A helical TALE protein molecule wrapped around a double helix of DNA. TALE stands for “Transcription Activator-Like Effectors”, they are produced by Xanthomonas bacteria when entering a plant cell. They manipulate the host cell by switching on certain genes that make the plant cell more susceptible to infection. TALE subunits bind to the nucleotides of DNA in a 1:1 ratio, and each subunit has a pair of amino acids that is specific to a single DNA base. This enables the TALEs to recognize and activate specific sequences of DNA.
As my old professor Carl Sagan said, ‘When you’re in love, you want to tell the world’. And I base my beliefs on the information and process that we call ‘science’. It fills me with joy to make discoveries everyday of things I’ve never seen before. It fills me with joy to know that we can pursue these answers. It is a wonderful and astonishing thing to me that we are - you and I are - somehow at least one of the ways that the universe knows itself. You and I are a product of the universe. Its astonishing that we have come to be because of the universe’s existence. And we are driven to pursue that - to find out where we came from…
The process of science, the way we know nature, is the most compelling thing to me.
wordfulwonderlous asked: Dear Hank, how do genes become 'dominant' or 'recessive'? When I ask my teacher this, she just says that she needs to go to a meeting. Thank you!
It isn’t the gene that’s dominant or recessive, it’s the trait. In biology, we call traits “alleles”. Things like “I have blue eyes” or “my blood cells do not function properly” are traits. Traits are caused by genes.
Traits that only require one copy of the same gene to show up are called “dominant” while traits that require two copies of the same gene are called “recessive.”
Real world example:
Red-headedness is a trait that is linked to a gene for the production of a protein being a little bit busted. If you have one functional copy of this protein, then the trait doesn’t show up because at least one gene is doing its job and making normal pigment. But if both of those genes have the “red hair” mutation then neither of them are producing the pigment properly and the allele “I’m a ginger” shows up.
In short, both genes are being expressed, but the expression of one (the dominant one) over-rides the expression of the other.
Of course, genetics is usually much more complicated than this and there aren’t actually very many traits that are pure recessive or pure dominant, but that’s often an entry point that we use when teaching biology.
In genetics classes, we exalt Mendel and his peas like they are the be-all and end-all of genetic interaction. But like Hank said, genetics is usually (likely always) much more complicated than simple, clear-cut “dominant” or “recessive”. We should still give peas a chance, but we need to make it clear that that’s the ground floor, and it’s the many, many, maaaaaany exceptions that make genetics interesting. That being said, I want to add a bit to Hank’s answer, because I think it’s missing something important.
I really disagree that the gene is not what’s “dominant” or “recessive” and I don’t like that we teach genetics that way. The gene is precisely what is dominant and recessive! I see that Hank is trying to make a distinction between the “gene” as a piece of DNA and “allele” as a particular version of that piece of DNA. But the gene is everything, and a trait, or phenotype, is simply the result of the DNA and RNA and protein that comes from it. Ever since Watson and Crick (and Franklin) and their double helix, we’ve known that phenotypes can ultimately be distilled down to DNA. (well, that’s not entirely true, we actually know that thanks to Avery, MacCleod, and McCarty, but they don’t roll quite as easily off of the tongue).
And once you understand that genes are behind it all, you can begin to understand the weirdness behind “dominant” and “recessive”. The key word is “dosage”. I’ll try to explain.
Say that red flowers are dominant to white. Flowers with two red (R) alleles have two “doses” of the R gene (RR), whose RNA makes a protein that ends up making a red pigment molecule. Flowers with one red and one white allele (Rr) make half as much of the R protein, but that’s still enough to make plenty of red pigment, so it’s still “dominant” to the white (technically called “haplosufficiency”) But with just r alleles (rr), there’s no red pigment made, so you see a white flower. That’s simple dominance! Easy! Sadly, genes rarely work that way.
But what if a Rr flower doesn’t make enough protein to make enough red pigment to make a totally red flower? What then? Then you’ll have a pink flower, not quite red (RR) and not quite white (rr), which we call incomplete dominance (which is a kind of of “haploINsufficiency”).
But what if a rr flower, instead of making NO pigment, makes a pigment that is actually white? RR is still red, rr is still white, and Rr is (probably) still pink (or maybe red and white speckled) … but neither is really recessive to the other. This is called codominance.
Now we can bring in even more confusing terms, like “wild-type”. Often students think that’s the same as “dominant”. But say in our first example, the “r” gene is wild-type. It would be haploinsufficient to R (because one wild-type “r” isn’t enough to overcome the “mutant” allele “R”), and recessive. So why do we call it “wild-type”? Simply because the DNA sequence of that allele is most common in the organism, not because it “works best”.
Don’t worry, it gets weirder. Proteins usually work in big complexes, bound to each other like a biochemical Voltron. Let’s say that “R” is the normal, fully-functional protein, which we know means that it has a normal DNA sequence. What if “r” has a mutation that makes the protein fold just a little bit differently than “R”? Then “Rr” will result in a bunch of broken Voltrons, protein complexes that are half-right and half-wrong. This is what happens to hemoglobin in sickle cell anemia, actually, which I hope you all view as a disease of tiny protein/robot cats from here on out.
This only scratches the surface of the incredibly interesting weirdness that is molecular genetics, like the fact that some organisms have three or four copies of a gene (like some plants) or that genes work in knotted networks so complicated that they make computers cry tears of silicon as they try to untangle them.
My main point is this: Textbook examples like Mendel’s peas and generic terms like “dominant” and “recessive” work best to teach you the simplest way that things work, in the same sort of way that you can understand how a soap-box racer and a Ferrari both have wheels and are both cars, but you only really understand how one of them works. Your teachers should prepare you to go forth and discover wonder in the exceptions.
My other point, of course, the one that started this whole thing, is this: Traits are most definitely the result of genes, and hopefully you now see that “dominant” and “recessive” and all those other terms really only make sense when you keep three letters in mind: D, N, and A
Anonymous asked: You seem good at answering science questions, so here's one the Internet hasn't been able to answer for me: might the science of lengthening life cause our species to devolve, so to speak? Does medicine interfere with the process of natural selection by ensuring most everyone lives to have the opportunity to reproduce? If so, what does that mean for our future? Could dependence on medicine weaken us? (I not saying we should prevent people from reproducing. I just want to know how this works.)
Well, technically there’s no such thing as de-evolution. All evolution is evolution. Like, if a cave-dwelling fish species loses the ability to see, that’s evolution. It has fewer capabilities, but also doesn’t have to waste resources building and maintaining useless eyeballs.
But I get what you’re saying. And it depends on your definition of evolution.
We’re evolving culturally and technologically MUCH FASTER than we are evolving genetically. That doesn’t mean we aren’t evolving. We continue to evolve genetically, though a lot of traits (like eyesight, to take a personal example) aren’t being selected for anymore.
But who cares…if we have lenses and lasers that can correct eyesight, what does it matter if people with bad vision end up procreating as much as people with good vision.
So yes, more people who would not have previously survived are surviving today, but calling this “devolution” is the exact opposite of the truth…in fact, it’s the result of much better (and faster) evolution than the Earth has ever seen.
Dangerous? Maybe. Devolution…definitely not.
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