Q: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
Beyond “The Selfish Gene” to “The Selfish Network”
The grasshopper is the gene, and the locust is the networked swarm.
David Dobbs has a very interesting article out in Aeon about the incompleteness of “selfish gene” theory and the rise of an idea called “genetic accommodation”. Accommodation is the appearance of a trait, say larger muscles or faster running, in response to the environment, within a single generation (it sounds Lamarckian, but it’s not). Dobbs’ article is full of some pretty high-level biology, but it’s a very crucial lesson on the realities of natural selection in complex creatures and complex populations.
Chances are, if you’re a student of genetics and evolution, you know about Richard Dawkins and “the selfish gene”. This theory, and the book of the same name, places the gene at the center of evolution, and presents the organism, you or I, as vehicles for their replication and selection. It is beautifully written, well thought-out, and it made Dawkins the star he is today.
Unfortunately, the idea of “selfish genes” is incomplete, at least according to many modern evolutionary biologists. In complex creatures, there are a host of changes in appearance, ability and behavior (so-called “phenotypes”) that do not result from discrete genetic mutations, but rather from changes in how those genes are expressed, and these often show in the same generation, not just in offspring.
Dobbs gives us the example of the locust and the grasshopper, which ( I did not know this), are the same species! When food goes scarce, the lone hopper morphs into a swarming species that can lay waste to fields at Biblical proportions. These changes are not at the level of DNA changes within the gene, they manifest in how that DNA is read and turned into proteins or whatever the gene product turns out to be.
There are two important keys here: 1) Genomes are full of mutations and differences, most of which are silent and don’t contribute to natural selection, and 2) in complicated creatures such as us, genes are subject to complex, squishy, variable networks, and it’s mutations in many genes within and between networks that often lead to phenotypes.
That’s an incomplete oversimplification itself, but if you’d like to dig deeper, read this PZ Myers piece on how evolution is about networks. As for me? I’ve studied molecular genetics for about ten years now, and while Dobbs is right that the simple “selfish gene” idea needs work, gene expression differences are also dependent on genes, and those genes can be mutated and selected, or not, so after a while this whole networked snake begins to eat its own tail.
Evolution is hard. Most people, if they even accept it, don’t get far enough in biology classes to see just how hard it is. In school, we begin our study of genetics with the study of Mendel’s peas, a simple and idealized example to demonstrate how statistics and ratios are at play in the distribution of genes. But then almost instantly, if we go on with our studies, we learn that these idealized scenarios are incomplete, and that’s not how the real world of natural selection and population genetics works. So we look for where our rules are broken, and we apply new, often complex, rules to fill in the gaps.
This is how science itself works. Our idealized classroom scenarios, like Dawkins’ “selfish gene” or Mendel’s peas, are important tools to have in our toolbox, but they are incomplete. It is important that learn to identify their deficiencies, and to use new observations to create new tools … and with them we are always working to build a better house.
Which we then hope is not flattened by a locust swarm.
Check out Die, Selfish Gene, Die by David Dobbs. What do you think?
Most of the people you are descended from are no more genetically related to you than strangers are.
From Veronique Greenwood’s fascinating look at just how interconnected our pool of shared ancestry is, and how genetics has changed the way we look at our genealogy: We Are All Princes, Paupers, And Part Of The Human family, at Nautilus.
Previously: Why everyone of European ancestry is related to Charlemagne, and anyone who was alive and reproduced in 3,000 BCE is an ancestor of everyone alive today.
Hello, my cousins. Nice to have you in the family.
Can Biotechnology and Genetic Engineering Save an American Icon?
It keeps smoldering at the roots / And sending up new shoots / Till another parasite / Shall come to end the blight
So wrote Robert Frost, in 1936, speaking hopefully of the American Chestnut tree and its fight against a fungal plague. The mighty trees were falling ill to toxic invaders, but naturalists hoped they would rise above the challenge on their own, fighting nature with nature.
This woody behemoth used to make up a quarter of American timber in Eastern forests. The might of these trees, evident in the photo above from ca. 1910, reminds me of towering redwoods, dwarfing the lumberjacks flanking their mighty trunks.
Unfortunately, Frost was wrong. The chestnut-killing tree fungus threatening the American Chestnut was accidentally imported by farmers along with a Japanese species of chestnut preferred by farmers at the time. Within half a century of hitting our shores, that blight had wiped out a quarter continent’s worth of old-growth American Chestnuts (a very sad Wikipedia entry catalogues the remaining few specimens).
But thanks to biotechnology and genetic engineering, William Powell and his lab at SUNY think they can engineer chestnuts resistant to the fungus. Traditional crosses with resistant species (like the Japanese species that started it all) haven’t worked, and forest management has proven equally fruitless (or nutless, to be precise). Powell and his lab have successfully inserted a gene into the tree’s genome that can break down the fungal toxin, and are spending a tense few years waiting for their saplings to mature in order to know if they may have created a way to save the species.
Becca Rosen takes a look at biotech’s fight to save the American Chestnut in a must-read at The Atlantic, check it out.
What I find so interesting is that the techniques being used to save this tree, and one day reintroduce it to the wild, are not that different from those that are used to create genetically modified crops. How does saving a dying species by inserting a gene differ from creating an herbicide-resistant soybean, or rice that produces extra vitamins? I have my opinions, but I want to know: What do you think?
Source: The Atlantic
The same process works going forward in time; in essence every one of us who has children and whose line does not go extinct is suspended at the center of an immense genetic hourglass. Just as we are descended from most of the people alive on the planet a few thousand years ago, several thousand years hence each of us will be an ancestor of the entire human race—or of no one at all.
There’s a famous old anecdote about Charlemagne that’s been used for ages to explain how interconnected we are among our biological pasts. It has been said that everyone of European ancestry is related to Charlemagne, the great King of the Franks, born in 742 AD. If you’re European, you’re royalty. How is that possible?
I’ll tell you another tidbit first: Not only do all Europeans share Charlemagne as an ancestor, they share everyone alive at the same time as Charlemagne as an ancestor. Everyone who had kids, anyway. Let me explain:
Everyone alive has two biological parents. They each have two parents themselves, for a total of four grandparents. For x number of generations that you travel back in time, you have 2^x direct grandparents of increasing separation. Extrapolate that back to Charlie’s time, and you’d need 1 trillion grandparents to cover all your ancestral bases. Michael from Vsauce did a video about it. Since that’s far more people than have ever been alive, we need to engage some incest to solve the problem. Not banjo-applesauce incest, just a bit of redrawing our family trees into family webs.
Somewhere, far enough back in the web of grandparents, we will find a person whose lines connect to every single person who comes after them. That zig-zagged trail of shared genetic history ends surprisingly recently (for Euros, again): A common European ancestor around 1400 AD. Go a bit farther, and we find a common Earthling ancestor around 3,000 BC. It’s neat stuff. But it’s all based in mathematical models, not real genetic data.
Until now. USC and UC Davis researchers Peter Ralph and Graham Coop have surveyed the genomes of 2,257 Europeans in order to put some real data behind those models. Because of the random shuffling of chromosome fragments that created your father’s sperm and your mother’s egg, you, your siblings and your cousins all share varying chunks of DNA. People who are more closely related share more of these chunks. Depending on how many chunks are shared between two people, we can calculate their approximate relation to each other. Using 2 million shared sequences and a lot of math, they proved the mathematical models correct. Turkish people are more related to other Turks than to someone from Portugal, but they are related enough that, not only do they share one common ancestor a few hundred years ago, but they share every ancestor if you go back a mere thousand years. The models guessed that a long time ago, but now we have the data to prove it.It’s likely that these patterns extend to other regions of Earth, although the numbers might be slightly (but not that) different.
Next time someone in your neck of the ethnic woods points out a famous relative or claims blue-blood descent, remind them that they aren’t so special. All street-sweepers are royalty, all nobles are peasants, and we are all Kings and Queens.
In ants and bees, there are no sex chromosomes. Instead, sex is determined by whether or not an egg was fertilized. If the egg isn’t fertilized, the offspring is male. If the egg is fertilized, it’s female. So male ants have no fathers, and they have half as many chromosomes as females. Poor little things.
I’ve always maintained that its not the number of chromosomes that matters, but rather how you use them.
The Science of Hair Loss and Balding by the AsapSCIENCE guys. Alopeciate it if you’d watch this video.
It’s not as simple as just your maternal grandfather, but that’s part of it. Scientists have identified one of the key proteins (and its target) that make men go bald. And did you know that the major commercial treatments for androgenetic alopecia (male-pattern baldness) were found by accident? Rogaine was a blood pressure drug and Propecia was for prostate enlargement!
I’m pretty confident that these flowing blond locks of mine are gonna stick around for a while … knock on (genetic) wood.
How Mendel’s Pea Plants Helped Us Understand Genetics (now with working video!)
TED Ed takes a look back at Gregor the Monk’s pioneering genetics experiments featuring the humble pea plant. When you remember that he figured all of this out before we had even discovered DNA or the molecular idea of a gene, it’s even more amazing.
That heterozygote dance looks like fun.
Previously: Awesome vintage illustrations of Mendelian genetic patterns featuring fluffy mice!
Sculpting a Catalogue of Apples
Apples, at least as we know them, are a freakshow born of agricultural genetics. While wild apples readily grow from seeds, perhaps every single variety we buy in stores is produced by grafting.
With more than 7,500 wild varieties, apples have incredible genetic diversity. This is how we’ve been able to develop so many variations of size, sweetness, texture and color. The side effect is that many apple varieties are such Frankenstein monsters that they literally can’t grow from seeds. Combine that with the complicated way that apples pollinate, and you’ve got a recipe for a clone army in an orchard.
This is great for farmers, because you get a consistent product, but bad for apples, because many of the wild varieties could be lost or forgotten. And should some pest, parasite or blight start attacking our genetically-engineered superfruits, we’re going to want those wild genes around to call on to save the day. It’s diversity that makes a population strong.
That’s why I love this project so much. It’s an archive of apple varieties using ceramic sculpture! So cool.
If you’d like to learn more about the history of the humble apple, read The Botany of Desire by Michael Pollan. Great book for foodies and science fans alike. If you want to get super-sciencey, here’s a cool paper in PLOS Genetics.
More via theatlantic:
In its original home, near Almaty in Kazakhstan, the apple can be the size of a cherry or a grapefruit. It can be mushy or so hard it will chip teeth. It can be purple- or pink-fleshed with green, orange, or white skin. It can be sickly sweet, battery-acid sour, or taste like a banana. Preserving this biodiversity can become a massive project, in life and art.
See more. [Images: Jessica Rath]