Some interesting stuff/citations/thoughts I like …

Oh great, now I’m worse than a fraud … practically a biologist

— Dr. Sheldon Cooper, Ph.D., Sc.D. ( a fictional character of THE BIG BANG THEORY sitcom)

I have taken a stand against atheism because I am convinced that it is perilously built on false premises and misinterpretations of evidence. . . . Properly understood, the evidence inexorably points to the existence of a creator God.

— Professor John Lennox (Mathematician, University of Oxford)

When you look at the narrative for hominin origins, it’s just a big mess — there’s no consensus whatsoever … People are working under completely different paradigms, and that’s something that I don’t see happening in other fields of science

— Sergio Almécija (a senior research scientist in the American Museum of Natural History’s Division of Anthropology)

There’s no reason to doubt that Darwin successfully explained the small adjustments by which an organism adapts to local circumstances: changes to fur density or wing style or beak shape. Yet there are many reasons to doubt whether he can answer the hard questions and explain the big picture—not the fine-tuning of existing species but the emergence of new ones. The origin of species is exactly what Darwin cannot explain.

— Professor David Gelernter (Computer science, Yale University)

Where is Anatomy Encoded in Living Systems?

Biologists don’t love to think about goal directed processes, the idea is there supposed to be emergence and kind of emergent complexity, but this idea that things are working towards a goal the way that any navigational system fundamentally does, is really not something that is very comfortable certainly for molecular biology …

— Michael Levin ( Developmental and synthetic biologist, Tufts University, USA)

All of us who study the origin of life find that the more we look into it, the more we feel it is too complex to have evolved anywhere. We all believe as an article of faith that life evolved from dead matter on this planet. It is just that life’s complexity is so great, it is hard for us to imagine that it did.

— Harold Urey ( Physical chemist, Nobel prize laureate, USA )

Origin of life is purely synthetic organic chemistry. There’s no way around it and I am perfectly situated to be commenting on this, to be critiquing the origin of life research. It is abiological, it is before biology takes over. This is purely synthetic organic chemistry and making these compounds it’s very simple four classes of compounds. You have to make them from what’s available on a presumed prebiotic earth and so the chemistry is not hard for synthetic organic chemists to follow …
Any trained synthetic organic chemist can follow me on this and I’ve never seen a synthetic organic chemist
disagree with me on this. In fact, the people that might disagree with me are biologists because they’ve never made anything.

Some might suggest that there are certain laws that we don’t yet know, undefined laws that would dictate the origin of first life. It’s very hard to comment on something that we don’t know anything about. However, one would have to have law upon law upon law upon law… One after another after another, to make the requisite molecules needed for life and then to have those requisite molecules assembled…
Because even if one had the molecules, which is very hard to do, how do you do the assembly?
We don’t know how to do that now…
If there’s some law to do this, remember just the interactome just the protein-protein interactions – within a single yeast cell the 3,000 proteins – it’s 10^79,000,000,000 on the possible combinations of just the interact on …
How do you get those to order? Of course, there is a large cascade of arrays that can get these to order but that always has life spawning life. We don’t dehydrate cells and get them to work together again …Cells will split and pass that information along to other cells. We don’t know how to spark these things and it can’t happen from a single unknown law…
You’d have to have unknown law upon unknown law upon unknown law …
Takes a lot of faith to do that. I’m not sure I have that level of faith, but if they do, good for them (for Darwinists)

— Professor James Tour (synthetic chemist / nanotechnologist, Rice University, Royal Society of Chemistry Centenary Prize winner )

Around 2007, I heard Dr Steven Benner (origin-of-life researcher) at JPL admit to a group of scientists and other employees that the problems in his field are so vexing, it was almost enough to make one become a creationist. The audience chuckled nervously. Such an admission must never be heard by the public. Benner listed problem after problem: chirality, genetic takeovers, accumulations of tar, and the difficulty of making ribose. When Benner is on camera, however, he smiles and talks about all the progress they’re making.

— David F. Coppedge, a former system administrator for the Cassini Mission to Saturn from 1997 to 2011, Jet Propulsion Laboratory ( JPL)

Origin of life research is a scam

… the scam is if we just make this RNA, we’ve got this you know this uh this fluke event we know how that’s simple let’s make this phosphodiester or let’s make ATP or ADP we’ve got that part nailed let’s now make this other molecule another molecule and how many molecules are going to be enough ? (an Youtube video auto-transcript)

— Lee Cronin ( synthetic chemist, origin-of-life researcher, University of Glasgow, UK )

Generalized self-driving is a hard problem, as it requires solving a large part of real-world AI. Didn’t expect it to be so hard, but the difficulty is obvious in retrospect.

— Elon Musk, chief engineer (SpaceX, Tesla)

Our finding casts serious doubts over literally thousands of studies that use phylogenetic trees of extant data to reconstruct the diversification history of taxa, especially for those taxa where fossils are rare, or that found correlations between environmental factors such as changing global temperatures and species extinction rates
… the results do not invalidate the theory of evolution itself. They do, however, put constraints on what type of information can be extracted from genetic data to reconstruct evolution’s path.

— Stilianos Louca, Department of Biology (University of Oregon)

I have been working with these traditional types of models for a decade now… I am one of the lead developers of a popular software package for estimating diversification rates from phylogenetic trees. And, as such, I thought I had a really good sense of how these models worked. I was wrong …

— Matthew W. Pennell (Biodiversity Research Centre, University of British Columbia)

Mutations are usually thought to be so rare, that when we see the same mutation in different individuals, the assumption is that those individuals shared an ancestor who passed the mutation to them both… But it’s possible that the mutation rate is so high in some of these non-B DNA regions that the same mutation could occur independently in several different individuals. If this is true, it would change how we think about evolution.

— Kateryna D Makova, biologist (Pennsylvania State University)

We have no idea how the molecules that compose living systems could have been devised such that they would work in concert to fulfill biology’s functions. We have no idea how the basic set of molecules, carbohydrates, nucleic acids, lipids and proteins were made and how they could have coupled in proper sequences, and then transformed into the ordered assemblies until there was the construction of a complex biological system, and eventually to that first cell. Nobody has any idea on how this was done when using our commonly understood mechanisms of chemical science. Those that say that they understand are generally wholly uninformed regarding chemical synthesis. Those that say, “Oh this is well worked out,” they know nothing—nothing—about chemical synthesis—nothing. … From a synthetic chemical perspective, neither I nor any of my colleagues can fathom a prebiotic molecular route to construction of a complex system. We cannot even figure out the prebiotic routes to the basic building blocks of life: carbohydrates, nucleic acids, lipids, and proteins. Chemists are collectively bewildered. Hence I say that no chemist understands prebiotic synthesis of the requisite building blocks, let alone assembly into a complex system. That’s how clueless we are. I have asked all of my colleagues—National Academy members, Nobel Prize winners—I sit with them in offices. Nobody understands this. So if your professors say it’s all worked out, if your teachers say it’s all worked out, they don’t know what they’re talking about…

— Professor James Tour (synthetic chemist / nanotechnologist, Rice University, Royal Society of Chemistry Centenary Prize winner )

There’s been quite a bit of mystery around how insects first arose, because for many millions of years you had nothing, and then just all of a sudden an explosion of insects … The rocks could have contained insect fossils. The fact that they don’t indicates the dearth of insects during this period is real and not just an artifact of bad luck with preservation …

— Sandra Schachat, a graduate student at Stanford’s School of Earth, Energy & Environmental Sciences (Stanford Earth)

For over 170 million years they dominated the land, from small creatures just a few feet long to some of the largest animals ever to have walked Earth. But despite their long evolutionary history, the origin of dinosaurs remains shrouded in mystery… The earliest definitive dinosaur is not one animal but an entire ecosystem containing a few different species. There’s no universally accepted dinosaur species that lived earlier in time.

— Josh Davis, Digital News Editor for Natural History Museum London UK

There is no dispute between me and Richard Dawkins and there never has been, because he’s a journalist, and journalists are people that report what the scientists have found and the arguments I’ve had have actually been with scientists doing research

— E.O. Wilson, biologist, Harvard (called the Darwin of the 20th century )

Do cells use passwords in cell-state transitions? Is cell signaling sometimes encrypted?

Organisms must maintain proper regulation including defense and healing. Life-threatening problems may be caused by pathogens or by a multicellular organism’s own cells through cancer or autoimmune disorders. Life evolved solutions to these problems that can be conceptualized through the lens of information security, which is a well-developed field in computer science. Here I argue that taking an information security view of cells is not merely semantics, but useful to explain features of signaling, regulation, and defense. An information security perspective also offers a conduit for cross-fertilization of advanced ideas from computer science and the potential for biology to inform computer science. First, I consider whether cells use passwords, i.e., initiation sequences that are required for subsequent signals to have effects, by analyzing the concept of pioneer transcription factors in chromatin regulation and cellular reprogramming. Second, I consider whether cells may encrypt signal transduction cascades. Encryption could benefit cells by making it more difficult for pathogens or oncogenes to hijack cell networks. By using numerous molecules, cells may gain a security advantage in particular against viruses, whose genome sizes are typically under selection pressure. I provide a simple conceptual argument for how cells may perform encryption through posttranslational modifications, complex formation, and chromatin accessibility. I invoke information theory to provide a criterion of an entropy spike to assess whether a signaling cascade has encryption-like features. I discuss how the frequently invoked concept of context dependency may oversimplify more advanced features of cell signaling networks, such as encryption. Therefore, by considering that biochemical networks may be even more complex than commonly realized we may be better able to understand defenses against pathogens and pathologies.
— Alex Root, molecular biologist ( Memorial Sloan Kettering Cancer Center, New York, NY, USA )

Evolution is slow and gradual except when it is fast. It is dynamic and creates huge changes over time, except when it keeps everything the same for millions of years. It explains both extreme complexity and elegant simplicity. It tells us how birds learned to fly and how some lost that ability. Evolution made cheetahs fast and turtles slow. Some creatures are made big and others small, some gloriously beautiful and some boringly gray. It forced fish to walk and walking animals to return to the sea. It diverges except when it converges. It produces exquisitely fine-tuned designs except when it produces junk. Evolution is random and without direction except when it moves toward a target. Life under evolution is a cruel battlefield, except when it demonstrates altruism. Evolution explains virtues and vice, love and hate, religion and atheism and it does all this with a growing number of ancillary hypotheses…It explains everything without explaining anything well.

— Matti Leisola, bioengineer (former Dean of Chemistry and Material Sciences at Helsinki University of Technology)

Mutation protection paradox

Unbounded random change of nucleotide codes through the accumulation of irreparable, advantageous, code-expanding, inheritable mutations at the level of individual nucleotides, as proposed by evolutionary theory, requires the mutation protection at the level of the individual nucleotides and at the higher levels of the code to be switched off or at least to dysfunction. Dysfunctioning mutation protection, however, is the origin of cancer and hereditary diseases, which reduce the capacity to live and to reproduce. Our mutation protection perspective of the evolutionary dynamics of digital and nucleotide codes thus reveals the presence of a paradox in evolutionary theory between the necessity and the disadvantage of dysfunctioning mutation protection. This mutation protection paradox, which is closely related with the paradox between evolvability and mutational robustness, needs further investigation.

— William DeJong (INI-Research, NL), Hans Degens (Institute for Biomedical Research, UK)

Viruses don’t have a structure derived from a common ancestor

Cells obtain membranes from other cells during cell division. According to this concept of ‘membrane heredity’, today’s cells have inherited membranes from the first cells that evolved, and provides evidence that cells are derived from a common ancestor. Viruses have no such inherited structure … In a phylogenetic tree, the characteristics of members of taxa are inherited from previous ancestors. Viruses cannot be included in the tree of life because they do not share characteristics with cells, and no single gene is shared by all viruses or viral lineages. While cellular life has a single, common origin, viruses are polyphyletic – they have many evolutionary origins.

— Vincent Racaniello, microbiologist, virologist ( Columbia University’s College of Physicians and Surgeons, US )

Animal DNA modifier captured from bacteria 60 million years ago

It is hard to imagine how a single, horizontally transferred gene would form a new regulatory system, because the existing regulatory systems are already very complicated …

It’s almost unbelievable, just try to picture, somewhere back in time, a piece of bacterial DNA happened to be fused to a piece of eukaryotic DNA. Both of them became joined in the rotifer’s genome and they formed a functional enzyme. That’s not so easy to do, even in the lab, and it happened naturally. And then this composite enzyme created this amazing regulatory system, and bdelloid rotifers were able to start using it to control all these jumping transposons. It’s like magic.

— Irina A. Yushenova, PhD., molecular biologist (University of Chicago, Marine Biological Laboratory, USA)

Some Problems in Proving the Existence of the Universal Common Ancestor of Life on Earth

Although overwhelming circumstantial evidence supports the existence of the universal common ancestor of all extant life on Earth, it is still an open question whether the universal common ancestor existed or not . Theobald (Nature 465, 219–222 (2010)) recently challenged this problem with a formal statistical test applied to aligned sequences of conservative proteins sampled from all domains of life and concluded that the universal common ancestor hypothesis holds. However, we point out that there is a fundamental flaw in Theobald’s method which used aligned sequences. We show that the alignment gives a strong bias for the common ancestor hypothesis, and we provide an example that Theobald’s method supports a common ancestor hypothesis for two apparently unrelated families of protein-encoding sequences (cytb and nd2 of mitochondria). This arouses suspicion about the effectiveness of the “formal” test.

— Masami Hasegawa ( Department of Statistical Modeling, Institute of Statistical Mathematics, Japan )

Most of evolutionary trees could be wrong

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.

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.
But now with molecular data, we can see that convergent (repeated) evolution happens all the time – things we thought were closely related often turn out to be far apart on the tree of life.
It means that convergent evolution has been fooling us – even the cleverest evolutionary biologists and anatomists – for over 100 years!

— Matthew A. Wills
( Milner Centre for Evolution, Department of Biology & Biochemistry, University of Bath, UK )

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.
— Dr. Jack Oyston
( Milner Centre for Evolution, Department of Biology & Biochemistry, University of Bath, UK )

DNA knots, tangles and supercoiling problems

[DNA molecule and cell nucleus] According to the usual comparison, it’s as if you had to pack 39 km of extremely thin thread into a tennis ball. Moreover, this thread is divided into 46 pieces (individual chromosomes) averaging, in our tennis-ball analogy, over 0.8 km long. Can it be at all possible not only to pack the chromosomes into the nucleus, but also to keep them from becoming hopelessly entangled?

All we can say currently is that we know some of the players addressing the problem. For example, there are enzymes called “topoisomerases” whose task is to help manage the spatial organization of chromosomes. Demonstrating a spatial insight and dexterity that might amaze those of us who have struggled to sort out tangled masses of thread, these enzymes manage to make just the right local cuts to the strands in order to relieve strain, allow necessary movement of genes or regions of the chromosome, and prevent a hopeless mass of knots.
Some topoisomerases cut just one strand of the double helix, allow it to wind or unwind around the other strand, and then reconnect the severed ends. This alters the supercoiling of the DNA. Other topoisomerases cut both strands, pass a loop of the chromosome through the gap thus created, and then seal the gap again. (Imagine trying this with miles of string crammed into a tennis ball)

— Stephen L. Talbott (Evolution scientist, The Nature Institute, USA)

The most common analytical method within population genetics is deeply flawed

It is expected that this method will give correct results because it is so frequently used. But it is neither a guarantee of reliability nor produces statistically robust conclusions

— Dr. Eran Elhaik (Associate Professor in molecular cell biology, Lund University, Sweden)

Techniques that offer such flexibility encourage bad science and are particularly dangerous in a world where there is intense pressure to publish.  If a researcher runs PCA several times, the temptation will always be to select the output that makes the best story

— Prof. William Amos (University of Cambridge)