August 1, 2011 | David F. Coppedge

Clue or Clueless on Plant Evolution

An article on The Scientist promised to provide “clues to plant evolution,” but the data seemed like clues to something else – namely, design.  The article was about how plant proteins interact with one another – the “interactome” (another word to add to genome and proteome).  Did the work actually fulfill evolutionary predictions?  Even if they claim it did, did it really?

The common water cress Arabidopsis thaliana has, for years now, been the “lab rat” of the plant world.  Two teams publishing in Science this week examined the plant’s interactome and compared their findings with evolutionary predictions.  Lo and behold, they found their predictions fulfilled.  So they claimed.  But The Scientist said this about the Braun et al. study,1 which mapped 8,000 proteins (30 percent of the plant’s protein-encoding genes) and how they network together when inserted into yeast cells:

The researchers also looked at the impact of these networks on evolution.  The protein products of duplicated genes, for example, might be expected to take on different functions, as one can maintain the original task while the other is free to accumulate mutations. But the researchers found that most gene duplicates in Arabidopsis tended to interact with many of the same proteins, even though those duplicates had originated more than 700 million years ago, suggesting that the interactome somehow reduces the freedom of duplicated proteins to diverge.

This seems a serious blow to a common notion among evolutionists that duplicated genes comprise raw material for evolutionary innovation.  The authors of the paper confirmed the problem: “Whether or not natural selection shapes the evolution of interactome networks remains unclear,” they said, even though gene duplication is considered “a major driving force of evolutionary novelty” among evolutionists, and has been studied in yeast.  “However, the difficulty in dating ancient gene duplication events and the low coverage of available protein-protein interaction data sets limit the interpretation of these studies.” 

So did their study help?  The yeast studies had hinted at “substantial and rapid divergence” of interactions.  “Yet, in Arabidopsis, paralogous pairs that have been diverging for ~700 million years still share more interactors than random protein pairs…, indicating that the long-term fate of paralogous proteins is not necessarily a complete divergence of their interaction profiles.”  To save the theory, they had to assume “variation of selective pressure at different times after the duplication event” and admit that “protein-protein interactions are only one of many constraints limiting sequence changes during evolution”.  No matter whether they expressed confidence in evolution.  Their own data seemed to contradict what they expected.

The other study by Mukhtar et al. in Science claimed victory for an evolutionary prediction.2  They watched how two very different plant pathogens attacked the plant’s protein network.  They announced, “Independently Evolved Virulence Effectors Converge onto Hubs in a Plant Immune System Network,” as if convergence is what they expected.  But The Scientist said,

Interestingly, rather than directly interacting with the immune system proteins, the effectors bound to Arabidopsis hub proteins, indicating that the pathogens induce immune responses indirectly.

Furthermore, despite the 2 billion years of evolution separating the two pathogens, they shared the strategy of targeting the hub proteins, and even interacted with 18 of the same major hubs. When the researchers knocked out those 18 genes individually in Arabidopsis plants and exposed the plants to the effector proteins, 15 of the mutants had an altered immune response.

“This is an unheard-of validation rate,” said Braun. “Even though [the pathogens] have independently evolved and their mode of attack is different, they are still converging on the highly connected proteins.

They could claim they predicted this, and they did: “Our hypothesis was that many effectors from evolutionarily diverse pathogens would converge onto a limited set of defense-related host targets and molecular machines, as opposed to each effector having evolved to target idiosyncratic, pathogen life-style–specific targets.”  But would it not have been just as valid a prediction to expect highly divergent attack modes by the pathogens after 2 billion years?  At least The Scientist seemed to think so.

For another opinion, look at what Christian R. Landry wrote of these studies in the same issue of Science.3  He took the side of Mukhtar et al. that the study confirmed their prediction of convergence.  But it might seem strange that plants, yeast, worms, and humans have all played the same evolutionary tune when evolving independently for two billion years:

With plant, animal, and fungal interactomes in hand, we can now ask whether more complex forms of life gave rise to specific network properties and architectures…. In addition, we can explore how interactomes have been shaped by the requirements of multicellular life—such as the need for intercellular communication, synchronization of cell division, cell specialization, and a transcriptional program that regulates cell development and differentiation. Plants and animals evolved multicellularity independently, and comparing the organization of their interactomes provides a unique opportunity to gain insight. For instance, genes that contributed to the evolution of multicellularity may be different in the two groups but could have given rise to similar interactomes. The Arabidopsis Interactome Mapping Consortium briefly touches on this issue, reporting that the overall topology of the Arabidopsis network is qualitatively similar to those of yeast, worm, and human.

If evolutionary theory can yield common design properties among vastly different organisms that have supposedly evolved independently for hundreds of millions of years, then it’s a theory that cannot lose.

1.  Pascal Braun et al. and the Arabidopsis Interactome Mapping Consortium, “Evidence for Network Evolution in an Arabidopsis Interactome Map, Science, 29 July 2011: Vol. 333 no. 6042 pp. 601-607; DOI: 10.1126/science.1203877.

2.  M. Shahid Mukhtar et al.,  “Independently Evolved Virulence Effectors Converge onto Hubs in a Plant Immune System Network,” Science, 29 July 2011: Vol. 333 no. 6042 pp. 596-601; DOI: 10.1126/science.1203659.

3. Christian R. Landry, “Cell Biology:  A Cellular Roadmap for the Plant Kingdom,”  Science, 29 July 2011: Vol. 333 no. 6042 pp. 532-533; DOI: 10.1126/science.1209753.

We keep showing you how evolutionists have rigged their game.  No matter what the data show, they win.  Independently evolving parts of the tree converge on similar designs?  Praise be to Darwin.  Irreducible complexity found?  Thank Darwin.  You can be sure that if the data above showed the very opposite (extreme divergence instead of convergence), Darwin would be praised for that, too.  What can a Darwin skeptic possibly do to expose this fraud?  Remember the three-step process for proving evolution:  (1) Assume evolution. (2) Observe a fact.  (3) Make up a story that forces the fact into the assumption of evolution.  They also employ Finagle’s Rule #6: “Do not believe in miracles.  Rely on them.”

Learn to watch for their miracle words.  In the final blockquote above, notice where Landry said, “we can now ask whether more complex forms of life gave rise to specific network properties and architectures.”  The phrase gave rise to is the miracle.  If you read evolutionary literature like we do, you find it replete with claims that such-and-such complex machinery emerged, arose, developed, came to light, originated, materialized, or appeared.  Miracles can also be seen when Natural Selection is personified as a driving force, tinkerer, or shaper of evolution. Call this lingo what it is: an appeal to miracles.  They merely assume evolution (Rule #1) did the hard work in a black box out of sight, out of mind. They feel no obligation to prove it empirically, the way you thought science had to be done.  Why?  Because they followed their three-step process, so a story suffices (Rule #3).  As Richard Goldschmidt said in 1952, “Evolution of the animal and plant world is considered by all those entitled to judgment to be a fact for which no further proof is needed.”  That’s why he could pile on the miracles with his Hopeful Monster hypothesis and not be drummed out of the science lab. 

So here’s the lesson.  Everybody is a supernaturalist, and everybody believes in miracles.  If you employ reason, you are a supernaturalist, because reason is not composed of particles in a big bang, but refers to a transcendent laws of logic that are universal, timeless and certain (claim otherwise and your claim can be shown to be self-refuting).  Likewise, everyone believes in miracles.  Evolutionists believe in miracles of chance.  Creationists believe in miracles that are designed for a purpose.  Don’t let anyone get away with this nonsense that evolutionists, as unbiased practitioners of the Scientific Method who have limited their explanations to natural causes, have removed miracles from science.  They just prefer their miracles over anyone else’s, and they have the power to expel anyone who points out their hypocrisy.

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Comments

  • RedReader says:

    “If you read evolutionary literature like we do, you find it replete with claims that such-and-such complex machinery emerged, arose, developed, came to light, originated, materialized, or appeared.” Yes, if such observations were empirical, we would SEE things “emerging, arising, developing, coming to light, originating, materializing, or appearing.”  No, what we SEE are living creatures—from smallest to largest—remaining within a set range of variability generation after generation. (See Michael Behe.)

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