Animals are doing surprisingly well in the radioactive areas around Chernobyl.

Imagine people’s worst fears are realized and the nuclear power plant at Diablo Canyon here in California has a Chernobyl-style meltdown. The effects on people are obvious: high rates of thyroid and other cancers, permanent resettlement elsewhere, increased rates of birth defects and so on. But as the area around Chernobyl is showing, the effects on the environment may be more subtle.

Over the break I watched a Nature special called, "Radioactive Wolves". This is a documentary about wildlife in a radioactive exclusion zone around Chernobyl.

Even though the area around Chernobyl is still so contaminated that humans can only go in for limited amounts of time, the wildlife appears to be doing surprisingly well. Birth defects are higher than in surrounding areas but life is thriving. Wolves are doing great, beavers have returned and everything looks hunky dory.

This seemed strange to me. I would think that so much radiation should be having pretty severe effects on these animals. And as noted in this in this NIH study, for certain individuals it definitely is.

The difference is in perspective. For the individual, the area around Chernobyl is terrible. Your kids have a higher rate of being stillborn or having birth defects, you have a much higher rate of developing various cancers, and so on. But for the species as a whole, things aren’t so bad. The higher background radiation appears to hardly be affecting their numbers at all.

Now this isn’t to say that the initial fallout wasn’t catastrophic to wildlife. It was. Untold numbers of animals died a terrible death in Chernobyl’s aftermath.

For the lucky survivors and new immigrants, though, Chernobyl is a different story. It is a chance to live a life without human interference. At least for now it looks like the high background radiation is preferable to man for these animals.

It is important that scientists keep studying this ecosystem though. The DNA of the animals in this area are under constant attack from the radiation. There may come a tipping point where the genetic burden becomes too high and populations start to crash. We’ll have to wait and see.

Additional Reading: NY Times Review of Radioactive Wolves

For now, sulfites are able to kill the yeast that might spoil this wine.

Wine sometimes tastes a bit funky because it was contaminated during fermentation with a yeast called Brettanomyces bruxellensis. This yeast can give wine a variety of interesting flavors like “…horse sweat, Band Aids, barnyard, and burnt plastic…”

Winemakers usually keep this from happening by killing off the yeast with those dreaded sulfites. But for awhile now, people in the know have been worrying about the emergence of a sulfite-resistant form of this yeast. And this is a well-founded fear.

Yeast, like bacteria, are fast growing microorganisms with lots of variation in their DNA. If you hit a population like this with something that kills them (like sulfites for B. bruxellensis or antibiotics for bacteria), some small percentage are probably going to be resistant. These resistant strains can then grow and replace the sensitive ones. The end result is sulfite-resistant yeast ruining our wines.

To try to head off this problem, a group of scientists in Australia has figured out this yeast’s DNA. The hope is that scientists will be able to use this data to determine how B. bruxellensis might evolve into a more resistant form.

Note that despite much trumpeting online, they haven’t really solved any problems with this knowledge yet. They have merely created the tool that might let them solve a potential future problem. And given how cheap and easy DNA sequencing is these days, it isn’t necessarily even an impressive feat of technological prowess.

Still, it may one day prove useful in allowing winemakers to more quickly defeat a sulfite-resistant strain. Which can only be a good thing for wine making.

I don’t want to end this before saying a nice word or two about B. bruxellensis. This yeast can spoil wines but it isn’t all bad.

For example, it gives Belgian beers their special taste. And some winemakers actively seek it to give their wine a bit of a “brett” taste.

Still, a sulfite-resistant form would definitely be a bad thing for most winemakers. So scientists should definitely stay vigilant and be ready to come up with quick solutions using this new tool (and whatever other ones they can find) when sulfite-resistant B. bruxellensis begin to appear.

Line up the blocks and help cure a disease!

Yesterday I discovered an online game called Phylo. No, it isn’t about Greek pastry dough. It has more to do with phylogenetics.

Phylogenetics is the study of how living things are related to each other. It takes advantage of the fact that DNA changes slowly over time. So the more distantly related two things are, the less DNA they will share.

You can also learn which bits of DNA are important for life (or good health) by seeing which ones stay pretty constant between various animals. Since these don’t change, they are probably being used for something. And if they get changed in people who have a disease, then they may be involved in that disease.

This is what Phylo is based on. In the game, you are trying to line up the DNA sequences of various animals to figure out which DNA is important and which isn’t. This is a lot harder than it sounds.

While DNA changes slowly, we’re dealing with some pretty long spans of time since two animals shared a common ancestor (i.e. had the same DNA). This means that the DNA can start to look pretty different.

Phylo gives you sets of DNA sequences that haven’t been lined up yet and has you try to line them up manually. Apparently people are still better at this than computers!

Lining these sequences up helps scientists discover which DNA bases are important. It can also give us some basic knowledge about the evolutionary relationship of various animals.

Since DNA sequence might be a little intimidating, Phylo uses colored blocks instead. Each different colored block represents one of the four DNA bases.

In the game, you have a certain amount of time to align the sequences as best you can. You want the fewest mismatches with the fewest gaps.

The game is pretty hard but it is engaging. And you’re doing your bit for science which is always a good thing.

What would make it even better is more explanation about what I am doing and why it is important. This could make the game fun and educational. (I’d also like to see the DNA sequences I aligned but that’s probably just me.)

So give it a whirl and do your bit to help humanity. And have a little fun in the process.

Nice list of top 5 citizen scientist games (Phylo is number 1).

By changing how a worm like this uses its genes, scientists have added the equivalent of 20 human years to their lifespans. And to their children and grandchildren's lifespans too.

One of the workhorses of longevity studies is a little flatworm called C. elegans. Lots of scientists have come up with lots of ways to get these little guys to live longer than usual. With enough tinkering, they can live 4 or 5 times as long as their wild brethren. That's like a human living to be 500!

Work out of the Brunet lab at Stanford added another chapter to this story. They tinkered with how a worm uses its genes and found these worms lived around 25% longer than normal.

That’s old news though. What is exciting is the new study that shows that the worms passed this trait down to their kids and their grandkids.

These worms inherited the pattern of how their genes were used from the original parent. And now the kids and grandkids live longer than worms that have the exact same set of genes. All because of how an ancestor used its genes.

The effect is not forever though. The great grandkids live about as long as worms with the same set of genes. Apparently gene usage patterns reset to normal after three generations or so.

As you’ve probably gathered, how our genes are used is as important as the genes we have. For example, every cell has the same set of genes. And yet, a blood cell is wildly different than a muscle cell. The difference comes from how each cell type uses the genes it has.

A big part of how a gene gets used is determined by various chemical marks attached to either nearby DNA or to the spools around which the DNA is wrapped. In this case it has to do with chemical marks on one of the worm’s spools or histones.

Most of the marks on DNA and histones are wiped clean once they are packed into a sperm or egg. This allows the fertilized egg to develop into all the different cell types needed for an adult worm (or person).

The specific changes made in this study linger for awhile longer and take three or so generations to wipe out. We don’t exactly know why yet but we do know that this is what we often see with epigenetic changes like this.

Epigenetics is a fancy way of saying something is passed down without a change in the gene itself. As scientists delve deeper and deeper into genetics, they are finding many traits that behave this way. Even in people.

So is this going to make us live longer? Not yet.

But it does suggest that if we can one day mimic these effects with a chemical, we may end up living longer. And so will our kids even if they don’t pop the same pill.

Cynthia Kenyon talks about one particular long lived mutant.

In the last 12 years, researchers have isolated taste receptors for sweet – as well as the lesser understood basic taste – umami. Umami (pronounced: ew-mommy) is often at the heart of intuitive succulent cooking. Grandmothers in southern Italy, for example, toss a handful of cherry tomatoes into a clear broth, or slip the rind of parmesan cheese into a pot of simmering beans.

“Without consciously knowing what they're doing, they add the taste of umami to the dish,” says Brooklyn-based cookbook author Rozanne Gold.

Wild mushrooms, fresh picked corn, dried seaweed and fish sauce all have lots of savory umami taste, and high levels of an amino acid called glutamate. Glutamic acid tips off the taste buds, and then an umami alert rushes to the brain.

Umami deepens flavor and adds meatiness, says Gold, who calls herself the "Diva of Simplicity."

Her latest book is Radically Simple: Brilliant Flavors with Breathtaking Ease.

“When you only have three ingredients to play with each one really counts, so instinctively I work with foods that are umami rich,” she said. “What MSG does for a dish, that already exists naturally in some foods.”

The concept is age-old but a Japanese chemist, Kikunae Ikeda coined the term “umami” in the early 1900s. Everyday taste testers struggle to categorize umami, says neuroscientist Alexander Bachmanov, because the taste rarely stands alone. And that, he says, may explain why a scientist, not a chef, finally gave umami a name.

You can put a sugar cube on your tongue to sample pure sweet, or lick sodium chloride to explain salty. Umami is harder to single out, says Bachmanov, a researcher at the Monell Chemical Senses Center in Philadelphia.

“If it's glutamic acid, it will also have some sourness in addition to umami. If it is monosodium glutamate (MSG), it will have a little bit of saltiness in addition to umami,” he said.

That something else, is now considered the fifth taste. When scientists isolated the first umami taste receptor in 2000, umami officially joined the big four–sour, salty bitter and sweet.

Bachmanov says our taste buds are “tuned-up” to taste glutamic acids, and there's likely an evolutionary reason why most people perceive umami as pleasant.

Our sense of taste is like a detection system, constantly analyzing and helping us decide whether to eat or avoid a food. Glutamic acid–the tip-off for the umami taste–is a building block of protein.

“If a food is sweet, it likely contains carbohydrates. If it has umami taste is probably has protein. Our body gets the indication that the food contains protein, that it's nutritious, good for us,” Bachmanov said.

My favorite ones are those where women sniff the shirts of various men and pick out the ones that smell the best to them. The ones they like best are usually from men whose immune systems are most different from theirs.

This makes some sense if you think about it. The strongest immune system is a varied one. It can fight off lots of different kinds of bacteria, parasites, and viruses.

And since our immune system is programmed by our genes and our genes come from mom and dad, the more different mom and dad’s genes are, the more varied your immune system will be. So ideally you would choose a mate that would give your children the stronger immune system. That mate would have an immune system very different from yours.

One way you might be able to find that particular mate is if different immune systems have different odors. The stinky guys share your immune system; the pleasant smelling ones have a different one.

This seems to be what is happening in these armpit smelling experiments. So at least some amount of attraction between people is happening with the nose.

But what I found even more interesting was that oral contraceptives mess with this system. Women on the pill tend to prefer the smell of men with similar immune systems. Some scientists think this is because pregnant women prefer family around them and family tends to have a similar immune system.

When I first read this I thought, “Wow, this is going to really mess up future generations’ immune systems. Maybe it even helps to explain the recent rise in allergies and autoimmune diseases.”

But then I caught myself and thought a little harder. It is probably not that likely that the recent increases in allergies and autoimmune diseases would have happened so quickly if the pill were the main culprit. And besides, there is undoubtedly more to human mate selection than smell!

We are complicated. There are all sorts of cues that cause someone to fall in love. Pheromones may play a role but they are certainly not the whole story.

For example, some studies use photos and ask women which men are the most attractive. The women in these studies tend to pick men with more similar immune systems (apparently there is some correlation between facial symmetry and the immune system).

And when scientists look at couples who actually have children together, they get mixed results. An early study pointed to Europeans having children with partners with different immune system genes. But a deeper look at that data and looking at a larger group of couples showed that this didn’t seem to be the case. Differing immune systems had little impact on who women chose to have children with.

The most that could be said was that women tended to avoid men with really similar immune systems. A bit similar was OK.

Of course we could already be seeing the effects of the pill in these studies. Maybe if the women in these studies hadn’t been on the pill when they met their partners, they might have chosen someone with a more dissimilar immune system.

Scientists need to look at people who did not meet while women were on the pill. Then we will have a better idea of how big a role your nose plays in choosing your soul mate. And how worried we should be about the pill’s effect on that selection.

Nice PBS video about the t-shirt smelling experiments.

Or my eyes? Or my smile? Or…?

Part of the reason for this is that most traits have not been studied in very much detail. Which makes sense in a world of finite research dollars.

As is right, we spend most of the limited money on trying to understand and find cures for diseases. Very little goes toward figuring out the chances that Junior will have grandpa’s nose.

The other big reason we can’t make good predictions is that the genetics behind most traits are surprisingly complex. Except maybe red hair, there really aren’t any simple dominant-recessive traits. Which means we don’t even have the parents with recessive traits to fall back on!

As you probably already know, we have two copies of each of our genes – one from mom and one from dad. These genes can come in different versions and some versions are dominant and some recessive. The dominant ones trump the recessive ones.

What this means is that if you have a recessive trait, then both of your copies of the gene in question should be the recessive version. So if two parents each had a recessive trait, then their child should end up with a recessive trait too. Because that is all the parents have to share.

This is why we can predict that two red haired parents will pretty much always have red haired kids (J.K. Rowling got the Weasleys right!). None of the other traits out there are so simple though.

Numerous studies have shown that ear lobe attachment, cleft chin, tongue rolling and whatever else you learned in high school biology are way more complicated than advertised. None of them are a simple, single gene, dominant/recessive trait. Even eye color is complicated.

Pretty much everyone knows that blue eyes are recessive to brown eyes. And so blue-eyed parents can’t have a brown eyed-child. Heck, one group of scientists even used this as a basis for an evolutionary model. Too bad it is wrong.

Blue-eyed parents can have brown-eyed kids. It isn’t as common as the other way around but it can and does happen.

So it is hard to guess what a child will look like just by seeing the parents. But if we could look at their DNA we could predict what their child might look like, right? No. In fact, we couldn’t predict what they looked like from their DNA.

People are often surprised to learn that even if scientists are given a complete genetic readout of a person, they would not be able to predict what he or she looks like. We could guess ethnic background and have a good shot at predicting if they had red hair. And that is pretty much it. Oh, except for eye color.

Scientists are starting to make real progress on figuring out eye color from a person’s DNA. By looking at six different markers they can predict whether someone has blue or brown eyes around 90% of the time. They are only right about hazel, green and other colors about 75% of the time.

So you can see that even “simple” eye color takes six genes to make any good predictions. How can anyone make a good prediction just from looking at two brown eyed people? They can’t without a good family history and even then, they can be fooled.

And that is with a well-studied trait where we have the markers and understand what is going on. All bets are off for the other traits. For now anyway.

And it is even cheaper than this if you want to focus on just your genes. 23andMe is offering that very service for less than 1,000 dollars. Your DNA is finally within your grasp!

This drop in price is great news for scientists. They can now get more DNA sequenced for less money. This is driving genetics forward at breakneck speed.

This will probably also be great news for patients. For example, in the near future cancer patients will get the DNA in their tumors sequenced so they get prescribed the right medicine. We aren’t there yet, but if costs keep dropping, we will be soon.

For casual consumers, though, affordable DNA sequencing is much less useful. In fact, it might even make a difficult situation worse.

Right now we can get the results of a million or so of our bits of DNA. Some of these SNPs are within genes and some are outside of genes.

These SNPs have been looked at in lots of experiments. This means we have at least some idea about how each relates to various diseases. The same won’t be true of the new data that will be made available to you.

There are going to be changes in your genes that scientists haven’t seen before. And in many cases they won’t be able to tell you whether a certain change matters or not. You will end up with a bunch of differences for which there is little or no information. If you’re a worrier, this is going to cause problems.

Let’s take an easy example, cystic fibrosis (CF). Most of the time CF is caused by one or more of a defined set of DNA differences in the CFTR gene. Genetic testing now looks for changes known to cause CF.

Unfortunately, CFTR is a gene with a lot of changes, many of which have no effect. What this means is that many of us will have differences in our CFTR gene that haven’t been seen before. Will they cause cystic fibrosis? For many differences, we won’t know for sure.

This information may ultimately be helpful for scientists if they find enough people with particular differences. But it may not be that helpful to you. In fact, if you’re a worrier, you may be unnecessarily concerned about your kids ending up with CF because of your unique version of the CFTR gene.

And this is the easy example. Other diseases happen when many different gene versions all work together in a certain way. Some combinations of these gene versions will lead to disease or increased risk of disease and some won’t. If you pile on enough genes, you suddenly have so many combinations that it becomes very difficult to make any really predictions with only a few people’s DNA.

Right now I think it is safe to say that with genetics, we have lots of data but little understanding. To increase our understanding of human genetics, everyone should probably throw their DNA into the ring for scientists to study. The question is when do you want to know the results of what scientists are finding. At an early stage when everything is muddled or at a more defined, later stage.

By reversing evolution, scientists may be able to transform chickens into dinosaurs one step at a time.

You may remember that in Jurassic Park, scientists sequenced some dinosaur DNA from a mosquito trapped in amber. They made a copy of this DNA, filled in the gaps with frog DNA and then created a dinosaur.

Although cool, we're not likely to get dinosaurs this way in the near future for a bunch of different reasons. The biggest for now (besides not having any dinosaur DNA) is that we can’t clone anything bigger than a bacterium with just a piece of DNA. To clone a multi-celled creature like a dinosaur, we need frozen or even better, live cells.

While this might be possible for some extinct animals including mammoths, 65 million years is just too long to find any frozen or viable cells. But there may be another way to one day create Jurassic Park. By messing with a chicken’s genes.

Current theories are that birds evolved from dinosaurs. This means that all the information for making a dinosaur was contained in bird DNA at one time. The trick is to figure out what this dinosaur DNA looked like and to change bird DNA accordingly and/or to unlock any hidden dinosaur DNA that may still be in bird DNA.

After 65 million years you might think all traces of dino-DNA would be lost in birds. Surprisingly, you’d be wrong. It looks like there is still some T-rex lurking in a chicken’s DNA.

In the last decade, scientists have been able to make chickens look a bit more dinosaur-like by changing how the chickens use the genes they already have. For example, they have been able to make a chicken’s tail look a bit more like a dinosaur’s.

A big difference between birds and dinosaurs is that dinosaurs have much longer tails. But this doesn’t hold up in a chicken embryo.

At a very early stage of development, chicken embryos have what looks like a very reptilian tail with 16 vertebrae. Later in development, though, most of the vertebrae disappear until only five are left.

What this means is that if scientists can figure out how to keep the vertebrae from disappearing, they might end up with a long tailed chicken. And they’ve actually managed to sort of do this already.

By changing when certain genes are turned on or off, they have managed to create a chicken with a tail that has eight vertebrae. Not quite a dinosaur but a step in that direction.

They have also been able to create a chicken with teeth. And even a snout! All of this without fundamentally changing a chicken’s genes but instead changing how they are used.

Now they probably won’t be able to make the chicken-dinosaur transition simply by changing how chicken genes are used. There are bound to have been some significant changes in certain key genes that will have to be replicated to really make a dinosaur. And for that we’ll need to figure out what dinosaur DNA looked like.

But still, we can make a lot of progress towards making a dinosaur by simply using the toolkit of current bird genes. In the end, we’ll probably be able to recreate something very much like a dinosaur. The question will then become whether we should.

QUEST story on how scientists can figure out ancient DNA from modern DNA.

These results from the "Interpretome" tool show that there is a bit of a Neanderthal in me.

As one of the whitest people on the planet, I almost certainly have mostly European ancestors. And if I had any doubts, my 23andMe ancestry results confirm the obvious…I am European through and through.

This means there is almost certainly some Neanderthal DNA squirreled away in my genome. But how much? I decided to try to find out.

First I asked 23andMe. They quickly replied that they didn’t do that, sorry. So as often happens, I needed to take my genome on a jaunt through the internet to find a tool that could give me the answer I was looking for.

I first went to my favorite, SNPedia. No luck though. Just a piece about the Neanderthal red hair version of the MC1R gene that hasn’t yet been found in humans.

Then I remembered a discussion at Stanford about which professor was genetically the most Neanderthal. Obviously they must have a way of figuring this out.

So I contacted Dr. Mike Snyder and he led me to Konrad Karczewski, a graduate student at Stanford. And he directed me to a tool called the Interpretome that he and some other Stanford folks had developed for their personalized medicine class.

This tool has a lot of cool features (feel free to explore) but I headed straight for the Neanderthal section. I plugged in my 23andMe raw data and out popped my results. There are definitely some Neanderthals in my family tree!

The site looks at 42 different markers and since we have two copies of each, there are 84 possible Neanderthal hits. I scored a 7 out of 84.

Now, since I don’t know if that is a lot, I asked Konrad about the kinds of ranges he sees. He said the average European has a score of around 7-10 which puts me at the lower end of average. He also said that someone in an online forum had reported a 26 but the highest Konrad had ever seen with his own eyes was 20. And that the lowest he has seen for Europeans or Asians was around 3-5.

So there you have it. I am on the low end of Neanderthalness for someone of European descent using these 42 SNPs. And less Neanderthal than a number of Stanford professors!

How cool are genetics when it lets me figure out that I am definitely a bit Neanderthal but not as Neanderthal as certain unnamed Stanford professors?

More Information

Neanderthals and you.