Noradrenergic Circuit Adaptations Underlying Predatory Aggression
Noradrenergic Circuit Adaptations Underlying Predatory Aggression
View/Type of Scholarly Publication
DissertationDate of Exam
15.12.2025Date of Publication
09.01.2026Advisor
Lightfoot, James W.Co-Referee
Grunwald Kadow, IlonaMetadata
Show full item record
Citable Links 
Abstract
Behaviors are adaptive traits shaped by natural selection. Nevertheless, the genetic, molecular, and neural modifications that underlie behavioral innovations remain poorly understood. Here, I identify specialized adaptations linked to the evolution of invertebrate aggression by leveraging a comparative nematode framework, Pristionchus pacificus versus Caenorhabditis elegans, to dissect the evolution of predatory aggression and its interface with territoriality and feeding. We combined high throughput tracking with a semi-supervised behavioral state labeling pipeline, cell type resolved perturbations, receptor mapping, and targeted CRISPR screens. Quantitative analyses revealed that octopamine and tyramine function as an antagonistic pair at the molecular level: tbh-1 loss (↓octopamine) reduced entry into the predatory state, tdc-1 loss (↓tyramine and ↓octopamine) rescued this effect. Furthermore, exogenous octopamine and tyramine also shifted state occupancy in opposite directions. Behavioral assays of CRISPR mutants showed that mutations in the octopamine receptors ser-3/ser-6 phenocopied tbh-1 deficits, whereas mutations in the tyramine associated ion channel, lgc-55 mirrored the rescue observed in tdc-1. Crucially, we found that while the neurotransmitter source remained conserved across species, the receptor expression has been rewired with differential expression observed across head sensory neurons. Notably, P. pacificus specific SER-3 expression is detected in IL2 sensory neurons and functional silencing of these reduces predatory search, biting, and feeding. This establishes the IL2 neurons as a sensory hub for prey detection and state gating. Comparative tests across another basal Diplogastrid species indicate that octopamine's pro-aggressive role is conserved within this family. Thus adaptations in noradrenergic circuits emerges as a central mechanism for shaping the evolution of aggressive behavioral states in nematodes.
Classification (DDC)
570 Biowissenschaften, BiologieEren, Güniz Göze: Noradrenergic Circuit Adaptations Underlying Predatory Aggression. - Bonn, 2026. - Dissertation, Rheinische Friedrich-Wilhelms-Universität Bonn.
Online-Ausgabe in bonndoc: https://nbn-resolving.org/urn:nbn:de:hbz:5-87028
Online-Ausgabe in bonndoc: https://nbn-resolving.org/urn:nbn:de:hbz:5-87028
@phdthesis{handle:20.500.11811/13809,
urn: https://nbn-resolving.org/urn:nbn:de:hbz:5-87028,
author = {{Güniz Göze Eren}},
title = {Noradrenergic Circuit Adaptations Underlying Predatory Aggression},
school = {Rheinische Friedrich-Wilhelms-Universität Bonn},
year = 2026,
month = jan,
note = {Behaviors are adaptive traits shaped by natural selection. Nevertheless, the genetic, molecular, and neural modifications that underlie behavioral innovations remain poorly understood. Here, I identify specialized adaptations linked to the evolution of invertebrate aggression by leveraging a comparative nematode framework, Pristionchus pacificus versus Caenorhabditis elegans, to dissect the evolution of predatory aggression and its interface with territoriality and feeding. We combined high throughput tracking with a semi-supervised behavioral state labeling pipeline, cell type resolved perturbations, receptor mapping, and targeted CRISPR screens. Quantitative analyses revealed that octopamine and tyramine function as an antagonistic pair at the molecular level: tbh-1 loss (↓octopamine) reduced entry into the predatory state, tdc-1 loss (↓tyramine and ↓octopamine) rescued this effect. Furthermore, exogenous octopamine and tyramine also shifted state occupancy in opposite directions. Behavioral assays of CRISPR mutants showed that mutations in the octopamine receptors ser-3/ser-6 phenocopied tbh-1 deficits, whereas mutations in the tyramine associated ion channel, lgc-55 mirrored the rescue observed in tdc-1. Crucially, we found that while the neurotransmitter source remained conserved across species, the receptor expression has been rewired with differential expression observed across head sensory neurons. Notably, P. pacificus specific SER-3 expression is detected in IL2 sensory neurons and functional silencing of these reduces predatory search, biting, and feeding. This establishes the IL2 neurons as a sensory hub for prey detection and state gating. Comparative tests across another basal Diplogastrid species indicate that octopamine's pro-aggressive role is conserved within this family. Thus adaptations in noradrenergic circuits emerges as a central mechanism for shaping the evolution of aggressive behavioral states in nematodes.},
url = {https://hdl.handle.net/20.500.11811/13809}
}
urn: https://nbn-resolving.org/urn:nbn:de:hbz:5-87028,
author = {{Güniz Göze Eren}},
title = {Noradrenergic Circuit Adaptations Underlying Predatory Aggression},
school = {Rheinische Friedrich-Wilhelms-Universität Bonn},
year = 2026,
month = jan,
note = {Behaviors are adaptive traits shaped by natural selection. Nevertheless, the genetic, molecular, and neural modifications that underlie behavioral innovations remain poorly understood. Here, I identify specialized adaptations linked to the evolution of invertebrate aggression by leveraging a comparative nematode framework, Pristionchus pacificus versus Caenorhabditis elegans, to dissect the evolution of predatory aggression and its interface with territoriality and feeding. We combined high throughput tracking with a semi-supervised behavioral state labeling pipeline, cell type resolved perturbations, receptor mapping, and targeted CRISPR screens. Quantitative analyses revealed that octopamine and tyramine function as an antagonistic pair at the molecular level: tbh-1 loss (↓octopamine) reduced entry into the predatory state, tdc-1 loss (↓tyramine and ↓octopamine) rescued this effect. Furthermore, exogenous octopamine and tyramine also shifted state occupancy in opposite directions. Behavioral assays of CRISPR mutants showed that mutations in the octopamine receptors ser-3/ser-6 phenocopied tbh-1 deficits, whereas mutations in the tyramine associated ion channel, lgc-55 mirrored the rescue observed in tdc-1. Crucially, we found that while the neurotransmitter source remained conserved across species, the receptor expression has been rewired with differential expression observed across head sensory neurons. Notably, P. pacificus specific SER-3 expression is detected in IL2 sensory neurons and functional silencing of these reduces predatory search, biting, and feeding. This establishes the IL2 neurons as a sensory hub for prey detection and state gating. Comparative tests across another basal Diplogastrid species indicate that octopamine's pro-aggressive role is conserved within this family. Thus adaptations in noradrenergic circuits emerges as a central mechanism for shaping the evolution of aggressive behavioral states in nematodes.},
url = {https://hdl.handle.net/20.500.11811/13809}
}
The following license files are associated with this item:
