least possible. If animals use this RNA transport to adapt, it would mean a new understanding of how evolution happens."

Think about that. There's nothing there about chance variation and unguided processes. There's a "tool" the animal can "use" to "adapt." That sounds like a pre-programmed plan for robustness in a world of change: a plan to keep the population stable when famine, drought, heat, cold, or other factors threaten. Once again, RNA plays the role of a messenger. Like the messenger RNA (mRNA) that ferries genetic information to the ribosome, the dsRNA ferries epigenetic information to other cells and to the next generation. One might imagine an email blast going out, "Attention, all cells: silence gene #59348h; famine detected!" This implies that both sender and receiver understand the protocols and have the necessary infrastructure to get the message out.

We're not out to support Lamarck or Darwin. Neither of them could account for new genetic information, body plans, or hierarchical design. What's intriguing is this "level of organization" that biologists "didn't know existed in animals before." Here is a new avenue where design-based research can take the lead.

Resistance is futile.

Sulfur Bacteria, Unchanged for Billions of Years, Confirm Darwinian Evolution. Come Again?  David Klinghoffer 

An organism's staying exactly the same for 2 billion years -- in other words, not evolving a bit -- supports the Darwinian theory of evolution, say scientists who studied fossils in rocks from the waters off the West Australian coast and uncovered the "greatest absence of evolution ever reported."

Nope, not The Onion. We read at Science Daily:

An international team of scientists has discovered the greatest absence of evolution ever reported -- a type of deep-sea microorganism that appears not to have evolved over more than 2 billion years. But the researchers say that the organisms' lack of evolution actually supports Charles Darwin's theory of evolution.

The findings are published online by the Proceedings of the National Academy of Sciences.

The scientists examined sulfur bacteria, microorganisms that are too small to see with the unaided eye, that are 1.8 billion years old and were preserved in rocks from Western Australia's coastal waters. Using cutting-edge technology, they found that the bacteria look the same as bacteria of the same region from 2.3 billion years ago -- and that both sets of ancient bacteria are indistinguishable from modern sulfur bacteria found in mud off of the coast of Chile.

"It seems astounding that life has not evolved for more than 2 billion years -- nearly half the history of Earth," said J. William Schopf, a UCLA professor of earth, planetary and space sciences in the UCLA College who was the study's lead author. "Given that evolution is a fact, this lack of evolution needs to be explained."

Given that Darwinian theory is a "fact," it must be shown that it is a "fact" regardless of evidence to the contrary. Well, given the premise, that would have to be so. The solution, please?

"The rule of biology is not to evolve unless the physical or biological environment changes, which is consistent with Darwin," said Schopf, who also is director of UCLA's Center for the Study of Evolution and the Origin of Life. The environment in which these microorganisms live has remained essentially unchanged for 3 billion years, he said.

"These microorganisms are well-adapted to their simple, very stable physical and biological environment," he said. "If they were in an environment that did not change but they nevertheless evolved, that would have shown that our understanding of Darwinian evolution was seriously flawed."

That was deft. It's not what they expected. But then again, it's exactly what they expected.

In summary, Darwinism is demonstrated when life evolves. It's also demonstrated when it does not. If the bacteria had changed, what would they have said? Since Darwinian evolution is a fact, you can be certain that too would be reconciled with the theory, like all evidence, one way or the other, come hell or high water.





  Ps. And now for the elephant in the room: If darwinian evolution had already produced the perfect replicator and vehicle for its selfish gene at the very beginning of life's  history.Shouldn't it have stop there  and then as per  the  claims of darwinists.

On darwinism's alleged 'tree of life'

Editor's note: This is Part 6 of a 10-part series based upon Casey Luskin's chapter,, "The Top Ten Scientific Problems with Biological and Chemical Evolution," in the volume More than Myth, edited by Paul Brown and Robert Stackpole (Chartwell Press, 2014). Previous installments can be found here:Problem 1, Problem 2, Problem 3, Problem 4, Problem 5. When the series is complete, the full chapter will be posted online.

When fossils failed to demonstrate that animals evolved from a common ancestor, evolutionary scientists turned to another type of evidence -- DNA sequence data -- to demonstrate a tree of life. In the 1960s, around the time the genetic code was first understood, biochemists Émile Zuckerkandl and Linus Pauling hypothesized that if DNA sequences could be used to produce evolutionary trees -- trees that matched those based upon morphological or anatomical characteristics -- this would furnish "the best available single proof of the reality of macro-evolution."⁹⁹ Thus began a decades-long effort to sequence the genes of many organisms and construct "molecular" based evolutionary ("phylogenetic") trees. The ultimate goal has been to construct a grand "tree of life," showing how all living organisms are related through universal common ancestry.

The Main Assumption

The basic logic behind building molecular trees is relatively simple. First, investigators choose a gene, or a suite of genes, found across multiple organisms. Next, those genes are analyzed to determine their nucleotide sequences, so the gene sequences of various organisms can then be compared. Finally, an evolutionary tree is constructed based upon the principle that the more similar the nucleotide sequence, the more closely related the species. A paper in the journalBiological Theory puts it this way:

[M]olecular systematics is (largely) based on the assumption, first clearly articulated

by Zuckerkandl and Pauling (1962), that degree of overall similarity reflects degree of relatedness.¹⁰⁰

This assumption is essentially an articulation of a major feature of the theory - the idea of universal common ancestry. Nonetheless, it's important to realize that it is a mere assumption to claim that genetic similarities between different species necessarily result common ancestry.

Operating strictly within a Darwinian paradigm, these assumptions flow naturally. As the aforementioned Biological Theory paper explains, the main assumption underlying molecular trees "derives from interpreting molecular similarity (or dissimilarity) between taxa in the context of a Darwinian model of continual and gradual change."¹⁰¹ So the theory is assumed to be true to construct a tree. But also, if Darwinian evolution is true, construction of trees using different sequences should reveal a reasonably consistent pattern across different genes or sequences.

This makes it all the more significant that efforts to build a grand "tree of life" using DNA or othebiological sequence data have not conformed to expectations. The basic problem is that one gene gives one version of the tree of life, while another gene gives a highly different, and conflicting, version of the tree. For example, as we'll discuss further below, the standard mammalian tree places humans more closely related to rodents than to elephants. But studies of a certain type of DNA called microRNA genes have suggested the opposite -- that humans were closer to elephants than rodents. Such conflicts between gene-based trees are extremely common.

The genetic data is thus not painting a consistent picture of common ancestry, showing the assumptions behind tree-building commonly fail. This leads to justifiable questions about whether universal common ancestry is correct.

Conflicts in the Base of the Tree of Life

Problems first arose when molecular biologists sequenced genes from the three basic domains of life -- bacteria, archaea, and eukarya -- but those genes did not allow these basic groups of life to be resolved into a treelike pattern. In 2009, the journal New Scientist published a cover story titled, "Why Darwin was wrong about the tree of life" which explained these quandaries

The problems began in the early 1990s when it became possible to sequence actual bacterial and archaeal genes rather than just RNA. Everybody expected these DNA sequences to confirm the RNA tree, and sometimes they did but, crucially, sometimes they did not. RNA, for example, might suggest that species A was more closely related to species B than species C, but a tree made from DNA would suggest the reverse.¹⁰²

This sort of data led biochemist W. Ford Doolittle to explain that "Molecular phylogenists will have failed to find the 'true tree,' not because their methods are inadequate or because they have chosen the wrong genes, but because the history of life cannot properly be represented as a tree."¹⁰³ New Scientist put it this way: "For a long time the holy grail was to build a tree of life ... But today the project lies in tatters, torn to pieces by an onslaught of negative evidence."¹⁰⁴

Many evolutionists sometimes reply that these problems arise only when studying microorganisms like bacteria -- organisms which can swap genes through a process called "horizontal gene transfer," thereby muddying the signal of evolutionary relationships. But this objection isn't quite true, since the tree of life is challenged even among higher organisms where such gene-swapping is not prevalent. Carl Woese, a pioneer of evolutionary molecular systematics, explains

Phylogenetic incongruities can be seen everywhere in the universal tree, from its root to the major branchings within and among the various taxa to the makeup of the primary groupings themselves.¹⁰⁵

Likewise, the New Scientist article notes that "research suggests that the evolution of animals and plants isn't exactly tree-like either."¹⁰⁶ The article explains what happened when microbiologist Michael Syvanen tried to create a tree showing evolutionary relationships using 2000 genes from a diverse group of animals:

He failed. The problem was that different genes told contradictory evolutionary stories. ... the genes were sending mixed signals. ... Roughly 50 per cent of its genes have one evolutionary history and 50 per cent another.¹⁰⁷

The data were so difficult to resolve into a tree that Syvanen lamented, "We've just annihilated the tree of life."¹⁰⁸ Many other papers in the technical literature recognize similar problems.

Conflicts Between Higher Branches

A 2009 paper in Trends in Ecology and Evolution notes that, "A major challenge for incorporating such large amounts of data into inference of species trees is that conflicting genealogical histories often exist in different genes throughout the genome."¹⁰⁹ Similarly, a paper in Genome Researchstudied the DNA sequences in various animal groups and found that "different proteins generate different phylogenetic tree[s]."¹¹⁰ A June, 2012 article in Nature reported that short strands of RNA called microRNAs "are tearing apart traditional ideas about the animal family tree." Dartmouth biologist Kevin Peterson who studies microRNAs lamented, "I've looked at thousands of microRNA genes, and I can't find a single example that would support the traditional tree." According to the article, microRNAs yielded "a radically different diagram for mammals: one that aligns humans more closely with elephants than with rodents." Peterson put it bluntly: "The microRNAs are totally unambiguous ... they give a totally different tree from what everyone else wants."¹¹¹

Conflicts Between Molecules and Morphology

Not all phylogenetic trees are constructed by comparing molecules like DNA from different species. Many trees are based upon comparing the form, structure, and body plan of different organisms -- also called "morphology." But conflicts between molecule-based trees and morphology-based trees are also common. A 2012 paper studying bat relationships made this clear, stating: "Incongruence between phylogenies derived from morphological versus molecular analyses, and between trees based on different subsets of molecular sequences has become pervasive as datasets have expanded rapidly in both characters and species."¹¹² This is hardly the only study to encounter conflicts between DNA-based trees and trees based upon anatomical or characteristics. Textbooks often claim common descent is supported using the example of a tree of animals based upon the enzyme cytochrome c which matches the traditional evolutionary tree based upon morphology.¹¹³ However, textbooks rarely mention that the tree based upon a different enzyme, cytochrome b, sharply conflicts with the standard evolutionary tree. As one article in Trends in Ecology and Evolution observed:

[T]he mitochondrial cytochrome b gene implied . . . an absurd phylogeny of mammals, regardless of the method of tree construction. Cats and whales fell within primates, grouping with simians (monkeys and apes) and strepsirhines (lemurs, bush-babies and lorises) to the exclusion of tarsiers. Cytochrome b is probably the most commonly sequenced gene in vertebrates, making this surprising result even more disconcerting.¹¹⁴

Strikingly, a different article in Trends in Ecology and Evolution concluded, "the wealth of competing morphological, as well as molecular proposals [of] the prevailing phylogenies of the mammalian orders would reduce [the mammalian tree] to an unresolved bush, the only consistent [evolutionary relationship] probably being the grouping of elephants and sea cows."¹¹⁵ Because of such conflicts, a major review article in Nature reported, "disparities between molecular and morphological trees" lead to "evolution wars" because "[e]volutionary trees constructed by studying biological molecules often don't resemble those drawn up from morphology."¹¹⁶

Finally, a study published in Science in 2005 tried to use genes to reconstruct the relationships of the animal phyla, but concluded that "[d]espite the amount of data and breadth of taxa analyzed, relationships among most [animal] phyla remained unresolved." The following year, the same authors published a scientific paper titled, "Bushes in the Tree of Life," which offered striking conclusions. The authors acknowledge that "a large fraction of single genes produce phylogenies of poor quality," observing that one study "omitted 35% of single genes from their data matrix, because those genes produced phylogenies at odds with conventional wisdom." The paper suggests that "certain critical parts of the [tree of life] may be difficult to resolve, regardless of the quantity of conventional data available." The paper even contends that "[t]he recurring discovery of persistently unresolved clades (bushes) should force a re-evaluation of several widely held assumptions of molecular systematics."¹¹⁷

Unfortunately, one assumption that these evolutionary biologists aren't willing to re-evaluate is the assumption that universal common ancestry is correct. They appeal to a myriad of ad hocarguments -- horizontal gene transfer, long branch attraction, rapid evolution, different rates of evolution, coalescent theory, incomplete sampling, flawed methodology, and convergent evolution -- to explain away inconvenient data which doesn't fit the coveted treelike pattern. As a 2012 paper stated, "phylogenetic conflict is common, and frequently the norm rather than the exception."¹¹⁸ At the end of the day, the dream that DNA sequence data would fit into a nice-neat tree of life has failed, and with it a key prediction of neo-Darwinian theory.

References:

[99.] Zuckerkandl and Pauling, "Evolutionary Divergence and Convergence in Proteins," 101.

[100.] Jeffrey H. Schwartz, Bruno Maresca, "Do Molecular Clocks Run at All? A Critique of Molecular Systematics," Biological Theory, 1(4):357-371, (2006).

[101.] Ibid.

[102.] Graham Lawton, "Why Darwin was wrong about the tree of life," New Scientist (January 21, 2009).

[103.] W. Ford Doolittle, "Phylogenetic Classification and the Universal Tree," Science, 284:2124-2128 (June 25, 1999).

[104.] Partly quoting Eric Bapteste, in Lawton, "Why Darwin was wrong about the tree of life" (internal quotations omitted).

[105.] Carl Woese "The Universal Ancestor," Proceedings of the National Academy of Sciences USA, 95:6854-9859 (June, 1998) (emphasis added).

[106.] Graham Lawton, "Why Darwin was wrong about the tree of life," New Scientist (January 21, 2009).

[107.] Partly quoting Michael Syvanen, in Lawton, "Why Darwin was wrong about the tree of life" (internal quotations omitted).

[108.] Michael Syvanen, quoted in Lawton, "Why Darwin was wrong about the tree of life."

[109.] James H. Degnan and Noah A. Rosenberg, "Gene tree discordance, phylogenetic inference and the multispecies coalescent," Trends in Ecology and Evolution, 24 (2009): 332-340.

[110.] Arcady R. Mushegian, James R. Garey, Jason Martin and Leo X. Liu, "Large-Scale Taxonomic Profiling of Eukaryotic Model Organisms: A Comparison of Orthologous Proteins Encoded by the Human, Fly, Nematode, and Yeast Genomes," Genome Research, 8 (1998): 590-598.

[111.] Elie Dolgin, "Rewriting Evolution," Nature, 486: 460-462 (June 28, 2012).

[112.] Liliana M. Dávalos, Andrea L. Cirranello, Jonathan H. Geisler, and Nancy B. Simmons, "Understanding phylogenetic incongruence: lessons from phyllostomid bats," Biological Reviews of the Cambridge Philosophical Society, 87:991-1024 (2012).

[113.] For example, see BSCS Biology: A Molecular Approach (Glencoe/McGraw Hill, 2006), 227; Sylvia S. Mader, Jeffrey A. Isaacson, Kimberly G. Lyle-Ippolito, Andrew T. Storfer, Inquiry Into Life, 13th ed. (McGraw Hill, 2011), 550.

[114.] See Michael S. Y. Lee, "Molecular Phylogenies Become Functional," Trends in Ecology and Evolution, 14: 177 (1999).

[115.]W. W. De Jong, "Molecules remodel the mammalian tree," Trends in Ecology and Evolution, 13(7), pp. 270-274 (July 7, 1998).

[116.] Trisha Gura, "Bones, Molecules or Both?," Nature, 406 (July 20, 2000): 230-233.

[117.] Antonis Rokas & Sean B. Carroll, "Bushes in the Tree of Life," PLoS Biology, 4(11): 1899-1904 (Nov., 2006) (internal citations and figures omitted).

[118.] Liliana M. Dávalos, Andrea L. Cirranello, Jonathan H. Geisler, and Nancy B. Simmons, "Understanding phylogenetic incongruence: lessons from phyllostomid bats," Biological Reviews of the Cambridge Philosophical Society, 87:991-1024 (2012).

Darwinism's quest for junk rolls on.

Why the "Onion Test" Fails as an Argument for "Junk DNA"

Jonathan M. November 2, 2011 6:00 AM

Briefly stated, the often cited "onion test" observes that onion cells have many times more DNA than human cells do. And since the onion is considered to be relatively simple as compared to us, this discrepancy -- it is argued -- can only be accounted for if the preponderance of its DNA is, in fact, junk or non-functional. Let's see whether the concept really holds any water.

The term "onion test" was first coined in April 2007 by the Canadian evolutionary biologist and genome biologist T. Ryan Gregory. In a post on his blog, Gregory wrote,

I am not sure how official this is, but here is a term I would like to coin right here on my blog: "The onion test." The onion test is a simple reality check for anyone who thinks they have come up with a universal function for non-coding DNA. Whatever your proposed function, ask yourself this question: Can I explain why an onion needs about five times more non-coding DNA for this function than a human?

The onion, Allium cepa, is a diploid (2n = 16) plant with a haploid genome size of about 17 pg. Human, Homo sapiens, is a diploid (2n = 46) animal with a haploid genome size of about 3.5 pg. This comparison is chosen more or less arbitrarily (there are far bigger genomes than onion, and far smaller ones than human), but it makes the problem of universal function for non-coding DNA clear.

Further, if you think perhaps onions are somehow special, consider that members of the genus Allium range in genome size from 7 pg to 31.5 pg. So why can A. altyncolicum make do with one fifth as much regulation, structural maintenance, protection against mutagens, or [insert preferred universal function] as A. ursinum?

There you have it. The onion test. To be applied to any ambitious claims that a universal function has been found for non-coding DNA.

This phenomenon is but one example of a larger issue typically known as the "C-value enigma." The C-value enigma describes the lack of correlation (among eukaryotes) between genome size and organismal complexity; a phenomenon which, curiously, does not extend to prokaryotic domains. The human genome comprises about 3 billion base pairs of DNA: Compare this to the genome size ofAmoeba dubia (670,000,000,000 bp). Indeed, the human genome is only marginally bigger than that of C. elegans and D. melanogaster. Among amphibians, the smallest genomes are just shy of 10 billion base pairs, while the largest are nearly 10^11 base pairs.

When I wrote on this subject at Uncommon Descent, Larry Moran protested that "[t]he Onion test is not about proving the existence of junk DNA and its not about explaining the C-Value Paradox,"but, rather, it's "a test for those people -- like Jonathan Wells -- who think that most of our genome has a function." He further wrote,

I hate to break it to you Jonathan M, you being such a great scientist and all, but the Onion Test is not an argument for junk DNA. It's a test of possible functional explanations. (Didn't I mention that already?) Jonathan M has completely misunderstood the Onion Test. Would it surprise you, dear readers, to learn that Jonathan Wells also flunks the test...This isn't rocket science."

This is a curious claim, not least because T. Ryan Gregory clearly wrote his original blog post with the intent of arguing that much of our DNA is junk. Indeed, he writes,

I do not endorse the use of the term "junk DNA," which I think has deviated far too much from its original meaning and is now little more than a loaded buzzword; the descriptive term "non-coding DNA" is what I use to refer to the majority of eukaryotic sequences (of various types) that do not encode protein products...Some non-coding DNA certainly has a function at the organismal level, but this does not justify a huge leap from "this bit of non-coding DNA [usually less than 5% of the genome] is functional" to "ergo, all non-coding DNA is functional."

While this may be true, as Jonathan Wells has noted, "it is the trend, more than the current total, that should worry any defender of junk DNA." Moran also claims that the "onion test" is not synonymous with the C-value enigma, but he doesn't make the difference very clear.

As I noted previously, the argument is only valid if one can justify the presumption that genome size has no bearing on organismal physiology. The problem is that this assumption can be demonstrated not to be the case.

Transcription Delays and Developmental Timing Mechanisms

Presumably a reflection of the selective-pressure on transcriptional economy with respect to highly expressed genes, genes that are highly expressed tend to have short introns (Castillo-Davis et al., 2002). Other genes are rich in introns: such as the 2400 kb human dystrophin gene, 99% of which is comprised of introns. The time taken to transcribe this gene into mRNA adds up to about 16 hours (Tennyson et al., 1995). To take another example, consider the Y chromosomal loci of Drosophila, which are very long (spanning millions of bases and consisting largely of introns): For instance, a locus such as DhDhc7(Y) is transcribed over the course of two to three days to give rise to a ~5,100,000 nucleotide pre-mRNA (see Reugels et al., 2000; Piergentili et al., 2007; and Redhouse et al., 2011). The time taken to transcribe respective stretches of DNA is not inconsequential to physiological fitness: Indeed, Swinburne and Silver (2010) report that "transcriptional delays have been shown to contribute to developmental timing."

On this, Larry Moran was curiously silent. Responding to the same article, Nick Matzke remarked that "if most of the genome has merely 'sequence independent' function, then Stephen Meyer's statement that the genome is 'chock-full of information' is unsupportable." While there is no doubt that SOME of the genome has a "sequence independent function," it is doubtful that most of the genome falls into such a category. Matzke is mistaken because, if the genetic elements possess a function, the design inference is not negated, even if that function is independent of exact sequence. Even in the case of repetitive DNA, the sequence can be highly relevant (see this paperby Richard Sternberg and James Shapiro on "Why Repetitive DNA is Essential to Genome Function"). Moreover, even if the function is sequence independent, there still might be specified complexity, triggering an explicit design inference.

Alternative Splicing and Genome Size

A second point I made was that the phenomena of alternative splicing and alternative polyadenylation may have some explanatory power when it comes to accounting for the C-value enigma. Alternative splicing allows the exons of pre-mRNA transcript to be spliced into a number of different isoforms to produce multiple proteins from the same transcript. I stated that the level of alternative splicing exhibited in humans (more than 90%, with an average of 2 or 3 transcripts per gene) is much higher than that for C. elegans (about 22%, with less than 2 transcripts per gene), and argued that this may, in part, explain why humans have only marginally more genes than C. elegans, which is otherwise seemingly paradoxical given the complexity of humans as compared to the roundworm. On this point, Moran wrote,

I don't agree with the facts. I don't think it's true that most human genes produce multiple functional copies of mRNA by alternative splicing.

But let's assume that it's true. Let's assume that a large fraction of putative junk DNA is there because it promotes alternative splicing. Why do onion cells need so much more alternative splicing and why do related species of onion differ so much in their need for alternative splicing? That's what the Onion Test asks.

On this point, Moran is not just in disagreement with me, he is also out-of-date with the literature by about ten years! As this 2008 article from Science Daily reports,

Nearly all human genes, about 94 percent, generate more than one form of their protein products, the team reports in the Nov. 2 online edition of Nature. Scientists' previous estimates ranged from a few percent 10 years ago to 50-plus percent more recently.

"A decade ago, alternative splicing of a gene was considered unusual, exotic ... but it turns out that's not true at all -- it's a nearly universal feature of human genes," said Christopher Burge, senior author of the paper and the Whitehead Career Development Associate Professor of Biology and Biological Engineering at MIT.

Wang et al. (2008), moreover, report in Nature,

Through alternative processing of pre-messenger RNAs, individual mammalian genes often produce multiple mRNA and protein isoforms that may have related, distinct or even opposing functions. Here we report an in-depth analysis of 15 diverse human tissue and cell line transcriptomes on the basis of deep sequencing of complementary DNA fragments, yielding a digital inventory of gene and mRNA isoform expression. Analyses in which sequence reads are mapped to exon-exon junctions indicated that 92-94% of human genes undergo alternative splicing, ~86% with a minor isoform frequency of 15% or more.

Moran also misunderstands the point of the argument, since it is not onion cells which would exhibit more alternative splicing but human ones (hence explaining why their genome size need not be as big as it might otherwise be). At any rate, this phenomenon on its own is not sufficient to account for the C-value enigma. Indeed, it is only one of a plethora of factors that make the issue far more complex than it is often portrayed.

Transcription Factors

I also noted that approximately 10% of human genes code for transcription factors (a special class of protein that binds to specific sequences of DNA, namely, enhancers or promoters which are adjacent to genes they regulate the expression of). In contrast, only about 5% of yeast genes code for transcription factors. When coupled with a much larger network of transcriptional enhancers and promoters, such a difference could result in a much larger set of gene expression patterns. This could lead to a non-linear increase in organismal complexity (see Levine and Tjian, 2003). Larry Moran conceded that "[he doesn't] even understand this point." Clearly, he didn't even bother to look up the cited paper. For if he had, he would have read the following:

The yeast genome encodes a total of 300 transcription factors; this includes both sequence-specific DNA-binding proteins and subunits of general transcription complexes such as TFIID9. In contrast, the genome sequences of C. elegans andDrosophila reveal at least 1,000 transcription factors in each organism. There may be as many as 3,000 transcription factors in humans. It would appear that organismal complexity correlates with an increase in both the ratio and absolute number of transcription factors per genome. Yeast contains an average of one transcription factor per 20 genes, while humans appear to contain one factor for every ten genes.Given the combinatorial nature of transcription regulation, even this twofold increase in the number of factors could produce a dramatic expansion in regulatory complexity. [emphasis added]

Limiting Factors

Another point missed by Moran and Matzke is that there are limiting factors on an organism's genome size. For example, in 2002, Andrew George published a paper in Trends in Immunologytitled, "Is the number of genes we possess limited by the presence of an adaptive immune system?" In the paper, he argued that gene count is limited by the presence of an adaptive immune system because of the potential for of self-recognition. As the paper explains,

The factors that are important in limiting the number of functional genes contained within the genome of an organism are presently unknown. Here, it is suggested that in organisms that contain an adaptive immune response, the number of genes in the genome might be limited by the need to delete autoreactive T cells, thus preventing autoimmunity. The more genes an organism has, the more autoantigens are generated, necessitating an increase in the proportion of T cells that are deleted. Is human complexity limited by the presence of an immune system? Although immunity is vital for health, the need to be tolerant to all "self" molecules could restrict the number of genes in our genome.

In a further correlation that has been established, organisms with rapid development typically have lower C-values, presumably because they don't have time to replicate lots of DNA between cell divisions.

In The Myth of Junk DNA, Jonathan Wells observes,

There is a strong positive correlation, however, between the amount of DNA and the volume of a cell and its nucleus -- which affects the rate of cell growth and division. Furthermore, in mammals there is a negative correlation between genome size and the rate of metabolism. Bats have very high metabolic rates and relatively small genomes. In birds, there is a negative correlation between C-value and resting metabolic rate. In salamanders, there is also a negative correlation between genome size and the rate of limb regeneration

In the case of bacteria, which have single replicons per chromosome, they face selective pressure to limit the accumulation of non-genic DNA which might make the replication times longer and thus slow rates of reproduction. This means that their genome size is correlated with gene number, and thus increases in proportion to structural and metabolic complexity.

On this point, the detractors have also remained oddly silent.

Genome Size and Cell Volume

A final point: For creatures as diverse as vertebrates, plants and protozoa (unicellular eukaryotes), there is a positive correlation between genome size and cell volume. Cavalier-Smith and others have suggested that DNA possesses a "structural role" in controlling nuclear volume, cell size and cell-cycle length.

Moran and Matzke want to know whether this phenomenon is a cause or an effect. Cavalier-Smith's view of "skeletal DNA," advocated in the cited paper, would suggest that "larger cells need more DNA," and that "smaller ones need less." Indeed, he explains that "If cell size declines, the nucleus will be too large compared with the cytoplasm for optimal efficiency and the drain on the cell's resources for replicating all that extra DNA and making all the histones it needs will be uneconomic." So, deletions are selectively favored over duplications. In the case of larger cells, the reverse is the case. When the cell size increases, Cavalier-Smith explains, "there is positive selection for a corresponding increase in nuclear volume; it is generally easier to achieve this by increasing the amount of DNA rather than by altering its folding parameters." Cavalier-Smith argues that the abundance of transposons (arising by duplication) is an effect (and not a cause) of the larger genomes. The larger amount of DNA thus provides a selective advantage by contributing to the skeleton and volume of the nucleus.

Conclusion

The so-called onion test, or indeed the "C-value enigma," is predicated on unsupportable assumptions about the physiological effects of -- and/or requirements for -- larger genomes, many of which are contradicted by the scientific evidence. As we learn ever more about the nature and functional inter-dependency of the genome, as the extent of genomic "dark matter" continues to shrink, those who continue to advocate the view that the preponderance of our genome is non-functional should find these facts disconcerting.