[For 40 years, scientists thought a specific gene was linked to
aggression in hamsters. Removing it, however, had violent
consequences.]
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GENE EDITING GONE WRONG: SCIENTISTS ACCIDENTALLY CREATE ANGRY
HAMSTERS
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Peter Rogers
June 16, 2022
Big Think [[link removed]]
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_ For 40 years, scientists thought a specific gene was linked to
aggression in hamsters. Removing it, however, had violent
consequences. _
In i and ii, a male hamster flank marks the corner of its cage. In
iii and iv, a larger female attacks and pins a smaller female., Jack
H. Taylor et al., PNAS, 2022)
KEY TAKEAWAYS
* Of all rodents, hamsters have a social organization and stress
response that is most human-like.
* To study aggression in hamsters, a team of scientists used gene
editing to create what they thought would be a calmer rodent. Instead,
the gene-edited rodents were angrier — chasing, biting, and pinning
down other same-sex hamsters.
* The research underscores that the field of behavioral genetics has
a long way to go.
Hamsters have a social organization and stress response that is more
human-like than any other rodent. Thus, behavioral scientists have
relied on hamsters to understand the forces that govern behavior.
According to a recent study
[[link removed]], however, these
forces are less well-understood than previously thought. The
researchers used gene-editing technology to delete a receptor thought
to cause aggression in hamsters. Instead of becoming more cuddly,
however, the hamsters got mean.
A gene that regulates aggression
In 1984
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a group of researchers set out to study the circadian rhythm
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small amounts of hormones into the brains of hamsters. One of the
hormones, arginine vasopressin (AVP), had an immediate and surprising
effect. It didn’t alter the hamsters’ sleep cycle, but it did
induce a dramatic behavioral change. The hamsters began soaking their
hips (where the scent glands are located) with saliva and rubbing
themselves vigorously against the wall of the cage, a behavior
indicative of aggressively claiming their territory.
Subsequent pharmacological studies
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examined the function of AVP’s receptor, called Avpr1a. According to
the studies, Avpr1a seemed to have sex-dependent effects. When male
hamsters received injections of Avpr1a _activators _(such as AVP),
they became more aggressive, whereas the female hamsters became less
aggressive. Alternatively, when hamsters received injections of
Avpr1a _inhibitors_, males became less aggressive, and females
becomes more aggressive. Almost four decades of studies overwhelmingly
showed that Avpr1a directly regulated aggression and anxiety-like
behavior [[link removed]].
One study, however, created an air of mystery around Avpr1a. In 2007
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a team of researchers at the University of Buffalo knocked out the
Avpr1a gene in male mice, expecting the mice to show reduced
aggression due to a lack of AVP signaling. However, the Avpr1a-lacking
mice were no more or less aggressive than normal mice. For over a
decade, this discrepancy was explained as being due to developmental
compensation — that is, the embryo compensated for the lack of
Avpr1a by modulating other behavioral pathways.
Angry hamsters
A team of researchers at Georgia State University led by Elliott
Albers and Kim Huhman, however, disagreed. The major gripe that they
had with the 2007 study was that Avpr1a was knocked out in _mice_,
rather than _hamsters_. Such differences matter. So, the researchers
used CRISPR-Cas9 gene-editing technology to mutate the Avpr1a receptor
gene (so that it was no longer functional) in male and female
hamsters.
The researchers believed that, by removing the hamster’s ability to
make Avpr1a, the hamsters would become less aggressive. Their
hypothesis was incorrect. To the contrary, all Avpr1a-lacking
hamsters, regardless of sex, exhibited far more aggressive behavior,
doing twice as much flank marking as well as chasing, biting, and
pinning down other same-sex hamsters.
The authors did not expect angry hamsters. “This suggests a
startling conclusion,” Albers said
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“Even though we know that [AVP] increases social behaviors by acting
within a number of brain regions, it is possible that the more global
effects of the Avpr1a receptor are inhibitory. We don’t understand
this system as well as we thought we did. The counterintuitive
findings tell us we need to start thinking about the actions of these
receptors across entire circuits of the brain and not just in specific
brain regions.”
_DR. PETER ROGERS grew up milking cows and building barns. This
provided him the transferable skills necessary for a smooth transition
into academic research. Three years of genetics research led to six
years of immunology research, which led to a PhD from Auburn
University. That led to three and half years of instructional design
research at Tufts University School of Medicine._
_His expertise includes biomedical sciences & technology, social
determinants of health, bovine birthing, training & development, and
cognitive psychology. He’s taught dozens of university courses,
ranging from Principles of Biology to Advanced Medical Immunology. He
is currently co-writing a book with his father, George Rogers,
called How to Correctly Hold a Flashlight: A Disagreement in Academic
and Agricultural Perspectives._
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