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A Nobel for CRISPR

The 2020 Chemistry Nobel has gone to Jennifer Doudna and Emmanuelle Charpentier for the discovery of CRISPR. An award in this area has been expected for some time – it’s obviously worthy – so the main thing people have been waiting for is to see when it would happen and who would be on it. We’ll get to that second part, but let’s start off with a CRISPR explainer. What is it, how does it work and why has everyone been so sure that it’s a lock for a Nobel?

The short answer is that CRISPR is the easiest, most versatile method for gene editing that has yet been discovered. It’s important to note that those discoveries are still coming; the fireworks have not stopped going off by any means. We’ll do “basic CRISPR” first, though, since everything builds off of that. The story of the discovery is actually a very good illustration of how science works – the good, the bad, and the baffling – and with that in mind, I’m going to spend more time on that part.

The acronym is not going to help very much, I fear: it stands for Clustered Regularly Interspaced Short Palindromic Repeats, which refers to some odd features found in the DNA sequences of many single-celled organisms. In 1987 these were discovered by Yoshizumi Ishino and his group at Osaka. They were cloning a completely unrelated bacterial gene and found these weirdo repeated short stretches of DNA all clustered together (but still separated by unrelated sequences), and no one had seen anything quite like them. This clearly wasn’t an accidental feature, but no one really knew what to make of them, either. It wasn’t until 1993 that the story was really picked up again, when J. D. A. van Empden and co-workers in the Netherlands were looking at repetitive DNA sequences as a way to tell different strains of M. tuberculosis bacteria apart, and noted the same sort of odd patterns.

That same year, Francisco Mojica (a grad student at the time) and co-workers at Alicante in Spain reported the same sort of thing in a really unrelated organism, Haloferax mediterranei. That’s an Archaea, the weird non-bacteria single-cell creatures that are found in many extreme environments, and Mojica was looking at gene transcription changes in that organism under various high-salt conditions (H. mediterranei is the sort of creature that gets stressed out when the salt concentration gets too low, to give you the idea). He was actually doing that (as this retrospective notes!) because he got totally scooped on his original project with the organism and then set out for the less-studied parts of its genome. Out there in what looked like a non-coding region, he found these same sort DNA repeats, 14 of them, each about 30 base pairs long and regularly spaced along in the organism’s genome. Bacterial sequencing was pretty strenuous work back in 1992, and these things were first thought to be an artifact of something that had gone wrong. But no, they were real. It was starting to become clear that this stuff (whatever it was) might have broader implications, but no one knew what those were.

Mojica kept digging into the problem: here’s a 2002 note that showed that these features (which he and his co-authors were then calling SRSRs, for Short Regularly Spaced Repeats) were found in dozens of bacteria and archaea and were probably the most widely distributed repeat sequences in prokaryotes in general. When they transcribed such a repeat region, they got an oddly wide array of proteins, which suggested that there was a lot of RNA processing going on downstream (confirmed by this 2002 work from another team on a different archaeon species).

Meanwhile, Ruud. Jansen at Utrecht, along with van Empden and others, worked out another piece of the puzzle. These repeats had been noted next to the open reading frames (ORFs) of proteins of unknown function, and they found that these were in fact always associated with them across different organisms. That paper suggested the “CRISPR” acronym to clear up the number of different terms that were appearing in the literature, and it stuck, as did the term for those “CRISPR-associated” genes: cas. But the origin and function of the repeats and their associated proteins were still a mystery. All of these were still confined to rather specialized microbiology journals and it was Just One of Those Things that no one had a handle on.

That changed in 2005. Three groups (including Mojica’s) found that those spacers between the repeat elements actually came (in some cases) from bacteriophage sequences or plasmids from other organisms. That rearranged people’s thinking, because it suggested that these weirdo repeat things were somehow involved in infection and defense mechanisms for the bacteria and Archaea themselves. But there were some hair-pulling difficulties along the way to getting the word out, because the discovery itself had been made some time before. Eric Lander’s history of the field (an article not without controversies of its own) illustrates what happened:

Mojica went out to celebrate with colleagues over cognac and returned the next morning to draft a paper. So began an 18-month odyssey of frustration. Recognizing the importance of the discovery, Mojica sent the paper to Nature. In November 2003, the journal rejected the paper without seeking external review; inexplicably, the editor claimed the key idea was already known. In January 2004, the Proceedings of the National Academy of Sciences decided that the paper lacked sufficient “novelty and importance” to justify sending it out to review. Molecular Microbiology and Nucleic Acid Research rejected the paper in turn. By now desperate and afraid of being scooped, Mojica sent the paper to Journal of Molecular Evolution. After 12 more months of review and revision, the paper reporting CRISPR’s likely function finally appeared on February 1, 2005. 

Here’s Mojica’s view on the history, for reference. This sort of thing has happened many a time in the history of science, in case you had any doubts. The other two groups trying to publish such results ran into similar difficulties: Gilles Vergnaud and his co-workers had their paper rejected by four journals in a row, and Alexander Bolotin’s paper lost months with a slow rejection as well.. But by 2007, this idea had been nailed down: if you challenged bacteria with various types of virus (phage), repeats showed up in their genomes with spacers between them based on chunks of that phage DNA. And in turn, if you went in and messed with those repeats and spacers, you altered the resistance profile of the bacterium to different phage infections. There was no doubt: this was part of an adaptive immune system in bacteria and Archaea.

And it was one that actually rewrote their genomes in order to work – that was the startling thing. There was some sort of mechanism that chopped up bacteriophage DNA and inserted pieces of it into the bacterial sequence in order to remember it for the next time it might show up. People had thought originally that such a system might work at the RNA level, but here it was operating on the DNA sequence instead. The number of papers in the field was taking off at this point – there was something new under the sun, and the uses for a completely new genome-editing tool were becoming apparent to anyone who spent a few minutes looking out the window and thinking about the possibilities.

Some of those cas proteins, in fact, turned out to be the endonucleases that did the double-stranded DNA cutting needed for these splices to occur. They needed more than one RNA species to guide them in that job, but Jennifer Doudna and Emmanuelle Charpentier re-engineered one (Cas9) from the bacterium S. pyogenes to make it more simple. Now it just needed one “guide RNA”, the sequence of which determined where in the genome the DNA would be cut. At the same time, Virginijus Šikšnys in Vilnius was working out the same sorts of details. He submitted his own paper to Cell, but it was rejected without review (!) It then spent months in review at PNAS, during which time Doudna and Charpentier’s work appeared in Science, and many are the people who will tell you that had preprint servers been more of a thing back then that his name might be on today’s Nobel citation as well.

This refashioning of the CRISPR system was very significant. The native bacterial system works, but it’s quite complex. The Doudna/Charpentier work opened up its use as a research tool, and molecular biology has never been the same. So there’s a story about the recognition of something strange in bacteria, a story about figuring out what that was and how it might work, and then a story about extending that into something new that could be used in other organisms entirely.

But there’s more – there’s generally more. The first people to get this to work in mammalian and indeed human cells (as opposed to bacteria and the like) were (in basically simultaneous publications) Feng Zhang and co-workers at the Broad Institute and George Church and co-workers at Harvard. Neither of them is on today’s citation, either, of course, and not everyone is happy about that, either (especially considering that there was a third slot left open). But that slot could also have been filled by Mojica, by Šikšnys, or by. . .well, you pick. Making the jump out of bacterial systems was non-trivial, and there were plenty of people who weren’t sure that it would even be possible. A human genome is a lot more complicated than a bacterial one, and its DNA is packaged and sequestered in totally different ways. Getting a bacterial enzyme into the right place in a human cell nucleus at the right time and in the right concentrations took a lot of work – just getting Cas9 and a guide RNA reliably into cells in the first place took a lot of work. But in the end, it could be done.

All these discoveries lead one to thoughts on the patent situation in this area, but it is too complex for human summary. I mean that nearly literally. In various jurisdictions, there are filings from multiple different institutions and companies (up to maybe eight at once) all fighting it out over the claim language and scope, and I just refuse to try to sort it out in my head. To add to the confusion, new variations and improvements on the technique are emerging constantly, leading a person to wonder what the eventual most valuable IP rights may turn out to be. There have already been a lot of twists and reversals in this area, but I have deliberately decided not to give it space in my head, for fear of crowding out something else.

But the reasons that such patent rights are so valuable, and that this area was Nobel-worthy to start with, are perfectly clear. CRISPR is the slickest way yet found to edit genome sequences in living organisms. You can silence particular genes, you can increase their expression, you can stick completely new things in pretty much wherever you feel like it. You can (in later variations) swap individual nucleotides around with extreme selectivity, and so on – it’s really like having magic powers. There are a lot of different Cas enzymes, and some of them do double-strand DNA breaking, while others do single-strand nicking and all sorts of things. They work with variation degrees of efficiency, selectivity, and fidelity, and the hunt is still very much on for improved versions.

So like any other molecular biology technique, CRISPR also has its hidden limitations that are still being worked out. That’s something to keep in mind when you hear about CRISPR babies, such as the hideously unethical human experiments in China in 2018. We are already trying to use CRISPR techniques to attack inborn genetic diseases such as sickle cell anemia, but think about that one: all those defective red blood cells come from a single tissue (the bone marrow) and we have already worked out techniques to transplant it (and, along the way, to kill off the original tissue in preparation for the new cells). That means that we have a much better chance of doing a clean swap, with cells that have been edited ex vivo and carefully sequenced to make sure that they’re what we think they are – and this on a disease whose genetic profile has been exhaustively studied for decades (and indeed was the first genetic disease ever characterized). The difference between that and stepping in to rewrite human embryos is huge, and we’re not going to be safely leaping that gap for a while yet.

That’s not least because in many cases we’re not sure what to rewrite. Inborn protein errors like sickle cell are clearly the place to start, but in many (most) cases the instructions are not quite so clear. Then you think about the genetic basis for (say) height, and it’s time to look out the window again. No, it’s going to be a while before we start cranking out the designer babies to order.

But where we’re using CRISPR every single day of the week is back in the research labs. It’s an astonishingly useful tool for producing new cell lines and looking at the phenotypes in organisms when you do such selective editing – you can accomplish things that were nearly (or completely) impossible. These new abilities have accelerated molecular biology noticeably, and it’s not like the field was lounging around much before. No, it’s hard to overstate the importance of CRISPR to basic research, and that’s where the clinical breakthroughs are born.

This was, then, one of those fields that has been recognized for years now as Definitely Going to Get a Nobel, No Doubt About It. And that day has come! Congratulations to Jennifer Doudna and Emmanuelle Charpentier, who are very deserving indeed and part of one of the great discoveries of 21st century biology so far.

51 comments on “A Nobel for CRISPR”

  1. steve says:

    Great summary

  2. Athaic says:

    As a former microbiologist, I’m not sure what’s the most jaw-dropping. Or baffling, as it was said.
    That bacteria are fiddling with their RNA.
    That bacteria are incorporating bits of phages into their genome, and not because the phage “told” them to do so.
    That bacteria have developed an immune system with a memory.
    That this was found in both bacteria and archaea, suggesting it was “put in place” early on during evolution. Or is it a case of convergent evolution?

    1. Barry says:

      Convergence seems astronomically unlikely. This machinery predates the split of eubacteria from archaea.

    2. JDK says:

      This suggests to me that viruses evolved very early and provided the necessity for Archaea to protect themselves. Parasites rule!

    3. Patrick says:

      Convergent evolution of broadly similar mechanisms is plausible, but convergent evolution of *exactly the same biochemical tricks* is presumably not.

  3. Chrispy says:

    I am still waiting for a “reverse transcribing” machinery that takes proteins and converts them to DNA sequence for later reference. We know the DNA->RNA->protein system is so well refined, surely there are organisms that run it in reverse?

    1. Ross Presser says:

      Ribosomes work with small tRNAs that have a common shape component that fits into the ribosome. A reverse ribosome, on the contrary, would have to be able to fit around parts of any possible protein in any possible folded configuration. And what benefit would it give the organism? “I found a neat protein, I’ll make some DNA now so I can recreate it in the future”?

      1. Aarti Sevilimedu says:

        In a roundabout way, isn’t that what antibodies do? Recognize protein bits, make other protein “counterparts” to them, which are encoded in DNA in B cells. Not exactly reverse translation, but the essence of the “function” is there. The sequence vs shape feature of nucleic acids vs proteins, probably makes this a cleverer solution than a more direct reverse (translation-transcription strategy), perhaps?

    2. Metaphysician says:

      I am not a biochemist, but my first thought is “factoring large numbers “. Which is to say, just because it can be done one way doesn’t mean it can be feasibly reversed.

    3. John Stamos says:

      While this would be great to have, the thermodynamics of the central dogma enzymes make this pretty much impossible. You’d need a totally different scheme of life. Nothing’s impossible but IMO…this won’t exist, not in this particular universe.

    4. chiz says:

      Reverse transcription is already a thing. I think you mean “reverse translation”.

    5. gippgig says:

      Reverse translation is far more possible than is generally believed. What is needed (besides unfolding proteins, which is easy) is for the aminoacyl-tRNA synthetases to be able to bind their amino acid at the end of a peptide or for the amino acid to be somehow “presented” to the synthetases (see elongation factors) after being cleaved off the end and a way to assemble a mRNA from the anticodons of the tRNAs. Today’s ribosome is highly optimized to only go in the forward direction but the protoribosome wouldn’t have been & I would not be surprised if life originated from bidirectional translation (possibly with the mRNA being assembled by splicing (so maybe that’s where introns came from, which would explain why tRNA introns are so frequently found next to the anticodon) rather than a polymerase, in which case nucleic acid replication would have come last!).

      1. chiz says:

        You need to clean up the protein first – undo the disulfide bonds, and remove all the post-translational modifications.

        1. Hugo says:

          In the proto-world there wouldn’t be so many modifications. Bacterial cytosolic enzymes are still not that modified.

  4. Barry says:

    If we are to contemplate deploying CRISPR/CAS9 clinically, we need to consider not only the Fidelity if the cuts, but also the different of the ligation. Mammalian DNAligase introduces to many errors to deploy this technology in any but the most dire conditions. But Liu’s single-base mutagenesis might be clean enough

  5. Katre says:

    A wonderful summary, although one that yet again makes me sad that there’s no dedicated Nobel for biochem, because it will be decades before we see another pure-chemistry prize.

    1. anon says:

      When I do chemistry outreach, I usually tell kids that chemistry applies to everything ranging from the sun to cells that make up our bodies to other cool materials. I think most chemists would share this view. Only when a Nobel prize is awarded to molecular biology or biochemistry, chemists suddenly claim discovering the molecular basis of a fundamentally important process is not chemistry.

      1. John Wayne says:

        We are guilty as charged.

        I think the only side effect one could ascribe to events like this one is that opportunities for basic investigation into what the heck matter is and how it works is criminally underfunded.

        1. sgcox says:

          And also disparaged by science tabloids.
          It is heart breaking to read about travails of Mojica and Šikšnys.

          Sir Peter Ratcliffe has in his office the rejection letter from Nature for the paper which was eventually published elsewhere and earned him Nobel prize last year.

          1. Some idiot says:

            c.f. Decca Records rejecting The Beatles (“Guitar groups are on the way out”).

      2. Albert says:

        Actually physics applies everywhere instead of chemistry. What happens in sun is a physics process, making hydrogen chloride from hydrogens is chemistry, yet making helium from hydrogen is not a chemical reaction.

    2. Jake says:

      When was the last ‘pure’ chemistry nobel in your opinion, b/c from here it looks like there was one just last year. (Not to mention 2017, 2016, 2014, 2013, 2011, 2010, 2007, 2005, 2001, ….)

  6. Hawaii Science says:

    I lived in Hilo Hawaii for a number of years, and I’m really proud that someone coming out of that community was able to get the Nobel Prize.

    1. Local Haole says:

      Agree. When my grandmother was born in Kohala, a century ago, it might as well have been on Mars. But us Honolulu kids are still pretty marginal and exotic on the Mainland. (Stop asking “when did you move to the US?” Especially on December 7th.) I’d give Nobelist Barry Obama at least partial credit for rising from the boondocks.

      1. confused says:

        >>Stop asking “when did you move to the US?”

        Wow, I thought it was amazingly ignorant when mainland-US people said that to Puerto Ricans. But people don’t realize that Hawaii *is an actual state* ????

        1. Local Haole says:

          Probably not, tbh. If you look at them quizzically, most will say, “oh, you know what I mean!” Mainlanders tend not to use “Mainland” much.

          More tragic, perhaps, is the “New Mexico USA” license plate.

  7. sitting in a vineyard pondering says:

    The whole concept of attribution in biological chemistry is very curious to me. This story is no different. Once the repeated elements were discovered, someone was going to figure it out. It was just a matter of when. But it’s not the 1800’s. No one does these things alone. Hundreds of people contributed, and each contributing an important bit. Our “first to publish” metric to reward science is increasingly idiotic, as Derek hints at. Indeed, perhaps for biological chemistry, even the concept of a prize to a few folks for a discovery is an anachronism. This is definitely not to say that Charpentier and Doudna are not deserving, it’s simply great biochemistry and an awesomely cool detective story (including contributions from yoghurt makers!). It’s just that it makes no sense to reward the final folks who put the block on top of a tower that hundreds built. It potentially also sends the wrong message to the public about how science works. But we use CRISPR every day and it’s very useful!

    1. c says:

      Agreed that this sort of award structure is part of the machinery that incentivises bad (or at least uncooperative) science.

      We need to move away from this ribbon clutching. Leave it to the athletes.

      1. Indeed, this reward structure impedes researchers’’ will to collaborate between labs in the course of managing this pandemic..

  8. Konstantinos Spingos says:

    Thank you!

  9. In Vivo Veritas says:

    An interesting correlate to this tale in the one being duked out by the patent lawyers. The Broad seems to win most of the battles, but the war is far from won……

  10. Erik Dienemann says:

    Fascinating stuff, most of which I don’t understand well, so take my following question with a large grain of salt. However, one high level question: is it correct to say the Nobel was for the “discovery of CRISPR” when that was discovered and the acronym invented by Mojica well before the work of the Nobel recipients? From what you wrote it seems more like they figured out ways to make the technology far more useful – I guess that’s a “discovery” but not sure. Maybe I’m being too picky…

    1. Local Haole says:

      An interesting comparison can be made with this week’s recognition of the hep C virus discovery, a long, stepwise process starting in blood banks and culminating decades later with the molecular biology done by Charlie Rice (the other RNA Nobel this week). The CRISPR prize is analogous only to that last bit, but it was far more spectacular. The big splash is arguably what Alfred Nobel intended to celebrate.

      The microbiology of CRISPR was really a crowd effort, so a muddle for awards, and not much to do with chemistry. Microbiologists are just not as attuned to finding general principles across disparate results as chemists are. And even broad-thinking people like Eugene Koonin, who connected a lot of the CRISPR dots, didn’t see the whole picture (as he admits).

      So I don’t think it’s too picky to raise the point you did. It was, in fact, such an obvious choice that the committee seems to have lazily gone with the popular “discovery of CRISPR” shorthand. The real breakthrough was cracking the code used by a *programmable* enzyme — the ribosome being the other one. Think about how many prizes were awarded for that, over a 45 year period.

      This week’s hep C and CRISPR prizes share another thing: they’re setting the stage for future Nobels, probably switching places in chemistry/medicine. Sofosbuvir etc was obliquely referenced by the committee presenter on Monday as a major advance.

      1. gcc says:

        I would just point out that the Nobel committee didn’t “lazily [go] with the popular ‘discovery of CRISPR’ shorthand.” The prize was awarded “for the development of a method for genome editing” not for the discovery of CRISPR per se (which was done by others before the work of Doudna and Charpentier).

  11. Not-an-epidemiologist says:

    Nice summary, but how about a shout-out for Martin Jinek, the postdoc in Doudna’s lab who drove (and actually did!) the bulk of the research and arguably had the greatest influence in taking CRISPR from an esoteric curiosity to the genome-editing wonder that it is? If anyone deserved a share of this Nobel, it was him.

    This essentially is the story of Jocelyn Bell Burnell all over again — the researcher at the coalface being ignored (yet again) in favour of the bigshot, grandstanding PI who sat in their office (and I write this as a PI myself, sitting in my home office, although for better or worse I’m not a bigshot). It’s not like the prize committee didn’t have another slot to fill in the list of awardees.

    1. Barry says:

      Jinek has established a lab of his own, and has a lot more to contribute.

      1. Nico says:

        Great interview, thanks!

    2. gcc says:

      Yes, not just Martin Jinek, but Krzysztof Chylinski as well. They were co-first authors on the key Science paper in which they demonstrated that the dual-tracrRNA:crRNA could be engineered into a single RNA and that they could trigger sequence-specific DNA cleavage of a target of their choice.

  12. Mourad Daoubi says:

    Yesterday, a lot of controversy have been stated in the different written and social media
    here in Spain. Specially, it was due to the none presence of Francisco Mojico between the Nobel prize ‘winners.
    The clear message was: “it is better to reward the applied research and not the fundamental one, even though there would be nothing to do without the latter, in reality”.
    I am fully agree with such paradigm and it is indeed the way to go.
    Thank you very much, Derek for the input (as always).

  13. JasonP says:

    Derek, thank you once again for taking a complex issue and distilling it such that this fascinating story is accessible to many! You skills as a writer are appreciated! This reads like a whodunit and draws your through the article. Kudos. Always appreciate good writing.

    Very interesting that prestige journals didn’t recognize the significance of some of this work and turned down the papers. Wonder what that says about the editors, reviewers, etc.? objectivity? ego? competition? over worked?

    1. Anon says:

      Semi-facetious post: Before CERN took the LHC operational, there was a seemingly serious publication by respected physicists who said that perhaps a time traveler from the future would journey back to prevent humans from operationalizing it. Seriously. See

      I wonder if the delays in publishing about CRISPR was some kind of intervention from future nature to keep us from genetically modifying ourselves. Jus a thought.

  14. passionlessDrone says:

    Can someone explain to a dummy how you achieve a necessary concentration of CRISPRD cells to beat back a genetic disease? That is, let’s say you have viral vector and know your payload, don’t you still have to deliver it to pretty much every cell? Let’s say that you wanted to fix something that was expressed just in the neocortex, or the eyes, or whatever. Do we have viral vectors that will target those areas? Just attach everywhere?


    1. Derek Lowe says:

      That is actually a key question! And that’s why you see it being applied to something like sickle cell first. In that case, you can generate a fully CRISPRed cell population out in a dish, then kill off the patient’s own bone marrow and transplant it all back in. That’s what I meant when I referred to a “clean swap”.

      But try it for, say, cystic fibrosis, where the problem is in the linings of the lungs. How do you deliver the vector(s) to get the CRISPR machinery into the cells while they’re still in the lungs? How many of them have to be affected by your therapy to make a difference? How long will that population last in there as the epithelial cells are slowly replaced – do you keep a constant ratio, or not? All very much open questions. It’s a much cleaner shot to pull out a localized stem cell population ex vivo and work on it there, nuke the patient’s own remaining tissue, and replace it with your modified version.

      1. Barry says:

        Doudna herself points to blood pathologies as the most promising applications for exactly these reasons. You can swap out a population of hematopoietic cells. Or for some defects (hemophilia) you don’t care where the gene product (clotting factor) is expressed as long as it shows up in the plasma compartment.

      2. metaphysician says:

        Yank the lungs out, grow new CRISPRed lungs, install in patient? Of course, if we could grow entire new functional lungs in a tank, we probably wouldn’t need gene therapy for the disease in question. . .

        1. cancer_man says:

          I think new lungs, kidneys and hearts will be common by 2030 so as you say, gene therapy wouldn’t be needed there.

    2. JIA says:

      That’s why the editing is typically applied to embryos: then the resulting adult organism is modified in all its cells. That’s how we create genetically modified mouse strains, and this is how He Jiankui modified a human (see Derek’s link) — not by treating an adult, and not by waiting for the baby to be born, but by treating an embryo and then implanting it.

  15. DataWatcher says:

    Interesting piece in today’s NYT (10/8) by Walter Isaacson, discussing the ethical implications of CRISP as we move forward. For some reason, I can’t find a link, but it’s in the Op-Ed section.

  16. TallDave says:

    yep we finally have a keyboard instead of being limited to mass copypasta

    now we learn to code

  17. István Ujváry says:

    Great piece. It was worth waiting for 😉
    Thanks, Derek.

  18. Robin E. Schlinger says:

    As it seems it was MIT that became Feng Zhang’s employer after he left Stanford with his chemical/bioengineering Ph.D., I am sure that in this “A Nobel for CRISPR” blog post you and commenter “In Vino Veritas” meant — in addition to referencing “the Broad” — to also reference this technology institute that, like Caltech, has a history of generally-unaddressed/unremedied gender discrimination. See and (Hopefully if/when this comment posts the 10/7/20 comment of In Vino Veritas will not have been deleted as at last viewing I saw that Marko’s comment of the same day, a comment that directed “In The Pipeline” readers to the CRISPR documentary “Human Nature,”, for some reason no longer appears?).

    A Stanford U bio sciences grad and currently-inactive California lawyer with a utility method patent, a woman who now has read Jon Cohen’s 9/11/20 article “The latest round in the CRISPR patent battle has an apparent victor, but the fight continues” and studied the PTO’s file on Serial No. 397,412 and the papers George Antheil’s family donated to Columbia University, I remain troubled by the surreptitious (and quite-arguably-dishonest) ways the U. S. Commerce Department acts through U. S. technology institutes and males (of both scientific and legal training) to keep female inventors from monetizing and controlling their breakthrough inventions.

    While I enthusiastically “second” the kudos offered to Drs. Doudna and Charpentier and recognition of the work of Francisco Mojica, Virginijus Siksnys, Martin Jinek, Krzysztof Chylinski…, should the two prize-winning women not want to “settle” I will be happy to testify to the PTAB about what I learned from my years researching Hedwig’s Kiesler’s secret communication system and the abandoned seventh claim of the patent application that led to the “routine” issuance of U. S. Pat. No. 2,292,387 with its six “apparatus” claims while PTO Serial Nos. 412,054 and 412,056 were pending and presumably were hidden — because of the imposition of War Department secrecy orders — from Serial No. 397,412 applicants Kiesler (aka Lamarr) and Antheil.

    This “hiding” is what seems to have prevented the SCOTUS deciding the case of NBC v US from knowing how encrypted radio transmissions could prevent/override interference when “frequency hopped” and combined with random signals known to academically-trained radio scientists as “pseudonoise,” something Robert Price and William W. Ward confirmed — see the latter’s 11/3/92 Lincoln Laboratory Journal article on NOMAC-Rake — and Canadian Scott Tilley’s find of a still-transmitting, circa-1960s military satellite seems to establish conclusively. (It was just about six months ago that NPR wrote on MIT’s “LES-5” that surely employs the 1940s’ and 1950s’ technologies on which Caltech grad students Bernard Oliver and John Pierce and a prominent resident of my and my mother’s hometown worked, this Pasadena CA resident being a greedy man whose consulting engineering services apparently were offered to Lamarr/Antheil in early 1941 and to their patent attorney at Los Angeles’s Lyon & Lyon well before then.)

    In extending my offer I act as a woman who has twice carried and birthed children and as a woman who heard David Baltimore speak in 2018 on how CRISPR-Cas9 would allow implantation in a woman’s uterus of multiple embryos for the benefit of science. Though Dr. Baltimore spoke of eradicating “Mendelian diseases,” I know from reading what appears here — — that this Nobel Prize winner’s employer with a history of viewing women as inferior — see the 1984-published writings of Dr. Margaret W. Rossiter — also was given (and seems to still maintain?) the “research fund” of Pasadena eugenicist and Human Betterment Foundation founder Ezra Gosney who, with George Ellery Hale, succeeded in eliminating the gender-diverse school Amos G. Throop founded in Pasadena CA in the late 1800s.

    ANY male scientist who speaks with Baltimore’s level of glee about the “Frankenstein Challenge” disturbs, but this disturbs even more now when women can read online how the PTAB is willing to give priority to the patent of a male scientist with institute associations despite the introduction of evidence such as that reflected in the 2015 email Shuailiang Lin sent Doudna (about how Zhang and his research team had not reduced to practice what they claimed to the PTO they had?).

    Thank you Derek for including (at least temporarily) the link to Adam Bolt’s well-reviewed film. And should “Marko” read this comment and be interested in further sharing please let this (London-based?) wine lover know my email address is There seems to be another “Robin Schlinger” — a woman with some connection to/with MIT — who years ago wrote and asked if I would relinquish this email address to her, but I did not agree to do that as Robin Schlinger is the name my parents gave me in 1955 and this email address one I had selected and used (and intended to continue using upon the advice of my sister Linda, another Pasadena CA native and Stanford U grad).

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