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Gene-editing experiment turns fluffy hamsters into ‘aggressive’ mutant rage monsters
https://metro.co.uk/2022/05/27/gene-editing-turns-fluffy-hamsters-into-aggressive-rage-monsters-16721041/
https://www.pnas.org/doi/10.1073/pnas.2121037119
CRISPR-Cas9 editing of the arginine–vasopressin V1a receptor produces paradoxical changes in social behavior in Syrian hamsters
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A team of scientists in the US have accidentally created overly-aggressive mutant hamsters following a gene-editing experiment.
Using the controversial CRISPR technology, researchers at Northwestern University were examining a hormone called vasopressin and its receptor, Avpr1a.
They opted to try and remove the latter from a group of Syrian hamsters, with the expectation it would increase bonding and co-operation between the lovable little critters.
That’s because Avpr1a is understood to regulate things like teamwork and friendship as well as dominance and bonding.
Their expectation proved to be wrong. Very wrong.
‘We were really surprised at the results,’ said Professor H Elliot Albers, the lead researcher on the study.
‘We anticipated that if we eliminated vasopressin activity, we would reduce both aggression and social communication.
‘But the opposite happened.’
The academics found the adorable bundles of fluff turned into mutant rage monsters exhibiting ‘high levels of aggression towards other same-sex individuals’.
All hamsters, regardless of genotype or sex, exhibited aggression (including chasing, biting, and pinning) when exposed to a nonaggressive, same-sex conspecific in a neutral arena.
Professor Albert admitted the results of the experiment were a ‘startling conclusion’.
The scientists chose to experiment with Syrian hamsters because, unlike mice, they have a social organisation that’s similar to humans.
Professor Albert explained: ‘Even though we know that vasopressin increases social behaviours 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.’
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So gene editing via crispr can produce a new breed infected with rage at the code/dna level.
Arginine–vasopressin (AVP) acting on V1a receptors (Avpr1as) represents a key signaling mechanism in a brain circuit that increases the expression of social communication and aggression. We produced Syrian hamsters that completely lack Avpr1as (Avpr1a knockout [KO] hamsters) using the CRISPR-Cas9 system to more fully examine the role of Avpr1a in the expression of social behaviors. We confirmed the absence of Avpr1as in these hamsters by demonstrating 1) a complete lack of Avpr1a-specific receptor binding throughout the brain, 2) a behavioral insensitivity to centrally administered AVP, and 3) an absence of the well-known blood-pressure response produced by activating Avpr1as. Unexpectedly, however, Avpr1a KO hamsters displayed more social communication behavior and aggression toward same-sex conspecifics than did their wild-type (WT) littermates.
Abstract
Studies from a variety of species indicate that arginine–vasopressin (AVP) and its V1a receptor (Avpr1a) play a critical role in the regulation of a range of social behaviors by their actions in the social behavior neural network. To further investigate the role of AVPRs in social behavior, we performed CRISPR-Cas9–mediated editing at the Avpr1a gene via pronuclear microinjections in Syrian hamsters (Mesocricetus auratus), a species used extensively in behavioral neuroendocrinology because they produce a rich suite of social behaviors. Using this germ-line gene-editing approach, we generated a stable line of hamsters with a frame-shift mutation in the Avpr1a gene resulting in the null expression of functional Avpr1as. Avpr1a knockout (KO) hamsters exhibited a complete lack of Avpr1a-specific autoradiographic binding throughout the brain, behavioral insensitivity to centrally administered AVP, and no pressor response to a peripherally injected Avpr1a-specific agonist, thus confirming the absence of functional Avpr1as in the brain and periphery. Contradictory to expectations, Avpr1a KO hamsters exhibited substantially higher levels of conspecific social communication (i.e., odor-stimulated flank marking) than their wild-type (WT) littermates. Furthermore, sex differences in aggression were absent, as both male and female KOs exhibited more aggression toward same-sex conspecifics than did their WT littermates. Taken together, these data emphasize the importance of comparative studies employing gene-editing approaches and suggest the startling possibility that Avpr1a-specific modulation of the social behavior neural network may be more inhibitory than permissive.
A key challenge in social neuroscience is to understand how genes act within defined neural circuits to regulate social and affective behaviors. The social behavior neural network (SBNN) is a complex circuit composed of an interconnected series of brain regions, or “nodes,” that govern many social behaviors, ranging from fear and aggression to affiliation (1–4). Much of the diversity and complexity of social behavior across species and among individuals is hypothesized to emerge from the functional interactions of elements of the entire SBNN circuit, and not from the activity of its individual components (3, 5). To address how social behavior emerges from such a complex neural network, it is essential to have advanced genetic tools capable of manipulating key neurochemical pathways across the entire circuit and to be able to compare the effects of these manipulations in a variety of species that exhibit rich and varied patterns of social behavior.
In the present study, we employed a CRISPR-Cas9 pronuclear germ-line gene-editing approach in Syrian hamsters (Mesocricetus auratus) to eliminate arginine–vasopressin (AVP) V1a receptors (Avpr1as) throughout the nodes of the SBNN (6–8).
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