I realize that I missed an opportunity, though! A week or so ago I was teaching my cell biology class about cell cycle regulation, and I was all about retinoblastoma, Rb, the gene product that acts as a regulator of the cell cycle — the cell will not proceed to the DNA synthesis phase unless Rb is deactivated by phosphorylation first. And then this week I was talking about the evolution of multicellularity, so I showed them unicellular algae like Chlamydomonas, and constitutive colonial protists like choanoflagellates, and of course I told them all about Volvox…but I failed to connect the two.

Now I read about the complexities of cell division in Chlamydomonas which could have played a role in the evolution of multicellularity, and from there I learn that differences in cell cycle can be traced to slight modifications of a few genes (no new genes required), in particular…Rb!

I wonder if the students would complain if we wound the class back to early November and started over? Probably.

Although today is a weird class day — it’s the day before Thanksgiving break, and I know from past experience that attendance will be very, very poor as students skip out to go home for vacation a day early; I also polled the class on Monday and learned that only about a quarter will show up (isn’t it nice that they’re honest about it?) I’m bribing them by promising pizza in class, but I’ve also told them it’ll just be a review/Q&A day. Maybe we can just sit down and have a conversation about science over pizza.

My latest WTF moment is this article, Human chromosomes are only half DNA, which presents this little fact as if it is surprising and ground-breaking.

A chromosome is believed to be an “organized structure containing most of the DNA of a living organism.” However, new research finds that DNA makes up only half of the material inside chromosomes – far less than was previously thought.

Instead, up to 47 percent of a chromosome’s structure is actually a mysterious sheath that surrounds the genetic material, researchers from the University of Edinburgh said in a statement.

Say what? A university PR department strikes again, and an oblivious journalist scribbles it up. This is not news. This is not new. I’ve no idea how long I’ve been teaching this, but it’s been ages. Here’s Alberts’ Molecular Biology of the Cell, 4th edition, from 2002.

The proteins that bind to the DNA to form eucaryotic chromosomes are traditionally divided into two general classes: the histones and the nonhistone chromosomal proteins. The complex of both classes of protein with the nuclear DNA of eucaryotic cells is known as chromatin. Histones are present in such enormous quantities in the cell (about 60 million molecules of each type per human cell) that their total mass in chromatin is about equal to that of the DNA.

And what’s with this “mysterious sheath” nonsense?

If you’re a reporter who’s never taken a basic cell biology class, you have no way of reasonably presenting the context around even a simple observation, so don’t even try, and never trust a university press release, because they’re typically written by people as ignorant of science as you are.

Kris Wager reports on the ongoing reproducibility crisis in Chinese research — as he mentions, it’s being called “fraud”, but that may be too strong a word, unless you want to call a lot of American science fraudulent, too. We’re in a strange state right now where the pursuit of arbitrary statistical validity at all costs has led to some distortion of our results.

Ken Ham has been having a grand time redefining evolution. It’s interesting in a twisted kind of way: the anti-evolutionists are now at the point of having to accept natural selection as true, and are simply declaring that sure, natural selection is fine, it’s just not evolution, which we hate.

Often evolutionists claim speciation is evidence of molecules to man evolution–they couldn't be more wrong https://t.co/EU5AmQxiIF

— Ken Ham (@aigkenham) November 18, 2016

Ask evolutionists for their best evidence for evolution and they'll usually point to speciation or drug resistance etc-they're not evolution

— Ken Ham (@aigkenham) November 18, 2016

He’s linking to an article by Georgia Purdom that is a fine example of selective use of information, and represents AiG’s weird stance. It begins with a hypothetical dialog. It’s really weird.

Let’s listen in on a hypothetical conversation between a biblical creationist (C) and an evolutionist (E) as they discuss some recent scientific news headlines:

E: Have you heard about the research findings regarding mouse evolution?

C: Are you referring to the finding of coat color change in beach mice?

E: Yes, isn’t it a wonderful example of evolution in action?

C: No, I think it’s a good example of natural selection in action, which is merely selecting information that already exists.

E: Well, what about antibiotic resistance in bacteria? Don’t you think that’s a good example of evolution occurring right before our eyes?

C: No, you seem to be confusing the terms “evolution” and “natural selection.”

E: But natural selection is the primary mechanism that drives evolution.

C: Natural selection doesn’t drive molecules-to-man evolution; you are giving natural selection a power that it does not have—one that can supposedly add new information to the genome, as molecules-to-man evolution requires. But natural selection simply can’t do that because it works with information that already exists.

You know, that last bit is actually sort of true: natural selection shapes, or selects, the variation that already exists (although, indirectly, natural selection does create new conditions in the environment by changing allele frequencies, and those changing frequencies can create new probabilities for recombination…but I’ll give her a pass on that for now, because it’ll just lead to arguments about defining “creative” vs. “unpredictable”). But evolutionary biologists already know about all that. She’s not saying anything that we’d find surprising.

She goes on, though.

From a creationist perspective natural selection is a process whereby organisms possessing specific characteristics (reflective of their genetic makeup) survive better than others in a given environment or under a given selective pressure (i.e., antibiotic resistance in bacteria). Those with certain characteristics live, and those without them diminish in number or die.

Hey, guess what? That’s what we’d say from an evolutionary perspective, too! Unfortunately, this state of blissful concordance cannot last.

The problem for evolutionists is that natural selection is nondirectional

Nope. That’s not really a problem, because a) selection is directional in the short term, shaping the population towards greater adaptedness to local conditions, and b) we generally don’t believe in any kind of long term directionality. It’s the creationists who believe in a mysterious molecules-to-man kind of pressure.

—should the environment change or the selective pressure be removed, those organisms with previously selected for characteristics are typically less able to deal with the changes and may be selected against because their genetic information has decreased…. Evolution of the molecules-to-man variety, requires directional change. Thus, the term “evolution” cannot be rightly used in the context of describing what natural selection can accomplish.

It is correct to note that selection is largely a conservative force — it prunes out variation from a population. So she is right that if natural selection were the only force operating on the gene pool, the distribution of variants would get smaller and smaller over time.

Gosh. If only there were some other forces acting on populations to produce a constant source of new information that apparently Answers in Genesis has never heard of. If only there were other processes that generated new genetic variants that natural selection could act on…

Surprise! There is! It’s called “mutation”.

No matter what the exact value of the human mutation rate, every single possible point mutation will happen in just a few generations somewhere among the seven billion or so people on Earth. And each individual who lives to the ripe old age of 60 (i.e. youngsters) will have experienced a huge number of somatic mutations.

Let’s also note that we have a large body of phenotypic variation, not all of which is genetic but which is observable, measurable, and quantifiable, and which AiG ignores. We also have deep information about population structure and patterns of inheritance and descent with modification that directly contradicts AiG’s claim that we are descended from a population of two people only 6,000 years ago.

You cannot imagine how stupid Purdom’s article looks to anyone who has some knowledge of genetics and populations, unless you actually know a little bit about those disciplines. She is willfully ignoring a huge part of genetics in order to make a truly idiotic argument.

We’ve all laughed at this clueless quote from fundies.

One of the most basic laws in the universe is the Second Law of Thermodynamics. This states that as time goes by, entropy in an environment will increase. Evolution argues differently against a law that is accepted EVERYWHERE BY EVERYONE. Evolution says that we started out simple, and over time became more complex. That just isn’t possible: UNLESS there is a giant outside source of energy supplying the Earth with huge amounts of energy. If there were such a source, scientists would certainly know about it.

Purdom has basically said the equivalent.

Natural selection reduces genetic variation in a population. Evolution says that we started out simple, and over time became more complex. That just isn’t possible: UNLESS there is a giant source of new mutations supplying the population with huge amounts of variants. If there were such a source, scientists would certainly know about it.

You bet we would.

Get ready, world, scientists are going to use CRISPR/Cas9 on human patients for the first time, extracting a population of cells, modifying their genomes, amplifying them in tissue culture, and then injecting the modified cells back into the human host. It’s being done in China, where the ethical constraints are a bit more loose, which isn’t always good…but in this case, it sounds like a good, safe (as safe as experimental therapies can be) approach.

They intend to use CRISPR/Cas9 to knock out the PD-1 gene in immune system cells. PD-1 is a cell surface molecule on T-cells that inhibits the cells, and acts as a constraint on immune system activity. The “PD” is short for “Programmed Death”, and what it does is compel the cells to commit suicide when stimulated — so if immune system cells get a bit overzealous and go on a rampage attacking healthy cells, they can be switched off. The immune system has multiple checkpoints to prevent it from going rogue, and this procedure will remove one of them. By knocking out the PD-1 gene, the scientists are creating particularly unrestrained cells that they hope will do a more effective job killing cancer cells, because cancer cells are known to use the signaling mechanisms that tell the immune system to die.

Are there drawbacks and risks? There are always drawbacks and risks. This technique is a variation on an existing pharmaceutical approach, which uses drugs that inhibit PD-1 in cancer patients, so we know a bit about its effects — it’s just that taking out the whole gene with CRISPR/Cas9 is a dramatically thorough way of demolishing the molecule. But we do have some drugs, like Nivolumab and Pembrolizumab, that target PD-1 already and are in clinical trials. We’ve also experimentally knocked out the gene in mice.

So, we have an idea of what could go wrong, and in the immortal words of Dr House, it’s lupus. Or lupus-like effects. By jacking up the immune system and removing one restraint on its activity, you can get complex system-wide problems, which Dr House will tell you are pretty hard to treat, but at least they’re not as severe as terminal cancer. They are also editing a terminal cell type — it’s not going to proliferate — so eventually, we hope after they’ve killed cancer cells, the injected cells will die of natural causes and the effect will fade away.

This is not a treatment that affects the germ cell line, so these patients, if they survive, will not be passing on an edited gene to their offspring. It’s also got to be a rather expensive therapy that has to be customized for each new patient, so it’s not going to be routine. It is a first step into the exciting world of genetically modifying humans, though.

Who else remembers the days of the BBS? Back in the 1980s I used to hang out on various dial-up bulletin boards, before the internet. They weren’t truly interactive — some used only a single phone line, a few fancy ones could handle a couple of simultaneous connections, but generally you’d log in, browse a couple of messages other people had left, maybe leave one yourself, and log out again, all at 300 baud. When the fancy 1200 baud modems came out (I bought one that was military surplus), my old Apple II struggled to keep up with the furious data rate, and I actually wrote my very own telecommunications program — in 6502 Assembler, of course, using the wonderful ORCA macro assembler package — and took the daring step of cutting a lead on my mother board to enable interrupts, and building the program around a custom interrupt handler just so it would stop dropping characters. I was a true nerd.

It all came rushing back with this article in the Atlantic, The Lost Civilization of Dial-Up Bulletin Board Systems. I abandoned them in the 1990s when the Internet became ubiquitously available, although still often through dial-up lines from home. Apparently some tiny number of them still hang on. There are actually 20 dial-up BBSes still running, somewhere?

But every mass extinction has its holdouts. Even today, a small community of people still run and call BBSes. Many seek the digital intimacy they lost years ago; 373 BBSes still operate, according to the Telnet BBS Guide, mostly in the United States. Many are set up to be accessible via internet-connected tools like Telnet, a text-based remote-login protocol originally designed for mainframes.

Did any direct-access, telephone-dial-up BBSes survive the internet’s proverbial asteroid? Sure enough, there are about 20 known dial-up BBSes in North America. And of those, only a handful have been running non-stop since the mid-1990s. These are the true dinosaurs walking among us. Who dares to run such antique systems, and why? Have any of them been left running by accident like the BBS in my dream? I had to find out.

Yes, why? I want to know. It turns out that many of them are just kept up for nostalgia’s sake, but others are…are you surprised to learn that they’re maintained by delusional right-wing paranoids?

Ten years ago, when I dipped back into BBSes, I still got a sense that many sysops ran them to provide a libertarian alternative to the internet. Among them, the unoppressed who wanted religious freedom, the unsurveilled who wanted freedom from surveillance, and those prepping for the day when BBSes would provide shelter after the internet came crashing down.

It was never an alternative to the Internet. It couldn’t be. You’d have to argue that the Post Office was just a slow version of blogging if you go down that path.