Biology Science Zoology

Of sex, food and worms: good science, badly reported

It is true: there is a newly-discovered set of neurons found in a type of worm that, when activated, causes the male of the species to forego food in search of sex. That this set of neurons was just discovered actually does matter to the lives of humans. Or at least, it could. But not because it confirms the cliche of men starving for sex:

Researchers may have figured out why men can prioritize sex over food. Well, some men.

It’s a matter of two “mystery” neurons, suggest researchers at University College London.

They found that these extra neurons — which are unique to males — allow them to remember and seek sex even at the expense of food and are also behind some sex-based differences in learning.

So, what happened?

C. elegans is a species of worm about which we know a surprising amount. In biology research, there are some species of plants and animals that, for one reason or another, get more attention than others. Elodia and Drosophila (fruit flies) are very common study species.

C. elegans is popular because it is a simple organism that happens to share a lot of common traits with more advanced forms of life like humans. By studying C. elegans, we can often make intelligent extrapolations about how things work in other species.

In particular, C. elegans has the distinction of being the only species of life for which we have a complete neuronal map. Every neuron, every synapse (connections between neurons), every feature of the neural network of the C. elegans has been long-since mapped and analyzed… at least, so we thought.

Two researchers at the University College of London, wife and husband team Dr. Arantza Barrios and Dr. Richard Poole, research the sexual dimorphism of C. elegans. Sexual dimorphism means that different sexes have different traits (think boobs. I know I do).

In the past, the dimorphism of C. elegans has always been studied in a different portion of the worm, where differences are more obvious: the tail. These researchers discovered one set of sexually-dimorphous neurons in the head of the animals, which they named the Mystery Neurons of the Male (MNM).

What they do turns out not to be much of a mystery at all: they learn to recognize the opposite sex as a priority stimulus. Don’t we all? When the opposite sex is near – which turn out to be hermophrodites, in the C. elegens’ case – the worm with active MNM will ignore other homeostatic functions – like eating – in favour of pursuing sexual reproduction.

So. There you have it: males of the C. elegens species will forego eating in favour of sex. Or at least, they will favour sexual reproduction over other things. Not quite the whiz-bang you were hoping for? Of course not, because non-science – and even some science – news sources want to focus on sex, sex, sex. Yet the reality of what the boffins in London discovered is way more important and honestly cooler.

Why it matters

Worms getting it on don’t seem terribly relevant to humans. And indeed, they are not. What really matters is, again, the fact that simple organisms like the C. elegens can give us clues to our own biology. In this case, science has been looking for the keys to understanding sexual dimorphism in human cognition. We know that some decision making in humans is consistently different from one sex to the other. While much of the scientific community has been certain that such a difference also existed in the brain’s wiring, science has thus far not been able to pin that difference down.

That a simple creature so far removed from us in the evolutionary tree should have such a simple device for continuing the species may indicate that a similar development across species. Or, it may not. It’s just way too early to tell.

The other, perhaps even more significant, discovery that this new development represents is the appearance of glial cells in such a simple organism. Here in Rochester, we know all about glial cells, because that’s what our neuroscientists specialize in.

Glial cells are, effectively, stem cells for the brain. They are part of the glimphatic system, and their job is to grow more neuronal  cells when old ones wear out or are damaged. Remember Nancy Reagan in the 80’s? Insisting that you could not grow brain cells back, so don’t do drugs? Well, the old bat was wrong. Do drugs: your glial cells will make more neurons, no sweat.

It’s is significant that glia create entirely new neuronal cells at different age stages, at least in the case of C. elegans. Rather than simply creating the same type of cell over and over again, it seems like glia (individual glial cells) can alter their behavior throughout the lifetime of an individual. It means glia are a lot more flexible than we knew, which may point the way towards therapies for neurodegenerative disease like Parkinson’s or Alzheimer’s.

So, maybe not the sexy news you were hoping for. If you’d been planning on filling out your 6pm news cast or your morning radio talk show? Sorry. But understanding the fundaments of human cognition and finding cures for wasting brain disease seems kind of important. But these messages got lost, because pee-pees and hoo-hahs. Maybe, if the media industry at large could stop giggling and take this more seriously, we could appreciate this amazing discovery for what it is.

But for now, dear reader, it’s just you and us.


Our Sunday visit from a snowy owl.

We’ve been keeping an eye on this girl all morning. At 8am, when I left to get the family some breakfast, our next door neighbor alerted me to the snowy owl sitting across the street on another neighbor’s roof. That neighbor no longer lives in the house, so I suppose it’s as quiet a place as any in the middle of the ‘burbs for a bird to stop.

As of 2pm, the bird is still sitting right there. Why, we don’t know. People tell me it’s normal, but she was getting harried by crows earlier and never moved. She’s still alert, with her head on a swivel. But not going anywhere. Such a beautiful bird, we wish her the best!

Biology Science

Mutatin’ Ain’t Easy: will #Ebola mutate and grow wings?

Have you ever wondered why it is that everybody else in the house is sick but you? Or why your entire office feels fine but you’re having a near-death booger experience in your increasingly-unlivable apartment bedroom? Infection seems like such a capricious event in the everyday world; it’s almost as if a virus must have your name written on it.

Every day in the news we hear about another threat of Influenza, coming from birds or pigs or some other nearby threat. The virus, we understand, has mutated and become infectious to humans. A disease spreading from pigs to humans seems to have made a pretty far leap in evolutionary terms.

Now that Western Africa seems on fire with the Ebola threat – and that threat has now reached American soil in Dallas – the growing concern is that Ebola will break out in massive numbers here. We are told that Ebola spreads through direct contact with bodily fluids – from saliva or blood or stool – and that it is not possible to spread the disease through the air as is the case with Influenza.

But some worry: if the virus can mutate, perhaps it will one day become airborne. Is this really possible?

Absolutely nothing in biology is terribly simple. But when thinking about mutations, it’s worth considering that a disease’s means of transmission is different from it’s means of infection.

Infection: the jewel thief’s keys.

When it comes to the disease’s means of infection, that is a question of very specific genetic coding. It’s a lot like a jewel thief’s keys.

Imagine twenty jewel thieves in a museum, each with a different set of keys. They all have the exact same “vector” of obtaining their booty: they’re all using their keys. There is nothing fundamentally different about each thief, they just have a different set of tools to work with. But since each one does have a slightly different set, many of them are going to be out of luck: they simply won’t have the right combination of keys to get them into the doors they want.

New jewel thieves come in and out all the time. They’re all carrying a different set of tools, but the most successful jewel thieves pass their keys along. Eventually, you end up with an incredibly-effective set of keys for a huge number of museums. Now, you have a giant outbreak of Influenza, maybe even as big as the 1919 outbreak.

A diagram of the Ebola virus, showing it’s incredible length and complexity.

Ebola is a huge virus containing an incredible number of genes. It dwarves Influenza’s 120nm (nanometres), ringing in at a healthy 960nm. That’s a whole lot of genes and a whopping set of keys. The number of tools they have to work with is much larger than Influenza to start. That makes Ebola hugely infectious, with deadly results.

So far, in the current outbreak in Africa, the fatality rate has been about 50%. But keep in mind: almost none of those poor people have gotten treatment, because the places where outbreaks are occurring are very, very poor.

Transmission: fish vs. birds.

Transmission is the means by which a virus moves from one host to another. You can also think of it as part of the virus’ living environment. A disease’s means of transmission is one of the defining characteristics of the disease precisely because of this. Like any other living creature, where it is found defines the environment it needs to survive. Fish don’t walk on land, birds don’t swim.

In the case of Ebola, there has never been a documented case of airborne transmission. The reason for this seems to be because the virus does not enter the lungs. Ebola will survive for several hours outside the body, but not forever. Like a fish out of water, Ebola exposed to air is a doomed creature.

On the other hand, Influenza is very present in the lungs as most anybody with the flu can attest. And it can survive for days outside of a living host. Of course, it can: it is an airborne virus that is designed to survive the Great Outdoors in search of a new victim.

Thus on the issue of transmission, Ebola and Influenza are profoundly different types of diseases. They exist in different environments for which they are uniquely designed. Crossing the border from one environment to another is not an easy feat for any species.

The upshot: will we see airborne Ebola, soon?

Evolution is a long time coming… So anything is possible. But we may see pigs on the wing – possibly with the flu – before we see airborne Ebola. Because there is nothing about one evolutionary scenario that is any less likely than the other. All kinds of animals and plants evolve in barely-noticeable ways to adapt to their environments. Raccoons are not natural city dwellers, for example. But that is a relatively simple adjustment, relative to the paradigm-altering change some in our society envision for the Ebola virus.

While nothing is impossible, Ebola is a well-established, very old virus. It is also devastatingly successful, in the right circumstances. If the environment doesn’t threaten it’s existence, it would be hard to imagine a scenario where it would need to mutate that much. Ebola is as likely to keep it’s current form as any other creature, maybe more so.

Influenza is highly-transmissible, but with a relatively modest infection rate. That’s why you’re sick and your cube mate isn’t. Ebola is a barely transmissible disease with a huge infection rate. On top of huge genetic differences about which this article does not make a pretense of delving into, it is enough to say that they are profoundly different species that should not be lumped together as just “viruses that can mutate.”