Sunday, January 24, 2016

Dog parks: tools to be used for good or evil

Dog parks can be valuable ways to exercise and socialize your dog. They can also be dangerous places where dogs can get hurt. And so we ask ourselves: are dog parks a good thing or a bad thing? I argue that they are neither. Like retractable leashes, they are just a tool that can be used well or badly.

Park design

The design of a dog park can have a lot to do with how well it functions. I think the size of the park is incredibly important. At my local park, we have a lot of space. And I use this space with my dogs. If there is a group of dogs that my dogs aren’t getting along well with, and I see trouble brewing, I move on to a different part of the park. In a small park, this wouldn't be possible.

Jenny at my fabulous local park

My local park also has a smaller area, separately fenced. It’s a great place to take a smaller dog when the park is full of big dogs, or to take a dog who needs a cooling down period after he's been acting like a bully. I don’t use this space much with my dogs, but it’s extremely helpful for a friend of mine who’s trying to teach her six month old to restrain his enthusiasm around other dogs by giving him time outs when he fails to control himself appropriately.

Park timing

I don’t go to the park when it’s crowded. Of course, it’s crowded at the times that are the most convenient for the most people: late afternoon, weekends, when the weather is lovely. I go in the mornings during the week. I lead a lifestyle which makes that possible (though I have to push back at work to protect that time). If you can only go to the park when it’s crowded, it might not be worth going at all. Tempers run high when dogs are packed in together with no real room to get away.

Dog management

This is the important one for me: I am always alert and managing my dogs. I keep an eye on them. One of them can have a short temper with other dogs, and I keep her moving, away from groups. If I see her meeting another dog, I am watching closely for her to get tense, and if I don't think it's going well, I call her away before something goes wrong.

This kind of management is hard for a lot of owners who don’t understand dog body language well. For this reason, I’ve founded a group at my local park with the goal of (among other things) providing educational material at the park to help owners understand how to identify and avoid problems before they start. Not everyone will be interested in this material, and that’s why it’s also important to me to attend a large park during low occupancy times.

Stuff happens

My dogs have been attacked at the park. One of my dogs has also been attacked while I was walking him on leash on a sidewalk. And once he got away from me and was almost hit by a car. That’s life. Is it more dangerous at the park than on a leash on the sidewalk? Possibly, though I’d love to see evidence one way or the other. Is it more dangerous to a young dog to fail to get his crazies out on leash, and then be at risk of being surrendered by a frustrated owner? Again, I can’t say, but there are risks to any choices about how we manage our dogs.

At the park, there are no cars, no cats, no children, no bicycles, no terrifying joggers just begging to be bitten. One of my park friends walked her dog on leash until he bit a roller blader who passed too close. Without the park, she would be unable to exercise her dog safely. My shy dog Jenny has made canine and human friends at the park that she is unable to make in situations in which she's restrained. She has made incredible gains in confidence. That has come at a risk, but to me, with a lot of careful management of the dog park environment, at the right park, with these dogs, it’s worth it.

Thursday, January 14, 2016

Too many pairs: DNA, chromatin, and chromosomes

Some facts:
  • Molecules of DNA are double-stranded, each strand a perfect complementary copy of the other.
  • Humans have 23 pairs of chromosomes.
  • Chromosomes are made of DNA.
  • We have two copies of each gene.
Where do these two copies of each gene come from — the complementary DNA? Or the pairs of chromosomes? In fact, what is the relationship between DNA and chromosomes? These questions have proven thorny for students in the past, so I'll try here to describe the two different ways in which genetic information is duplicated in a cell.

1. Complementary copies of DNA strands

Molecules of DNA duplicate the information they carry. Each base in a DNA strand is bonded to its complement on the opposite strand: A bonds to T, C bonds to G. It’s like a backup mechanism: if something happens to one part of the strand, the other half is there with the complement of the information. So that’s the first way in which genetic information is paired. And the important part about this pairing is that the pairs are exact complements of each other, like mirror images: the information is duplicated precisely and does not vary.

Part of a DNA strand, demonstrating complementary bases in matching colors
This double-stranded molecule of DNA, then, is wrapped up tightly around proteins called histones, and this set of spools of DNA and histones all together is a material called chromatin.
Chromatin: light blue/green strands of DNA wrapped around bright blue histones.

2. Two copies of each chromosome

Chromosomes are made out of chromatin. In a lot of the pictures of chromosomes in which you can see the chromatin that makes it up, the chromatin looks sort of like yarn woven into a sweater. That’s a reasonable way to think of chromosomes: big structures (big enough that we can see them with a not-too-powerful microscope) made from this yarn-like chromatin.

Cartoon of chromosome made of yarn-like chromatin. (Image by Magnus Manske at Wikipedia.)
 A particular gene is always on a particular chromosome in a given species. For example, the gene for oxytocin, OXT, is always on chromosome 24 in dogs and chromosome 20 in humans. So your chromosomes are very orderly, each one containing a specific set of genes.

Humans have 23 pairs of chromosomes. Dogs have 39 pairs. In fact, Wikipedia has a whole page devoted to the number of pairs of chromosomes in different species. We think of chromosomes as looking like big X. The X is actually the two separate chromosomes in a pair, stuck together during the process of cell division. Usually those two arms of the X are separate in the cell.

Image by JWSchmidt at Wikipedia

In a pair of chromosomes, one chromosome is made of chromatin from one (double) strand of DNA and proteins, which you got from your mother; and the other chromosome is made of chromatin from another (double) strand of DNA and proteins, which you got from your father. So you have, for example, two copies of chromosome 20, one from your mother and one from your father.

Human chromosomes: 23 pairs.
These pairs of chromosomes are the second way in which your genetic information is paired. But this is very different from the exact copy pairing of strands of DNA. Your version of the OXT gene on the chromosome you got from your mother may be slightly different from your version of the OXT gene on the chromosome you got from your father. Where her version had a G-C, his version may have an A-T. (Or it may be just the same.)

DNA differences on two different copies of the same chromosome (see the difference highlighted in blue).
So we have two versions of each gene, one on each chromosome in a matched pair. For a particular gene, we may have two identical copies (in which case we are “homozygous” for that gene) or we may have two different versions (in which case we are “heterozygous” for that gene).

So, yes, we essentially have four instances of each gene in each cell. That’s four instances, but a maximum of two versions of the gene (the doubled instances on a double strand of DNA are always identical complements; it’s only when you compare instances between chromosomes that you may see differences).

In the minds of geneticists, it’s the two versions in the pair of chromosomes which really count. That’s the pair that could differ, after all. And that’s why you'll hear that we have “two” copies of each gene, even though the gene is paired both in the DNA and again between chromosomes.

Wednesday, January 13, 2016

Science for the people

One of my students in the online genetics class I’m teaching commented to me that it was a little sad that we were marketing the class as “not too difficult.” Science is only as hard as you make it, she said. It shouldn’t be something scary.

It shouldn’t be, but for a lot of people it is. As a freshman in college I figured I should take college level biology as an elective so that I had a solid groundwork in how life works. (I was a medieval studies major.) But talking to my pre-med friends convinced me otherwise. Science classes were for people who were all in: they were only for scientists, not dabblers. They were hard work. Lots of hard work.

When I decided to go back to school to become a veterinarian, I took that introductory biology course, and a lot of other science courses. I learned a lot of information I’d never use again (and have since forgotten), particularly in chemistry and physics. I wasn’t eligible to learn the things I wanted to learn until I’d jumped through these hoops.

I hope that these days, with online classes, the tide is starting to turn. I don’t think people should have to take a year of basic biology in order to learn a little about genetics. I don’t think people should have to learn about photosynthesis and the difference between monocots and dicots (those are groups of plants, by the way) in order to learn neurobiology. It is perfectly possible to design science courses for people who are not pre-med or pre-vet undergraduates. But sometimes, when I’m telling people about this great new genetics course I'm teaching and they look slightly alarmed, I'm saddened by the history of how we've traditionally taught science courses.

More than thirty people signed up for the genetics course. I hope I’ve designed something that’s worth their while.

Monday, January 11, 2016

The future of behavior medication?

We don’t actually know how behavior medications work. We know how they change the operations of cells — for example, we know facts like “this medication makes cells slower to recycle this particular chemical.” But we don’t have a good idea of how those cellular-level changes result in behavior-level changes. We don’t know how these medications make individuals feel better.

And that’s a problem, because not every individual responds to a particular behavior med in the same way. A pathologically fearful dog might have nasty side effects on one med, no response to a second, and then respond beautifully to a third. It’s hard on owners to have to try a variety of medications before finding the right one, especially as it takes a month or two to be sure that a particular medication is or isn’t working. (Oh, yeah, and the same is true for humans who use these drugs.)

If we knew how these medications worked, we might be able to figure out who they would work on without so much cumbersome trial-and-error. Imagine taking your shy dog to a veterinary behaviorist, who would do a genetic test and prescribe the right drug based on the results, to go along with behavior modification exercises.

My current work focuses on gene networks that differ in the brain between animals who are shy and aggressive and animals who are confident and friendly. I've always felt that my requests for funding have been a little hand-wavy as I have argued that surely my findings may help us understand behavioral medications better... You know, someday. Someday maybe my findings will help us design better medications, in fact. But that day seemed a really long way off.

Until I read Ed Yong's story “CRISPR’s most exciting uses have nothing to do with gene editing”. CRISPR is a fancy new gene editing technology that has everyone talking about science fiction coming to pass: being able to edit human (and animal) genes to make designer babies (and animals). Edit out the gene variants for genetic diseases before a baby is born! (But hopefully don't slide down the slippery slope to editing height, skin color, eye color, personality...)

But it turns out that CRISPR may have a more subtle use: gene regulation. Soon, scientists may be able use it to tell individual genes to turn on and off (to make more or less of their product). Rather than permanently editing genes in embryos, we could temporarily modify the output of genes in adults. Suddenly my quest to find the sets of genes affecting shyness seems less quixotic. Maybe my discoveries (do you like how I assume I’ll have discoveries? Let’s just pretend it’s a sure thing) won't have to wait for drug discovery work to be useful. Maybe we’ll be able to directly turn the volume up or down on those particular genes, directly affecting pathological shyness.

Scary? Yeah, it's not something I foresee being used therapeutically in the next few years, not until we understand the brain well enough to be able to predict side effects. But it’s really cool to imagine that some day we may have this sort of fine-tuned control over psychological diseases.