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
So many bells ringing here from my long forgotten biology classes.
Astronomers have discovered the largest known structure in the universe, a clump of active galactic cores that stretch 4 billion light-years from end to end. The structure is a light quasar group (LQG), a collection of extremely luminous Galactic Nulcei powered by supermassive central black holes.
So that’s cool and everything, but maybe some of you would be interested to know why this is a significant find? Beyond just its record-setting bigness.
Since Einstein, physicists have accepted something called the Cosmological Principle, which states that the universe looks the same everywhere if you view it on a large enough scale. You might find some weird shit over here, and some other freaky shit over there, but if you pull back the camera far enough, you’ll find that same weird and/or freaky shit cropping up over and over again in a fairly regular distribution. This is because the universe is (probably) infinite in size and (we are pretty darn sure) has, and has always had, the same forces acting on it everywhere.
So why is this new LQG so radical? (It stands for ‘Large Quasar Group,’ btw, not ‘Light Quasar Group.’)
Well, let’s try to comprehend the scale we’re dealing with. A ‘megaparsec,’ written Mpc, is about 3.2 million light years long. The Milky Way is about 0.03 Mpc across (or 100,000 light years). The distance between our galaxy and Andromeda, our closest galactic neighbor, is 0.75 Mpc, or 2.5 million light years. LQGs are usually about 200 Mpc across. Assuming a logarithmic distribution of weird shit outliers (if you don’t know how logarithmic distribution curves work, don’t worry about it), cosmologists predicted that nothing in the universe should be more than 370 Mpc across.
This new LQG is 1200 Mpc long. That’s four billion light years. Four BILLION LIGHT YEARS. Just to travel from one side to the other of this one thing. I mean for fuck’s sake, the universe is only about 14 billion years old! How many of these things could there be?
Right now it looks like the Cosmological Principle might be out the window, unless physicists can find some way to make the existence of this new LQG work with the math (and boy, are they trying). And that’s totally baffling. It would mean—well, we don’t have any idea what it would mean. That the universe isn’t essentially uniform? That some ‘special’ physics apply/applied in some places but not in others? That Something Happened that is totally outside our current ability to understand or quantify stuff happening?
By the way, no one lives there. The radiation from so many quasars would sterilize rock.
If you love a flower, don’t pick it up. Because if you pick it up, it dies and it ceases to be what you love. So if you love a flower, let it be. Love is not about possession. Love is about appreciation.
Never really understood why people like receiving flowers. You receive something beautifully dead that wouldn’t be dead if people would be more sensible about things they adore.
Alpacas are so much cuter than llamas.
YOU FORGOT THE FOLLOWING POINTS:
- LLAMAS HAVE BIG TEETH TO RIP OUT YOUR F#@&ING THROAT
- ALPACAS HAVE FUZZY LIPS TO NUZZLE YOU GENTLY TO SLEEP
- LLAMAS WILL CHARGE AFTER YOU IF THEY SMELL FOOD AND FEAR
- ALPACAS AMBLE ALONG LIKE THE WORLD IS MADE OF GUMDROPS
- LLAMAS ARE THE DEVIL INCARNATE
- ALPACAS ARE NOT THE DEVIL INCARNATE
The Non Program Pavilion / Jesús Torres García • Architects
1. For A Gorgeous, New Experience: Necessary Provisions
This new kid on the block is one surprising little hidden gem. Tucked away in the depths of Upper Bukit Timah, Necessary Provisions is everything you’d want from a cafe. Surreal lighting, dark walls, streaming sunlight, plants, gorgeous bakes, killer iced espresso and milk, and beer on tap. It’s worth the trek.
2. For A Happening Arts Scene: Artistry
Artistry is known for being a happening hotspot for arts events. It’s where budding artists share their work, and aspiring artistes take the stage at night. This is probably the only cafe you could get service from a “cute angmoh” ;) Remember to give him a pat on the back for his passion to support the local arts scene, and of course, for serving gorgeous cups of coffee.
3. For All Things Coffee: Chye Seng Huat Hardware
While quickly becoming a coffee institution, CSHH still manages to be a cosy space. The gorgeously modified industrial-chic interior of this old hardwarestore provides the perfect setting for enjoying a good cup of coffee. If you’refeeling adventurous, give their galvanized ale a try- literally coffee beer. It’s strangely good!
Sometimes you just need to shake things up to help them get better.
That’s the idea Drexel University researchers have used to develop a novel treatment for chronic wounds. A team of doctors and biomedical engineers has found that applying low-frequency, low-intensity ultrasound directly to wounds causes them to heal significantly faster.
They created a small, wearable ultrasound applicator that is placed over wounds called venous ulcers, which account for 80 percent of all chronic wounds on the lower extremities. Such ulcers afflict 500,000 Americans annually. The device is tuned to deliver sound waves at 20 kilohertz for 15 minutes. A small initial study they completed with it found that just four applications triggered complete healing.
birdandmoon: ‘Cause we are living in a bacterial world, and I am a bacterial girl.
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