Whole genome sequencing has not found any single gene variation responsible for extreme longevity, according to a paper published in PLOS ONE:
We have sequenced the genomes of 17 supercentenarians (over 110 years of age) to see if we could uncover the genetic basis for their extreme longevity. We analyzed rare protein-altering variants, but found no strong evidence for enrichment of either a single variant or a single gene harboring different variants in female Caucasian supercentenarians compared to controls.
The full genomic sequences have been published, allowing other researchers to build on the data set.
In recent years, the possibility of reviving extinct species by recreating their genomes has become a reality. First on deck for "de-extinction" are the woolly mammoth and passenger pigeon. But is this a good idea? KQED's QUEST takes a look: "Reawakening Extinct Species"
Over the last couple of days, you might have heard about the "duon" — a "second" genetic code that's being hyped as a radical new "breakthrough" in science.
Based solely on the number of words I've put in quotations here, you can probably guess that the actual news doesn't really match the hype.
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How can a mild-mannered grasshopper turn into a ferocious locust? Why are humans humans when we have share 80 percent of the same genetic material with a cow?
In a fascinating long read at Aeon, David Dobbs delves into the differences between genetic change (evolution as you probably learned it in school) and genetic expression (the amazing powers of natural selection that scientists are only now starting to really understand).
Distributed today to all users of the 23andMe home genetic testing service, after the FDA ordered the firm to halt sales of new kits:
Dear 23andMe Customers,
I wanted to reach out to you about the FDA letter that was sent to 23andMe last Friday.
It is absolutely critical that our consumers get high quality genetic data that they can trust. We have worked extensively with our lab partner to make sure that the results we return are accurate. We stand behind the data that we return to customers - but we recognize that the FDA needs to be convinced of the quality of our data as well.
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At what point does interesting-but-potentially-incorrect-or-misleading information become a potential threat to health? How do you regulate a product that current regulations were never set up to handle? The University of Michigan's Risk Science Center put together this quick cartoon that neatly summarizes the problems and questions at the heart of the FDA's crackdown on 23andMe, which Xeni wrote about on Monday.
A couple of other smart takes on this that have come out in the past couple of days:
• Genomics expert Michael Eisen delves deeper into the question of how we should regulate personal genetic testing.
• Journalist David Dobbs rounded up some diverse opinions. You should pay attention to his blog. He's been doing a lot of great reporting on genetics and culture and is planning on publishing a longer piece on the 23andMe stuff later this week.
Is the yeti actually some hybrid of ancient polar bear and brown bear? University of Oxford geneticist Bryan Sykes has analyzed DNA from what's purported to be yeti hair samples.
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The answer is yes — but only in certain circumstances and that "yes" comes with a whole bunch of caveats. At Discover, Emily Sohn has a nice basic primer on what we know now about intelligence testing
and what your score on an IQ test does and doesn't mean.
Turns out, whether or not you are a ginger is not determined by the simple genetics of a single gene. In fact, the pigment that causes red hair is likely present in many brunettes. What matters more seems to be how much of the ginger-hiding brunette pigment you have — and the genetics that determine that are a lot more complicated. Which, frankly, makes the brunette-guy-with-red-beard phenomenon make a whole lot more sense.
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Besides magnetism, there's another thing that the Insane Clown Posse was on-track in categorizing as a mind-blowing mystery — Why do Shaggy 2 Dope's kids look just like him? As with the magnets, this is another situation where the obvious answer (it's genetics!) masks a much more complicated issue that science hasn't totally figured out yet. At Pacific Standard, Michael White explains why genetics is still messing with our heads, almost 150 years after Mendel:
The problem: most of the genetic differences discovered have only a very small effect. And when you add up all those effects, the result can’t possibly explain the full influence of our genes on those traits. For example, researchers have identified hundreds of DNA differences between people that influence the very strongly heritable trait of human height, but the total effect of those differences added together explains only about 10 percent of the genetic influence on height. In other words, we still can’t explain why tall parents have tall children.
Scientists have named this discrepancy the “missing heritability,” and they’ve spent the last half-decade trying to find it.
Down's syndrome happens when a human being ends up with an extra copy of chromosome 21 — three copies, instead of the normal two. But scientists say they might have found a way to make that extra chromosome functionally irrelevant. If they're right, it could lead to treatments that could someday reduce the symptoms of Down's. The trick is connected to another extra chromosome that the human body "turns off" all the time — the X. Women have two X chromosomes, of course, but only one ever gets to express itself
. Scientists put the same mechanism to use on chromosome 21
in petri dish experiments.
Nine people who have not recently made any sweeping judgements about biotechnology.
Last week, I told you about the US Supreme Court ruling that made it illegal to patent naturally occurring DNA. In that article, I talked briefly about the fact that the new ruling doesn't cover all DNA. It's still perfectly legal to patent synthetic DNA, and the court documents referred specifically to complementary DNA (aka cDNA).
This is where things get murky. Complementary DNA is a thing that can be both natural and synthetic. And, as a laboratory creation, it's an important step in a common method of replicating naturally occurring DNA. All of which leaves some holes in the idea that the Supreme Court ruling is a simple "win" for open-access science, patent activists, and patients. After all, if you can't patent a gene, but you can patent the laboratory copy of the gene, what's that mean? It's sort of like not being able to patent a novel, but being able to patent a copy of its contents that's had all the white space removed. It seems like everybody is a bit confused by this. So I wanted to take a moment to at least clarify what cDNA is and what some people, on different sides of the science/law/biotech divides, are thinking about it.
It starts with some stuff you learned back in junior high — how information from your DNA gets turned into actual working proteins.
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History has shown us that even some of the greatest scientific luminaries, towering figures such as the naturalist Charles Darwin, the twice-Nobel-Laureate chemist Linus Pauling, and the embodiment of genius — Albert Einstein — have made some serious blunders.Read the rest
In an unanimous decision, the United States Supreme Court ruled today that companies can't patent genes, or parts of genes — at least, so long as that genetic material is identical to what occurs in nature. The lawsuit dealt specifically with Myriad Genetics, the company that isolated and has claimed a patent on BRCA 1 and BRCA 2 — genes associated with an increased risk of breast and ovarian cancers. From a practical perspective, Myriad's hold on the genes has meant that tests for genetic cancer risk are strikingly expensive — Xeni paid more than $3000 for hers. It's also meant that, if you get a positive result, there's been nowhere you could go for a second opinion.
That's a big deal. Mutations in the BRCA 1 and 2 genes mean an increased risk of cancer, but there's more than one kind of mutation that can happen. In fact, BRCA 1, alone, has hundreds of known mutations. Some increase your risk of cancer. But, even if you narrow it down to just those, they don't all increase the risk by the same amount. The health choices you make could be very different depending on whether you have an 80% risk of developing breast cancer by age 90 (the worst-case scenario for BRCA 1 mutations), or something much lower. That's the kind of situation where you might really like to have more than one lab run more than one kind of test.
This ruling opens the door for that, and the competition should (theoretically) also lower the cost.
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Genetically speaking, identical twins ought to be two copies of the same person. Environmentally speaking, if the twins grow up together, they ought to even be influenced by the same things. But if you actually pay attention to identical twins, they aren't identical in personality or interests. How do naturally occurring clones become individual people?
That's the subject of a mouse study that Scicurious writes about on her blog. Fascinating stuff.
Short answer: We don't know
. What makes this story by Erin Wayman interesting is the way it carefully breaks down an almost Hollywood-ready narrative and finds the fascinating uncertainty lurking underneath. The truth is, uncertainty is cool. Because it means there's more stuff left to discover.
The coelacanth is one of a small handful of living fishes that are probably closely related much more ancient, extinct creatures — including, the first fish to haul itself up onto land. Now scientists have sequenced its genes and are digging through the data in search of genetic clues to how fish and land-dwelling animals are connected to one another
. Among the finds so far, a gene that seems to be connected to how animals grow placentas. Coelacanths don't have placentas, but they do have eggs that hatch inside their own bodies.