Purpose and Desire

Purpose and Desire: What Makes Something “Alive” and Why Modern Darwinism Has Failed to Explain It is the new book by physiologist J. Scott Turner, author of The Tinkerer’s Accomplice: How Design Emerges from Life Itself.

The book may make some “skeptics” uncomfortable, but maybe they should read it anyways.

From the book:

I have come to believe that there is something presently wrong with how we scientists think about life, its existence, its origins, and its evolution.

Without a coherent theory of life, whatever we think about life doesn’t hold water. This applies to the major contribution we claim that the modern science of life offers to the popular culture: Darwinism.

… there sits at the heart of modern Darwinism an unresolved tautology that undermines its validity.

… do we have a coherent theory of evolution? The firmly settled answer to this question is supposed to be “yes” …

I intend to argue in this book that the answer to my question might actually be “no.”

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The Mystery of Evolution: One Down

My kids just informed me that they have seen an okapi evolving, or transitioning into a zebra

Okapi’s stripes appear to be no doubt the same as zebra’s…

Zebra, Equus quagga, Masai Mara Reserve, Kenya : Stock Photo

Well, at least we have one example of species transitioning into another…out of 10 billion and this one looks like a stunner….

I have to run!

I’ll fill in the rest when I get back…

Update!

It turns out that okapi is considered to be more closely related to giraffe than to zebra…if at all…That is surprising…because okapi and zebra do look alike just okapi is missing some stripes…No wonder my kids fell for it…as did some experts…

“…The okapi and the giraffe were assigned to the same order (Artiodactyla) because they both have cloven hooves, and to the same family (Giraffidae) because they share certain distinctive features: Both have large eyes and ears, thin lips and a long, extensible tongue that allows them to lick their entire face (even the ears); their backs slope upward from rump to withers; they also share the same dental formula: ( i 0/3, c 0/1, pm 3/3, m 3/3) × 3 = 32. Both, unlike any other mammal, have molars with rugose enamel and bony horns that remain covered with skin throughout life (Nowak 1999, vol. 2, p. 1085).

Yet the rump and legs of an okapi are covered with black-and-white stripes exactly like those of a zebra. Perhaps, then, if okapis had solid hooves instead of cloven ones, they would be classified as perissodactyls (Order Perissodactyla) and would be considered more closely related to zebras than to giraffes. An okapi is about the same size as a Burchell’s zebra.

The chromosome count of an okapi is also like that of a zebra, to which it is not supposed to be related, and unlike that of a giraffe. Giraffes have 30 chromosomes (Taylor et al. 1967; Hösli and Lang 1970; Koulisher et al. 1971), whereas okapis have a variable chromosome number of 44-46, depending on the animal in question; most seem to have 2n = 45 (Ulbrich and Schmitt 1969; Hösli and Lang 1970; Koulisher 1978). The chromosome number of Grevy’s zebra is 2n = 46 and plains zebras have 2n = 44 (Benirschke and Malouf 1967). Variation in chromosome count is itself unusual among mammals, but common in hybrids…”

The 14-16 chromosome difference between giraffe and okapi is striking isn’t it?

Improbable Destinies

Improbable Destinies: Fate, Chance, and the Future of Evolution

I love books like this. Pure wonder about the living world. The beauty. The mystery. Shattering the myths of Darwinism while still clinging desperately to them.

We learn that Darwinism has retarded evolutionary thought for at least a century because the picture that Darwin gave us (which his disciples followed for over a hundred years) was false. Evolution can be tested. It can be observed within human lifetimes. It doesn’t require the infinitesimal insensible aggregations over millenia previously thought. Evolution can be really really fast. Which ought to be good news for young earth creationists.

We also learn that the oft-heard claim that degree of similarity implies degree of relatedness is false. That some species A looks very much like some species B doesn’t at all mean that they are more closely related than some other species which is visibly different.

Another nail in the coffin.

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The Mysteries of Evolution: 6. Endosymbiosis-The second miracle of life after the origin of life

This is one of the most fundamental mysteries of evolution and the origins of multicellular life often called endosymbiosis, which is supposed to explain the origin of eukaryotic cell.

It doesn’t!  Here is why…

What I found perplexing, or even disturbing, is that although it is presented as scientific fact of evolution, as evolution itself often is, there is absolutely not one fact to support that endosybiosis happened or could have happened…

And this the fact…

How could that be?

First of all, the difference between prokaryotic and eukaryotic cell is so staggering that even proposing such quantum leap in evolutionary change goes beyond macroevolutionary claim…

Here are some facts: Continue reading

Invited responses to my nylonase research and the question of “New Proteins Without God’s Help”

Susumo Ohno (who coined the term “junkDNA”) published a paper in 1984 through the National Academy of Sciences that was used by the NCSE, Ken Miller and Dennis Venema to claim “proteins can evolve without God’s help”. At the request of John Sanford, a courtesy associate research professor at Cornell, I was recruited to write a paper to refute Ohno’s evolutionary hypothesis on nylonases. I wrote it under John’s guidance based on his intuitions about genetics, his life-long specialty of 40 years and for which he became famous as attested by the fact he is one of the few geneticists who had their work featured in the Smithsonian National Museum of American History.

The actual paper is now in review, but it is not intended to be published in any journal, but will be released in a variety of channels shortly. It is hoped the material can be used by others to actually create papers that enter peer review. The motivation for releasing the paper in this way is to counter Venema’s book while it is still hot off the press.
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The embarrassing “science” of the origins of life: The missing piece of evidence that persuaded scientists to believe in abiogenesis

What comes to your mind when you hear or read the word science? To most the word science correlates with fact, proof or  even truth.

In my countless debates over the years with scientist and supporters of the origins of life (OOL) or evolution, I’ve often asked the question what convinced them so strongly about something, like abiogenesis. The answers I often got would be:

“…I believe it,  because I believe in science…”

Is it really science? 

No doubt to many, whether scientists or not, the word science is often paralleled with trustworthiness, credibility, reliability, soundness and even authority and influence.

”If something is dubbed as “science”, you’d better believe!” – many would say.

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When did nylon-eating proteins actually evolve the ability to eat nylon?

It has been widely advertised that nylon eating genes evolved after 1940. I have no problem with that claim in principle since new antibiotic and malaria resistances have evolved since 1940. Even though I can easily accept the possibility of post-1940 nylon-eating evolution in principle, where is the slam dunk evidence that this is actually the case? Did a significant portion of the ability for bacteria to digest nylon take place after 1940 (or 1935 when nylon was first created)?
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The Arrival of the Fittest: a book review

Andreas Wagner’s book,The Arrival of the Fittest has been mentioned many times (just try a site search as I’ve just done) since it was published. Petrushka pointed it out in a comment

For anyone interested in whether RMNS can create stuff, I recommend a relatively new book, Arrival of the Fittest. I just bought the Kindle version an haven’t finished, but it has a lot to say about how goldilocks mutations occur.

Much later Mung writes:

Reminds me of petrushka, who is always plugging Andreas Wagner’s Arrival of the Fittest, but will never post an OP on it for discussion.

So I’ve taken the hint and bought the book at last. I can see why people have recommended it. Continue reading

Mind blowing presentation by George Church at the NIH

Last week, George Church talked at the school where I take part-time evening classes. I provide a link to that talk. He talked about re-engineered codons (something I’m grateful to Rumraket for introducing me to), stem cell research, human animal chimeras, aging therapies, human genome re-engineering, and just a little bit about ENCODE. Though I have ethical concerns about human/animal chimeras, and human genome re-engineering (like what happens if you mess up), Church goes into the technologies and raises questions as to what our world may look like in the not too distant future. Not that I’m trying to make a point about ID or God by linking this video, but it shows how rapidly we may be forced to deal with certain issues.

I personally don’t have too much problem with GMO foods. After all, my YEC friend John Sanford created the gene gun through which a large fraction of genetically engineered crops on the planet were made at one time. But one thing that bothers me is genetically engineered bacteria. Church discussed super bacteria created for research applications. I can imagine an accident where germs are created accidentally that become really hard to kill and we basically have an apocalypse. Maybe that will be the fulfillment of prophecy by Jesus, “there will be famines and pestilence”.

Here is the video (with Francis Collins speaking at the start):
https://videocast.nih.gov/summary.asp?Live=21803&bhcp=1

Here is a description of the talk:
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Larry Moran’s Exit Exam

Attached is Larry Moran’s exit exam for biochemistry and molecular biology. Exit Exam for Biochemistry.

I probably will not get a lot of these right on the first try, but it is a good learning experience. When I don’t know the answer, I can look it up, so this is a good chance to review important concepts.

I will provide answers I think Professor Moran wants students to give, and then I’ll provide my own answers which I think he might dock points for if he were grading. I always try to give the answer the professor is expecting even if I disagree. It shows that I am trying to understanding of what he was trying to teach. It’s not a confession of belief on my part.

For example:

21.How much of your genome is functional?

Answer I think Larry is expecting:

10%, because of the limits mutational load imposes on a genome the size of a human’s and their reproductive excess. But even the 10% number is likely high since the Muller Limit of 1 mutation/person/generation might allow even less than 10% function for the human genome.

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The Glories of Global Warming and the Faint Young Sun Paradox

It is a little known fact that scientists who argue that the paleontological record of life is hundreds of millions of years old, when confronted with astrophysical facts, must eventually rely heavily on the hypothesis of finely tuned, large scale global warming. The problem is known as the Faith Young Sun Paradox. A few claim they have solved the paradox, but many remain skeptical of the solutions. But one fact remains, it is an acknowledged scientific paradox. And beyond this paradox, the question of Solar System evolution on the whole has some theological implications.

Astrophysicists concluded that when the sun was young, it was not as bright as it is now. As the sun ages it creates more and more heat, eventually incinerating the Earth before the sun eventually burns out. This is due to the change in products and reactants in the nuclear fusion process that powers the sun. This nuclear evolution of the sun will drive the evolution of the solar system, unless Jesus returns…
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Mouse Utopia, Mutational Meltdown, Extinction by Natural Selection

The National Institute of Mental Health (NIMH) of the National Institutes of Health (NIH) sponsored the work of John Calhoun on social behaviors. Here were the results of one of his experiments:

On July 9th, 1968, eight white mice were placed into a strange box at the National Institute of Health in Bethesda, Maryland. Maybe “box” isn’t the right word for it; the space was more like a room, known as Universe 25, about the size of a small storage unit. The mice themselves were bright and healthy, hand-picked from the institute’s breeding stock. They were given the run of the place, which had everything they might need: food, water, climate control, hundreds of nesting boxes to choose from, and a lush floor of shredded paper and ground corn cob.

This is a far cry from a wild mouse’s life—no cats, no traps, no long winters. It’s even better than your average lab mouse’s, which is constantly interrupted by white-coated humans with scalpels or syringes. The residents of Universe 25 were mostly left alone, save for one man who would peer at them from above, and his team of similarly interested assistants. They must have thought they were the luckiest mice in the world. They couldn’t have known the truth: that within a few years, they and their descendants would all be dead.
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New data on human genomic diversity

The extent of variation present in human populations and the consequences of genetic load seem to be topics of perennial interest here (see, for example, recent comments in the Evolution Visualized thread).  Recent issues of Nature have published a flurry of papers aimed at getting a better handle on just how much genetic diversity is likely to exist among humans.   One notable paper from last August is the following:

Analysis of protein-coding genetic variation in 60,706 humans

In this study, Monkol Lek and many, many colleagues sequenced the exomes–i.e., the portion of DNA sequences that code for proteins along with some accompanying untranslated regions–of more than 60,000 people.  The results were pretty spectacular.  The paper is incredibly dense, but here are some highlights:

  • The authors found more than 7 million reliably identified variants.  Most were single base pair substitutions, but the variants also include more than 300,000 insertions/deletions.
  • On average, 1 out of every 8 nucleotides is variable.  However, the overwhelming majority of variants are rare.  That is they are found in only a single or a few individuals
  • The frequency of different kinds of variants is proportional to both the rate at which they occur as well as the extent to which they are likely to be deleterious.  This is not at all surprising, but it’s neatly demonstrated.  For example,  63.1% of all possible CpG transitions (i.e., a cytosine adjacent to a guanine that mutates to a thymine) were observed, while only 3% of possible transversions were present.  CpG transitions are among the most common type of substitution in mammals, while transversions are less frequent.  Likewise, the proportion of possible synonymous variants that were actually observed was much higher than the proportion of possible nonsynonymous variants that were observed, which is consistent with the generally accepted notion that nonsynonymous mutations are usually subject to stronger purify selection than synonymous mutations.
  • They identified almost 180,000 different protein truncation variants (PTVs), which are protein-coding genes predicted to be shortened due to an introduced stop codon, a frameshift, or removal of a critical splice site.  Amazingly (to me at least), the average genome in their dataset includes 85 PTVs in the heterozygous state and almost 35 PTVs in the homozygous state.
  • They identified more than 100 variants previously thought to contribute to disease phenotypes that are present at anomalously high frequencies in human populations (> 1%).  Based on the fact that the evidence of pathogenicity for most of these variants is actually extremely weak, the authors suggest that these variants are most likely benign.

There is a lot more in the paper that’s worth chewing over, so give it a read.  This is easily the largest dataset of its type ever generated, but it has limitations.  The sampling is heavily biased toward Europeans, and there is likely some variation missing, especially in Central and Middle Eastern Asia.

I imagine that within a few years, we’ll have datasets of similar size consisting of high-coverage, whole genome sequences, which will no doubt show even larger amounts of genomic variation.  It’s an exciting time to be interested in biology!

Some evidence ALUs and SINES aren’t junk and garbologists are wrong

Larry Moran, Dan Graur and other garbologists (promoters of the junkDNA perspective), have argued SINES and ALU elements are non-functional junk. That claim may have been a quasi-defensible position a decade ago, but real science marches forward. Dan Graur can only whine and complain about the hundreds of millions of dollars spent at the NIH and elsewhere that now strengthens his unwitting claim in 2013, “If ENCODE is right, Evolution is wrong.”

Larry said in Junk in Your Genome: SINES
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Dynamics of genome evolution in E. coli

Hi All,

The Lenski lab has just published a new paper in Nature that looks at the dynamics of genome evolution in E. coli populations over the course of the LTEE.  Here is the abstract:

Tempo and mode of genome evolution in a 50,000-generation experiment

Adaptation by natural selection depends on the rates, effects and interactions of many mutations, making it difficult to determine what proportion of mutations in an evolving lineage are beneficial. Here we analysed 264 complete genomes from 12 Escherichia coli populations to characterize their dynamics over 50,000 generations. The populations that retained the ancestral mutation rate support a model in which most fixed mutations are beneficial, the fraction of beneficial mutations declines as fitness rises, and neutral mutations accumulate at a constant rate. We also compared these populations to mutation-accumulation lines evolved under a bottlenecking regime that minimizes selection. Nonsynonymous mutations, intergenic mutations, insertions and deletions are overrepresented in the long-term populations, further supporting the inference that most mutations that reached high frequency were favoured by selection. These results illuminate the shifting balance of forces that govern genome evolution in populations adapting to a new environment.

I’m assuming the whole thing is pay-walled, but a pre-print copy (which may or may not be identical to the final version) is freely available here.

I’ve only read the abstract thus far, but the paper seems likely to touch on a variety of topics that folks here like to discuss. Have at it!

What is the Plan?

A prominent ID supporter at UD, gpuccio, has this to say:

My simple point is: reasoning in terms of design, intention and plans is a true science promoter which can help give new perspective to our approach to biology. Questions simply change. The question is no more:

how did this sequence evolve by some non existent neo darwinian mechanism giving reproductive advantage?

but rather:

why was this functional information introduced at this stage? what is the plan? what functions (even completely unrelated to sheer survival and reproduction) are being engineered here?

 

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“Species”

On the thread entitled “Species Kinds”, commenter phoodoo asks:

What’s the definition of a species?

A simple question but hard to answer. Talking of populations of interbreeding individuals immediately creates problems when looking at asexual organisms, especially the prokaryotes: bacteria and archaea. How to delineate a species temporally is also problematic. Allan Miller links to an excellent basic resource on defining a species and the Wikipedia entry does not shy away from the difficulties.

In case phoodoo thought his question was being ignored, I thought I’d open this thread to allow discussion without derailing the thread on “kinds”.

Thorp, Shannon: Inspiration for Alternative Perspectives on the ID vs. Naturalism Debate

The writings and life work of Ed Thorp, professor at MIT, influenced many of my notions of ID (though Thorp and Shannon are not ID proponents). I happened upon a forgotten mathematical paper by Ed Thorp in 1961 in the Proceedings of the National Academy of Sciences that launched his stellar career into Wall Street. If the TSZ regulars are tired of talking and arguing ID, then I offer a link to Thorp’s landmark paper. That 1961 PNAS article consists of a mere three pages. It is terse, and almost shocking in its economy of words and straightforward English. The paper can be downloaded from:

A Favorable Strategy for Twenty One, Proceedings National Academy of Sciences.

Thorp was a colleague of Claude Shannon (founder of information theory, and inventor of the notion of “bit”) at MIT. Thorp managed to publish his theory about blackjack through the sponsorship of Shannon. He was able to scientifically prove his theories in the casinos and Wall Street and went on to make hundreds of millions of dollars through his scientific approach to estimating and profiting from expected value. Thorp was the central figure in the real life stories featured in the book
Fortune’s Formula: The Untold Story of the Scientific Betting System that Beat the Casino’s and Wall Street by William Poundstone.
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Impractical Naturalism of Dan Graur vs. the NIH

I’ll be making a presentation at AM-NAT 2016, and Dan Graur will be the poster boy of impractical naturalism. Below are some things I collected from his websites, some of which I view as highly anti-science. The aim of my presentation isn’t to settle the question of God or no God or ultimate questions of whether godless naturalism is the best description of reality. The goal is to suggest there are some unspoken naturalistic creeds that often take priority over experiments and observations. In a manner of speaking, there are some interpretations of naturalism that actually go against dispassionate examination of how the natural world actually operates.
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