Dust and Starlight · Episode 9

Who wrote the genetic code?

Every living cell reads its DNA code three letters at a time, using a molecular machine called the ribosome. Science explains how the code works but not yet how it began; Psalm 139:16 says "in your book they were all written."

From Episode 9: Written in Your Book. Host Daniel Voss with Dr. Julia Hartmann, molecular biologist (protein biochemistry and gene regulation).

Chapters

  1. 0:00 Intro
  2. 0:19 Cold open
  3. 1:29 The Text Itself
  4. 4:53 A Code, Not a Chemical
  5. 8:13 The Chemist's Hand
  6. 11:12 A Needle in Sequence Space
  7. 15:05 A Personal Detour
  8. 18:13 Blueprints That Won't Bend
  9. 23:32 Okay, but let's be honest
  10. 30:45 What Do We Do With a Story Like This

Transcript

Voices are AI-generated, and the host and guests are fictional characters. The facts and sources are real and listed below.

Cold open

Daniel: Right now, inside you — inside every cell you've got — there's a little machine reading.

Julia: You're starting with the ribosome.

Daniel: I'm starting with the ribosome. It's reading a message. Three letters at a time. And every three letters, it grabs one building block and snaps it onto a chain. Snap. Snap. Snap. Several every second. When it hits the word that means "stop," it stops, lets go, and that chain folds itself up into a working machine.

Julia: And if a letter in the message is wrong —

Daniel: — the machine can come out wrong. Or not fold at all. So here's the question this whole episode is about. Somebody wrote that message. Or nobody did. There's a line in the Psalms, three thousand years old, give or take — "In your book they were all written." I think David knew something. And I'm not going to pretend I don't have a side.

Julia: You never do.

Daniel: I'm Daniel Voss. Joined by molecular biologist Dr. Julia Hartmann, this is Episode 9: Written in Your Book.

The Text Itself

Daniel: Okay. Scripture first, on the table, before any biology. Psalm one thirty-nine. David's writing. Verse thirteen. "For you formed my inmost being. You knit me together in my mother's womb. I will give thanks to you, for I am fearfully and wonderfully made. Your works are wonderful. My soul knows that very well."

Julia: "Knit me together." Huh. I — sorry, go on.

Daniel: No, no, hold that, we're coming back to knitting. Verse fifteen. "My frame wasn't hidden from you, when I was made in secret, woven together in the depths of the earth." The Hebrew word behind "woven together" is "raqam." It's an embroidery word. It's the word for — like, a craftsman working different colored threads into a pattern. Not a pile of thread. A PATTERN.

Julia: Okay, that's — that's a very specific image.

Daniel: It gets more specific. Verse sixteen. "Your eyes saw my body. In your book they were all written, the days that were ordained for me, when as yet there were none of them." And the word translated "my body" there is "golmi." One word. It means the unformed mass. The embryo, before it looks like anything.

Julia: So God sees the — the unshaped thing, and there's already a book.

Daniel: There's already a book. The plan comes before the body. Now, I want to be careful — the book in verse sixteen is literally about his days. His life. I'm not going to tell you David was writing a genetics paper.

Julia: Thank you.

Daniel: But the picture he reaches for — a body woven to a pattern, from a book, before it has a shape — that's the picture. And he got it three thousand years before anybody knew there was a text inside a cell.

Julia: I'm going to stay out of the Hebrew. That's your lane. What's the second passage?

Daniel: Genesis one. And it's a phrase, not a verse. "After their kind." Plants "after their kind." Sea creatures "after their kind." Livestock, creeping things — "after their kind." It shows up ten times in that one chapter. Ten.

Julia: Ten? I never counted.

Daniel: Nobody counts! The Hebrew word is "min." And look, I'll be straight — "min" is not the modern word "species." Nobody knows exactly where the line of a "kind" falls. But the idea's clear. Living things reproduce inside boundaries. A LOT of variety inside the boundary. But the boundary's there.

Julia: Hm. Okay. I can already tell where you're taking that.

Daniel: You can?

Julia: Gene networks. You're going to hit me with gene networks.

Daniel: Later. Later. One more, just one line. Paul, Romans one twenty. "For the invisible things of him since the creation of the world are clearly seen, being perceived through the things that are made." So the claim is — you can look at what's made and see something about the maker. That's — honestly, that's the whole episode in a sentence.

A Code, Not a Chemical

Daniel: Okay, Julia. Your turn. You spend your days inside cells. Is it fair — is it actually fair to call DNA a message? Or is that just preacher poetry?

Julia: No, it's fair. It's — it's what we call it. We call it a code. The genetic code. DNA is a sequence of four chemical letters, and the ORDER of those letters is what matters. The cell copies a stretch of it into RNA, the ribosome reads the RNA three letters at a time, and each three-letter word stands for one amino acid. String the amino acids together in the right order and you get a protein.

Daniel: And the order is everything.

Julia: The order is everything. Same letters, different order — different protein, or no protein. It's like — okay, "listen" and "silent." Same six letters.

Daniel: Oh, I like that.

Julia: I stole it from a textbook, don't give me credit.

Daniel: And here's the part that keeps me up at night. The machine that reads the code — the ribosome, and all the helper machines around it — how do those get built?

Julia: From instructions in the code.

Daniel: From instructions in the code! So you need the reader to read the book, and the book to build the reader.

Julia: Yeah. It's a loop. Every biology student hits that and goes "wait —"

Daniel: "— wait, which came first?"

Julia: Exactly that. That's the RNA world's whole reason to exist, honestly. We'll get there.

Daniel: And it's not just biologists who see a code. Bill Gates, in his book "The Road Ahead." Quote, "DNA is like a computer program but far, far more advanced than any software ever created." And Gates is not writing a sermon.

Julia: No. And it's not just the software people. Richard Dawkins opens "The Blind Watchmaker" — first line of the book — "Biology is the study of complicated things that give the appearance of having been designed for a purpose."

Daniel: The APPEARANCE of design.

Julia: He'd stress "appearance." Yes.

Daniel: Of course he would. But even he starts there. The thing looks designed. The argument is about whether you believe your eyes.

Julia: Or whether something else can produce that look.

Daniel: Right. And that's the fight. So let me bring in the man whose case we're walking through today. Stephen Meyer. PhD in the philosophy of science from Cambridge. Runs the Center for Science and Culture at the Discovery Institute in Seattle. Two books — "Signature in the Cell," two thousand nine, and "Darwin's Doubt," two thousand thirteen. His argument, stripped down, is this. In everything we've ever watched happen, when you find functional, specific information — a code, a message, software — the only cause we've ever seen produce it is a mind.

Julia: And that's — okay, I'll say it now so I don't have to keep saying it. That's a minority position in my field.

Daniel: Minority. Not crazy.

Julia: Minority. Let's see if it's crazy.

Daniel: Fair enough.

The Chemist's Hand

Daniel: Back in Episode Five we spent a whole episode on the origin of life, and I don't want to repeat all of it. But there's one piece that belongs here. The RNA world.

Julia: The idea that before DNA and proteins, you had RNA doing both jobs — storing information AND doing chemistry.

Daniel: And it's the leading idea. And here's what gets me. Two of the big names in that field — Gerald Joyce at Scripps and Leslie Orgel at the Salk Institute — they described the RNA world as, quote, "the molecular biologist's dream." And in the same breath, "the prebiotic chemist's nightmare."

Julia: That's — yeah, that's a real line. It's famous.

Daniel: The DREAM, because once you have self-copying RNA, a lot of things make sense. The NIGHTMARE, because getting there from dirt and water is —

Julia: — really, really hard. It's really hard. I'm not going to fight you on that.

Daniel: So here's Meyer's point, and I think it's sharp. Look at the experiments that make progress. Who's doing the work? The chemist. Picks the pure starting chemicals. Picks the order. Pulls out the stuff that would ruin the reaction. Adds the next ingredient at exactly the right step. His argument is that the experiment ends up demonstrating the thing it was trying to replace. An intelligent agent, making it work.

Julia: Okay — that's where I push back. Because that's not fair to someone like John Sutherland.

Daniel: Tell me about Sutherland.

Julia: Two thousand nine, in Nature. Sutherland's group in Manchester showed a route to two of the RNA building blocks — the pyrimidine ones — starting from simple molecules chemists think were around on the early Earth. And they did something clever. They skipped the step everybody had been stuck on for decades.

Daniel: And did a chemist set it up?

Julia: Well — yes. Obviously a chemist set it up. That's what an experiment IS.

Daniel: That's my point!

Julia: No, but — hang on, Daniel — the question is whether the conditions they chose could plausibly exist in nature. A chemist who builds a model of a river isn't proving rivers need engineers.

Daniel: Okay. That's a good line. I'll give you that line.

Julia: Thank you.

Daniel: But — and here's where I land — it's two building blocks, out of four. From carefully chosen feedstocks. In sequence. And even your own field calls the next steps a nightmare. So every time the chemistry gets further, it gets further because somebody very smart is steering. At some point you have to ask — is the steering the experiment, or is it the answer?

Julia: That's — I don't love it. But I understand why you ask it.

A Needle in Sequence Space

Daniel: Okay. Proteins. This is the one I've been waiting for.

Julia: I can hear that.

Daniel: Say a protein is a hundred and fifty amino acids long. Pretty ordinary size. And there are twenty kinds of amino acids to choose from at each spot. How many possible sequences is that?

Julia: Twenty to the hundred and fiftieth power. It's — it's a number that doesn't mean anything to a human brain. It's vastly more than the number of atoms in the universe.

Daniel: And most of those sequences —

Julia: — are garbage. Yeah. They don't fold. They're floppy, they clump, they do nothing.

Daniel: So how rare are the ones that work? Because that's the whole question. That's the needle.

Julia: That's a real, live question, yes.

Daniel: Douglas Axe. Two thousand four, Journal of Molecular Biology. He did actual experiments. Took a real enzyme, a piece of a beta-lactamase — the kind of enzyme bacteria use to break down penicillin — and started changing its sequence, and measuring what still worked. And from that, his estimate for how many sequences of that size would fold into a working enzyme like it —

Julia: One in ten to the seventy-seventh.

Daniel: One in ten to the SEVENTY-SEVENTH. That's a one with seventy-seven zeros after it.

Julia: And I have to jump in right here. Because that number is not the only number.

Daniel: I knew you would.

Julia: Of course I would, it's my job. Two thousand one, Nature. Anthony Keefe and Jack Szostak — Szostak's the Nobel laureate we talked about in Episode Five. They built a library of about six trillion random proteins, eighty amino acids long, and fished out the ones that could grab onto ATP. The cell's energy molecule. And their estimate was about one in ten to the eleventh.

Daniel: Eleven.

Julia: Eleven. Not seventy-seven. That's sixty-six zeros of difference.

Daniel: Okay, but — can I — they're not measuring the same thing, are they?

Julia: No. They're not.

Daniel: Axe is asking, how rare is a sequence that folds into a real working enzyme, one that does a job in a living cell. Szostak's asking, how rare is a sequence that can stick to one molecule. Sticking is not working. A magnet sticks to your fridge. That doesn't make it an engine.

Julia: Okay, that's — that's a little unfair, but it's not WRONG. Binding is a much lower bar than catalysis. Most people in my field would say Axe's number is too harsh and Szostak's is too easy for a real enzyme, and the truth sits somewhere in the middle. We honestly don't have a settled figure.

Daniel: And here's the other thing about Szostak's experiment. Who built the library?

Julia: Oh, don't —

Daniel: Who picked the target? Who ran the fishing?

Julia: Szostak did. Yes. I walked into that.

Daniel: You walked right into it. And here's the piece people skip. Natural selection is real. I'm not denying it. But it can only keep something after the mutation has already shown up. It doesn't see ahead. It can't aim. So if the working sequences are really rare, selection's standing there with nothing to pick.

Julia: That — yes. Selection acts on what variation hands it. That's just true. The whole argument turns on how rare "rare" is.

Daniel: And nobody's measured it and gotten a number that makes the problem go away.

Julia: Nobody's gotten a number everybody agrees on. I'll say it that way.

A Personal Detour

Daniel: Can I tell you something personal? It kind of goes with all this.

Julia: Please.

Daniel: My sister had her first baby last spring. And I went with her to one of the scans — the twenty-week one, her husband was stuck at work. And I'm sitting in this little dark room, and the tech's moving the wand around, and then — there's this —

Julia: The heartbeat.

Daniel: The heartbeat. And four chambers. The tech's pointing, "that's the left ventricle," and I'm just — I'm a grown man, and I'm crying in a chair in a dark room. And my sister looks over and goes, "Danny, are you okay?" And I couldn't even — I said "I'm fine," and I was very much not fine.

Julia: That's the right reaction, honestly.

Daniel: And all I could think was, "you knit me together in my mother's womb." Because that's what I was watching. Knitting. From a book.

Julia: Is the baby here now?

Daniel: She's here. Four months old. Grace. And last week I'm holding her, and she grabs my finger — you know how they do, that grip —

Julia: They're strong.

Daniel: They're SO strong! And I'm looking at this little hand, and five fingers, and fingernails — tiny, perfect fingernails — and I'm thinking, every one of those was on a schedule. Something told the cells, "now fingers, not a flipper, and stop HERE." And my sister's watching me and she goes, "you're doing the thing again." Because apparently I have a face I make.

Julia: The crying face?

Daniel: Almost the crying face. I'm going to be the weird uncle. I've accepted it.

Julia: Can I — mine's knitting too, actually.

Daniel: Really?

Julia: My grandmother. She knitted everything. Sweaters, scarves, these horrible Christmas vests —

Daniel: Oh no. The vests.

Julia: — and she had this rule. If you drop one stitch, you don't keep going. You go back. Because one dropped stitch, three rows down, and the whole thing — it starts to pull. It puckers. You can't hide it. And when I started grad school, my first real project was a protein I was supposed to make in bacteria and purify. Weeks. And it came out as this — this gray sludge at the bottom of the tube. Useless. And it turned out I had ONE letter wrong in the gene. One. Out of hundreds.

Daniel: One dropped stitch.

Julia: One dropped stitch. And I called my grandmother that night, just to complain, and she said, in German — I'll spare you the German — she said, "So. Now you know why I go back."

Daniel: I love her.

Julia: Everyone did. I'll be honest, I didn't think about Psalm one thirty-nine then. I'm thinking about it now.

Blueprints That Won't Bend

Daniel: Okay. Gene networks. You saw it coming.

Julia: I did.

Daniel: Explain it better than I can, because this is your lane.

Julia: Okay. So — genes don't just sit there making proteins. A lot of them are switches. They turn OTHER genes on and off, in the right place and the right order, while an embryo builds itself. And these switches are wired together into networks. Developmental gene regulatory networks — people just say dGRNs. They're basically the construction schedule for a body plan.

Daniel: And the man who spent his life mapping them was —

Julia: Eric Davidson. At Caltech. A giant. He spent decades mapping the network that builds a sea urchin embryo.

Daniel: And here's what Davidson wrote, in two thousand eleven, in the journal Developmental Biology. Quote. "There is always an observable consequence if a dGRN subcircuit is interrupted. Since these consequences are always catastrophically bad, flexibility is minimal."

Julia: Yes. He wrote that.

Daniel: Catastrophically bad. Flexibility minimal. So the core of the construction plan — you touch it, and the body either doesn't form or doesn't live. And Meyer asks the obvious question. If you can't change the core plan without killing the animal, how do you get a new body plan by changing it one small step at a time?

Julia: Okay. I have to say something about Davidson here, and I'd be dishonest if I didn't.

Daniel: Go.

Julia: Davidson was not a design guy. At all. He thought body plans evolved. His point was that they evolved through changes in these networks, and that the textbook story — small changes in proteins, one at a time — was the wrong picture. He was fighting with his own field about HOW. Not WHETHER.

Daniel: That's fair, and I'll say it clearly — Davidson didn't agree with Meyer's conclusion. But the observation is his. Not Meyer's. The core circuits don't bend. That's Davidson's own data.

Julia: The core circuits, yes. The edges of the network do change, though. There's a lovely example — stickleback fish. There are populations of them in lakes that lost their pelvic spines. And in two thousand ten, a team showed why — a little switch region near a gene called Pitx1 got deleted. Not the gene itself. Just the switch that turns it on in the pelvis. And the fish were fine. Better than fine, in those lakes.

Daniel: And what did the fish gain?

Julia: It lost — okay, it lost a structure.

Daniel: It lost a structure. It stayed a stickleback. That's "after its kind," Julia. That's exactly what Genesis describes. Tons of variation — spines, no spines, size, color — inside the boundary. What nobody's shown is the boundary moving. A brand-new body plan, built from scratch.

Julia: You're going to make me say "after its kind" on air, aren't you.

Daniel: You don't have to say it. I just did. Ten times.

Julia: Okay, okay.

Daniel: Okay, but my favorite example of variation inside the boundary isn't a fish. It's the octopus.

Julia: Oh — the cold-water study. I love that paper.

Daniel: Two thousand twenty-three, in Cell. Joshua Rosenthal's team. They took California two-spot octopuses, chilled the water in their tanks, and within hours — hours — the octopuses were editing the messages coming off their genes. More than twenty thousand spots. Rewriting the instructions for proteins in their nervous system.

Julia: And I have to be precise, because people get this wrong all the time. It's the RNA they're editing. The working copies. The DNA doesn't change at all.

Daniel: Right. The master copy stays locked. They're editing the photocopies. And one of the edits makes a motor protein in their nerve cells run slower. Another one changes how a protein handles calcium at the synapse. Tuning the nervous system to the cold. And they saw it in wild octopuses too, not just in the lab.

Julia: It's genuinely astonishing. There's an enzyme family — ADAR — that does the editing, and octopuses use it on a scale almost nothing else does.

Daniel: So here's my question. When the water turns cold, does the octopus go out and invent a new system?

Julia: No. The system's already there. It just gets used differently.

Daniel: It's already there. Built in. Waiting. That's not an animal inventing its way forward, Julia. That's an animal that came with a thermostat. It stays an octopus. It just adjusts. After its kind.

Julia: I'd say the editing system itself evolved.

Daniel: And I'd say somebody who knew the water would get cold put it there.

Julia: That's where we differ. But I'll grant you — it looks a lot more like a feature than an accident.

Okay, but let's be honest

Daniel: Okay. This is the part of the show where I have to take the hits. So — I'll start with an email, actually, because it's the best version of the objection. A listener wrote in after Episode Eight. And the gist was, "isn't all of this just God-of-the-gaps? You find something science can't explain yet, and you stick God in the hole. And then science fills the hole, and God gets smaller."

Julia: Can I say I agree with your listener?

Daniel: I figured.

Julia: So let me make the strongest case. The best one I've got. First — new genes aren't a mystery. Susumu Ohno wrote a whole book on this in nineteen seventy, "Evolution by Gene Duplication." A gene gets copied by accident. Now you have a spare. The original keeps doing its job, and the spare is free to drift and change and maybe — maybe — find a new job. We see the fingerprints of that all over every genome.

Daniel: Okay —

Julia: Second. Nylon. Nylon didn't exist until the nineteen thirties. And by the nineteen seventies, Japanese researchers found bacteria in the wastewater of a nylon factory that could EAT the leftover bits of nylon. An enzyme for a chemical that didn't exist forty years earlier. That's new function.

Daniel: Can I —

Julia: And — sorry, I'm on a roll — genes don't even need a parent gene. We find what we call de novo genes. Stretches of DNA that used to be junk, that picked up the right signals and started making a protein. In two thousand six, a team found five of them in fruit flies. Brand new. From nothing coding.

Daniel: From nothing coding. Okay, hold that one, because I want to ask about it —

Julia: One more. One more. Richard Lenski's experiment. Twelve populations of E. coli, started in nineteen eighty-eight, still running. And around generation thirty-one thousand five hundred, one population learned to eat citrate in the presence of oxygen — something E. coli normally can't do. Watched. In a lab. New capability.

Daniel: Okay. Those are real. All four are real. So let me take them one at a time, and you tell me where I'm wrong.

Julia: Deal.

Daniel: Nylon. In two thousand five, a Japanese team — Seiji Negoro's group — solved the actual structure of that nylon enzyme. And what did it turn out to be?

Julia: It's — it has the same fold as a family of existing enzymes. Esterases. The beta-lactamase fold, actually.

Daniel: The BETA-LACTAMASE fold. The exact enzyme family Douglas Axe was studying. So the nylon enzyme isn't a new fold. It's an old, existing enzyme, with a few changes in its pocket, doing a new trick. And in two thousand seven, the same group showed just two changes in a related enzyme pushed its activity way up.

Julia: Yeah. That's — yes. It's tinkering with something that already worked.

Daniel: Tinkering. Not writing. Now your de novo genes. What do those proteins look like? Are they nice folded little machines?

Julia: Mostly — no. They tend to be short. The typical one's under a hundred amino acids. And a lot of them are what we call disordered. They don't settle into a stable shape.

Daniel: So they don't fold.

Julia: A lot of them don't, no. Some pick up structure over time, that's an active research area, but —

Daniel: — but the thing Axe was asking about, a real folded enzyme, a machine —

Julia: — isn't what pops out of junk DNA. No. Not usually. Short, floppy, and often we don't even know what they do yet.

Daniel: I'm not trying to score cheap points. That's genuinely interesting. But a floppy string that does we-don't-know-what is a long way from a ribosome.

Julia: It's a long way. I'll grant you it's a long way.

Daniel: Okay. Lenski. What was the actual mutation?

Julia: The key one was a duplication. A chunk of DNA got copied, and a citrate-transport gene that was always there — but switched off when oxygen's around — landed next to a switch that's switched ON when oxygen's around.

Daniel: So an existing gene, moved next to an existing switch.

Julia: Yes.

Daniel: And how long did it take?

Julia: More than thirty thousand generations, in that population, and the other eleven hadn't gotten it at all. They'd tested — the paper says billions of mutations.

Daniel: Billions of tries. One population. And the prize was flipping on a gene that was already there. Julia, I'm not saying that's nothing. It's genuinely beautiful work. But if that's the best we can watch happen — if that's the showcase — it sounds a lot more like my side than yours. It sounds like good mutations are rare, and new machines are rarer still.

Julia: Okay. I'll — I'll give you something real. Everything I just listed — duplication, nylon, citrate, even the de novo genes — is change built on top of machinery that already exists. I don't have an example, in a lab or anywhere, of a brand-new protein fold, or a brand-new body plan, being built from nothing while someone watched. Nobody does.

Daniel: Thank you.

Julia: And I'll give you the bigger one. Where did the FIRST information come from? Before there was anything to duplicate? Before there was a cell? That's open. Genuinely open. Francis Crick — who co-discovered the structure of DNA, and was no friend of religion — wrote in nineteen eighty-one that, quote, "the origin of life appears at the moment to be almost a miracle, so many are the conditions which would have had to have been satisfied to get it going."

Daniel: Almost a miracle. From Crick.

Julia: He then went looking for a natural answer, to be clear.

Daniel: Of course.

Julia: And I haven't changed my mind on the big picture. Common descent is the leading scientific theory for good reasons, and I think it's true. But I can't tell you honestly that we know where the first code came from. We don't.

Daniel: And that's why this isn't God-of-the-gaps. God-of-the-gaps says "we don't know, so God." Meyer's argument says "we DO know something." We know what writes code. We've watched it every single day of human history. Minds write code. Every book, every program, every blueprint anybody's ever traced back to its source — a mind. So when you find code at the bottom of every living thing, pointing to a mind isn't filling a gap. It's following the one cause we've actually seen work.

Julia: I'd still say a cause we haven't found yet could be out there.

Daniel: Could be. But you don't build a case on a cause nobody's seen. You build it on the one everybody's seen.

Julia: That's — — that's a better answer than your listener's going to expect.

What Do We Do With a Story Like This

Daniel: Okay. Let me try pulling it together, and you tell me where I'm overreaching.

Julia: You'll overreach. I'll tell you.

Daniel: Here's what I think we've shown. One — the cell runs on a code. Not a metaphor. The biologists call it a code. Two — the working sequences in that code are rare. How rare is argued, but even the friendly number is one in a hundred billion, for the simplest job. Three — the core of the construction plan for a body doesn't bend without breaking. That's Davidson's own finding. Four — everything we've actually watched evolution do is tinkering with what's already there. And five — the origin of the first code is, to use Crick's word, almost a miracle.

Julia: Where you overreach — and you knew this was coming —

Daniel: I did.

Julia: — is jumping from "we don't have a full natural explanation" to "therefore there isn't one." Science has closed gaps before that people swore were permanent. I'd rather keep looking.

Daniel: And you should keep looking. I want you to. But I'm not jumping from ignorance. I'm jumping from what we know. And here's where I stop being a science host and just talk as me. I believe Psalm one thirty-nine is true. I believe somebody saw my unformed body, and there was already a book. That doesn't come from a microscope. It comes from the same God who told Paul you could see Him in the things He made. The microscope just keeps agreeing.

Julia: I'll say this. I came in thinking this was a gaps argument, and it's — it's more careful than that. I don't share your conclusion. But I understand now why you look at that ribosome and see handwriting.

Daniel: That's all I'm asking anybody to do. Look at it long enough to see why.

Julia: And my grandmother would say — go back and check the stitches.

Daniel: She would. She'd be right.

Daniel: Somewhere tonight, a little machine in one of your cells is reading three letters at a time, and it hasn't dropped a stitch yet. You were knit together. You were written down before you had a shape. Think about who might be holding the pen. We'll be back.

Sources

  1. Psalm 139:13-16 and Genesis 1:11-25 (World English Bible, public domain), ebible.org/eng-web. Hebrew notes: "raqam" and "golmi" — biblehub.com/lexicon/psalms/139-16.htm and commentaries on Psalm 139:15; "min" — Strong's H4327, biblehub.com/hebrew/4327.htm (the phrase occurs ten times in Genesis 1; "min" is not equivalent to modern "species").
  2. Romans 1:20 (World English Bible).
  3. The genetic code, transcription and translation: standard molecular biology (three-nucleotide codons, one amino acid per codon, stop codons).
  4. Bill Gates, The Road Ahead (Viking, 1995): "DNA is like a computer program but far, far more advanced than any software ever created." Widely cited; page number not verified.
  5. Richard Dawkins, The Blind Watchmaker (1986), opening line: "Biology is the study of complicated things that give the appearance of having been designed for a purpose."
  6. Stephen C. Meyer: PhD, philosophy of science, University of Cambridge; director, Discovery Institute's Center for Science and Culture. Signature in the Cell (HarperOne, 2009); Darwin's Doubt (HarperOne, 2013, New York Times bestseller) — discovery.org/p/meyer; stephencmeyer.org/cv.
  7. Gerald F. Joyce and Leslie E. Orgel, "Prospects for understanding the origin of the RNA world," in The RNA World, 2nd ed., ed. Gesteland, Cech, and Atkins (Cold Spring Harbor Laboratory Press, 1999): the RNA world as "the molecular biologist's dream" and "the prebiotic chemist's nightmare."
  8. M. W. Powner, B. Gerland, and J. D. Sutherland, "Synthesis of activated pyrimidine ribonucleotides in prebiotically plausible conditions," Nature 459, 239-242 (2009) — nature.com/articles/nature08013.
  9. Douglas D. Axe, "Estimating the prevalence of protein sequences adopting functional enzyme folds," Journal of Molecular Biology 341, 1295-1315 (2004): as low as 1 in 10^77 — pubmed.ncbi.nlm.nih.gov/15321723.
  10. Anthony D. Keefe and Jack W. Szostak, "Functional proteins from a random-sequence library," Nature 410, 715-718 (2001): a library of about 6 x 10^12 random 80-mers; about 1 in 10^11 bind ATP — nature.com/articles/35070613.
  11. Eric H. Davidson, "Evolutionary bioscience as regulatory systems biology," Developmental Biology 357, 35-40 (2011): "There is always an observable consequence if a dGRN subcircuit is interrupted. Since these consequences are always catastrophically bad, flexibility is minimal." Davidson held that body plans evolved through changes in gene regulatory networks; see E. H. Davidson and D. H. Erwin, "Gene regulatory networks and the evolution of animal body plans," Science 311, 796-800 (2006).
  12. Y. F. Chan et al., "Adaptive evolution of pelvic reduction in sticklebacks by recurrent deletion of a Pitx1 enhancer," Science 327, 302-305 (2010) — pubmed.ncbi.nlm.nih.gov/20007865.
  13. Susumu Ohno, Evolution by Gene Duplication (Springer-Verlag, 1970).
  14. Nylon-degrading bacteria: isolated from nylon-factory wastewater in Japan in the 1970s (Kinoshita, Okada, and colleagues). S. Negoro et al., "X-ray crystallographic analysis of 6-aminohexanoate-dimer hydrolase: molecular basis for the birth of a nylon oligomer-degrading enzyme," Journal of Biological Chemistry 280, 39644-39652 (2005): a pre-existing esterase with the beta-lactamase fold, altered in the catalytic cleft; a 2007 study by the same group showed two substitutions (G181D, H266N) raised a related enzyme's activity to about 85% of the nylonase's. Summary: en.wikipedia.org/wiki/Nylon-eating_bacteria.
  15. Z. D. Blount, C. Z. Borland, and R. E. Lenski, "Historical contingency and the evolution of a key innovation in an experimental population of Escherichia coli," PNAS 105, 7899-7906 (2008): 12 populations founded in 1988; Cit+ arose in one population by about 31,500 generations, after "billions of mutations" were tested — pnas.org/doi/10.1073/pnas.0803151105. Z. D. Blount et al., "Genomic analysis of a key innovation in an experimental Escherichia coli population," Nature 489, 513-518 (2012): a tandem duplication placed citT under the aerobically active rnk promoter — nature.com/articles/nature11514.
  16. Francis Crick, Life Itself: Its Origin and Nature (Simon & Schuster, 1981), p. 88: "the origin of life appears at the moment to be almost a miracle, so many are the conditions which would have had to have been satisfied to get it going." Crick went on to propose directed panspermia.
  17. Michael J. Behe, "Experimental evolution, loss-of-function mutations, and 'the first rule of adaptive evolution,'" Quarterly Review of Biology 85, 419-445 (2010) — background for the "tinkering, not writing" reading of Lenski's results (not quoted on air).