Ten-hundred word challenge, Part 3: Worm Sperm and Brain Pain

9:03:00 AM

In our third installment of the Ten Hundred Word Challenge inspired by this XKCD Up-Goer Five comic (and aided by this Up-Goer Five text-editor), we present two cases of complicated biology made simple. Aggie writes about fear changing our brains, and Paul writes about tiny worm sperm. Read on to learn more! And then, if you’re interested in writing your own, contact us at bfsablog@gmail.com.


Simplified explanation:

When we get into trouble or bad things happen that can hurt us, our brain responds by waking up parts of the brain that control fear. Fear is important in bad situations because it helps us escape the bad stuff fast, so that we don't get hurt.

However, if bad stuff happens a lot, or if something very bad happens, our brains can over-respond. If parts of the brain that control fear are excited too much or too often, they become broken and don't work as they should. These fear parts of the brain start to become excited by normal, safe situations, and over-respond to small, annoying stuff. When our brain over-respond like this, stuff that is usually safe can make us nervous or afraid. Eventually, we become sad and scared all the time, and our brain becomes sick.

We can't avoid bad stuff. However, we can help our brain get stronger, so that when bad stuff happens, it doesn't hurt our brain. I study ways to help make our brain stronger and work better. It turns out that walking, running, or anything that makes us move around is good for our brain. When we take time to move around every day, our brain begin to change in small ways. Over time, these small changes make our brains stronger. Even when really bad things happen, our brain can still work like they're supposed to, and we don't become sad or afraid.

I've found that moving around when you're young can make your brain even stronger and work even better. When you're young, your brain has not quite grown up yet and it's easier to change, so a little bit of running or walking can change the brain in big ways.

Real explanation:

Stressors are aversive experiences that awaken an organism’s biological stress response. The stress response ensures survival in dangerous situations. When the brain senses a threat, it immediately alarms brain regions that control important survival behaviors, such as fear and panic, which helps us behave appropriately to escape the threat.

However, if we experience frequent or intense stressors, our brain’s stress response can become harmful. Frequent or intense stress can over-stimulate brain regions that control fear and panic behavior. This produces changes in brain chemistry that enable these regions to overreact, even to non-threatening situations. When the brain’s stress centers react to situations that aren’t dangerous it can lead to psychiatric disorders such as anxiety.

Since avoiding or preventing stressors is not feasible, finding ways to make our brains more resistant to the harmful effects of stress is important. I study the impact of exercise on brain health. Habitual exercise increases many molecules that support and improve brain health. Increases in certain molecules within brain regions that control fear and panic behavior can help these regions function appropriately, even in the face of intense stress. This way, exercise can help prevent stress-related psychiatric disorders.

I’ve found that exercise is most effective at promoting mental health early in life, when the brain is still developing. Exercising when you’re young can potentially produce more robust and permanent improvements in brain health, arming your brain against stress for life.  


Simplified explanation:

I used to study tiny tiny little animals. They were about as big as, and looked something like, this: ~  

Usually, these tiny animals made lots and lots of babies.  But one sick kind couldn't make babies.  I wanted to see if I could help the sick ones make babies.  So I broke them again and made them even more sick!  But when I broke the new part that made up for the part that broke them so they couldn't make babies in the first place. Now they could make babies again. So, they got better by being even more broken!  How cool is that?  It turns out that the thing I broke also made up for broken parts that made lots of other kinds of these animals not able to have babies. By breaking more parts, I figured out how those parts worked with the first parts that broke to help these tiny animals have babies.  Well, I thought I figured it out. My friend, who also studies how tiny animals make babies, just figured out that it may not quite work the way I thought it did.  Oh well, that's how these things go. I wonder if I could do this same thing for people to help them have babies if they couldn't.  That would be fun, but it's not nice to keep breaking people.  They don't like that.

Real explanation:

In graduate school I worked on sperm development in the nematode Caenorhabditis elegans, a model organism for developmental genetics. Our lab studied sperm-defective mutants.  

I was most interested in the final stage of sperm development, called spermiogenesis.  During spermiogenesis, a spherical non-motile spermatid “activates” to become a mature crawling spermatozoon. Yes, worm sperm move by crawling with a pseudopod instead of swimming with a flagellum. 

In my first month in the lab, I did a genetic screen.  I started with a temperature sensitive spermiogenesis mutant, which was sterile at room temperature but fertile at a chilly 15°C.  I grew a population of several million of these mutants at the permissive temperature, mutagenized them, shifted the population to room temperature, and selected for rare fertile suppressor mutants.  The screen yielded many suppressors, and I spent the remainder of my graduate career mapping, cloning, and characterizing them (this was in the days before whole-genome sequencing!).  Most of the mutations turned out to be different alleles of the same gene, spe-6.  We still don’t know exactly what SPE-6 does, but my model was that it acts to prevent premature spermiogenesis until the spermatid receives the activation signal. 

Aggie Mika, 4th year PhD candidate in Integrative Physiology
Paul Muhlrad, Science Communications Manager in Molecular, Cellular, and Developmental Biology

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