Nigel S Atkinson
· ProfessorVerifiedUniversity of Texas at Austin · Biochemistry and Molecular Biology
Active 1960–2025
About
Nigel S. Atkinson is a Professor in the Department of Neuroscience at the University of Texas at Austin, affiliated with the Interdisciplinary Neuroscience Program and Interdisciplinary Life Sciences Graduate Programs. His research focuses on the molecular mechanisms underlying alcohol tolerance, utilizing the fruit fly Drosophila as a model organism. His work involves studying how the nervous system adapts to alcohol exposure through genetics and molecular biology, including the analysis of alcohol-induced histone modifications to identify genes and DNA elements important for tolerance production. Notably, he has demonstrated that the BK-type Ca2+-activated K+ channel gene is induced by sedation and is required for tolerance, with increased expression counteracting the drug's effects during intoxication and contributing to withdrawal phenotypes after clearance. His research extends to mapping drug-responsive DNA elements and exploring genomic responses to understand addiction-related behaviors. Dr. Atkinson's educational background includes a B.S. in Microbiology from Texas A&M University, a Ph.D. studying yeast RNA processing at Hershey Medical Center of Penn State University, and postdoctoral work at the University of Wisconsin-Madison in Drosophila neurogenetics, where he cloned the first BK-type Ca2+-activated K+ channel gene.
Research topics
- Genetics
- Biochemistry
- Biology
- Neuroscience
- Zoology
- Psychiatry
- Ecology
- Medicine
- Psychology
Selected publications
PPI-ID: Streamlining protein-protein interaction prediction through domain and SLiM mapping
PLoS Computational Biology · 2025-10-16 · 1 citations
articleOpen accessSenior authorCorrespondingAlphaFold-Multimer models protein complexes and facilitates protein-protein interaction (PPI) prediction. Mapping of protein interaction domains and motifs onto the 3D structure can lend credence to the model and provide insight into the function of a given interaction. Furthermore, limiting structure prediction to only the domains and motifs that are likely to interact can reduce the computational demand and produce a higher quality model. To satisfy these needs, we built the Protein-Protein Interaction Identifier (PPI-ID). PPI-ID maps interaction domains and motifs onto molecular structures and filters for those that are sufficiently close to interact. Once an interface is found, PPI-ID labels interacting amino acids. Given only sequences, PPI-ID predicts regions for AlphaFold-Multimer modeling, reporting potential interactions only when each protein has one-half of a paired sequence. Testing with known dimers confirms high accuracy of the tool.
Journal of Biological Chemistry · 2025-05-01
articleOpen accessSenior authorAnimations are effective media that enable researchers to explore, communicate, and gain new insights into complex biological processes.However, the technical complexity and steep learning curve of traditional 3D animation software have hindered their widespread adoption in scientific research.This project addresses these challenges by developing accessible software tools that empower researchers to create their own molecular models and animations.Leveraging the open-source animation software Blender, we are building a suite of tools specifically tailored for molecular animations.These tools will allow users to import Protein Data Bank (PDB) and AlphaFold structural models directly into Blender and build customized molecular representations.Researchers will be able to define conformational states of molecular complexes and generate animated trajectories that transition between these states.Additionally, the tools will support the creation of simplified animations to visualize molecular interactions and movements, offering an intuitive means of depicting complex biological processes.All tools will be implemented as free Blender addons, using Python scripting and Blender's Geometry Nodes procedural system.To enhance accessibility and promote collaboration within the scientific community, we are also developing platforms for archiving, annotating, and sharing animated molecular models.These platforms will enable broader dissemination and use of molecular animations in research and science communication.
Frontiers in Behavioral Neuroscience · 2025-12-10
articleOpen accessSenior authorCorrespondinggene uses alternative messenger RNA (mRNA) processing to encode two different nuclear factor kappa Bs (NF-κBs). The DifA isoform is a canonical NF-κB transcription factor that is important for activation of the immune response. Our primary interest is the DifB isoform, which is neuron-specific and expressed in the mushroom bodies and antennal lobes of the adult brain. The DifB protein lacks a nuclear localization signal and does not enter the nucleus. Instead, it localizes to the cell body surrounding the nucleus, to axonal-dendritic projections, and to the synapse. DifB is an unusual member of the NF-κB superfamily, as it acts outside the nucleus to modulate behavior. The DifB isoform has been shown to modulate the sensitivity of the adult to sedation by alcohol. Here, we conducted a survey to determine whether the DifB NF-κB is important for other fly behaviors. We observed that a DifB-specific mutation strongly suppresses male courtship. However, despite the expression of DifB in the mushroom bodies, a DifB null allele does not interfere with learning in a learned-suppression-of-phototaxis assay. Finally, both DifA-specific and DifB-specific mutations caused flies to have a circadian long rhythm phenotype, although the circadian phenotype cannot be scored in male DifB mutants because of a sexually dimorphic locomotor defect.
PPI-ID: Streamlining Protein-Protein Interaction Prediction through Domain and SLiM Mapping
bioRxiv (Cold Spring Harbor Laboratory) · 2025-04-25 · 2 citations
preprintOpen accessSenior authorCorrespondingABSTRACT AlphaFold-Multimer models protein complexes and facilitates protein-protein interaction (PPI) prediction. Mapping of protein interaction domains and motifs onto the 3D structure can lend credence to the model and provide insight into the function of a given interaction. Furthermore, limiting structure prediction to only the domains and motifs that are likely to interact can reduce the computational demand and produce a higher quality model. To satisfy these needs, we built the Protein-Protein Interaction Identifier (PPI-ID). PPI-ID maps interaction domains and motifs onto molecular structures and filters for those that are sufficiently close to interact. Once an interface is found, PPI-ID labels interacting amino acids. Given only sequences, PPI-ID predicts regions for AlphaFold-Multimer modeling, reporting potential interactions only when each protein has one-half of a paired sequence. Testing with known dimers confirms high accuracy of the tool.
The Role of Toll and Nonnuclear NF-κB Signaling in the Response to Alcohol
Cells · 2023-05-30 · 5 citations
reviewOpen access1st authorCorrespondingAn understanding of neuroimmune signaling has become central to a description of how alcohol causes addiction and how it damages people with an AUD. It is well known that the neuroimmune system influences neural activity via changes in gene expression. This review discusses the roles played by CNS Toll-like receptor (TLR) signaling in the response to alcohol. Also discussed are observations in Drosophila that show how TLR signaling pathways can be co-opted by the nervous system and potentially shape behavior to a far greater extent and in ways different than generally recognized. For example, in Drosophila, TLRs substitute for neurotrophin receptors and an NF-κB at the end of a TLR pathway influences alcohol responsivity by acting non-genomically.
Neuroscience Insights · 2021-01-01 · 2 citations
reviewOpen access1st authorCorrespondingIntraspecies aggression is commonly focused on securing reproductive resources such as food, territory, and mates, and it is often males who do the fighting. In humans, individual acts of overt physical aggression seem maladaptive and probably represent dysregulation of the pathways underlying aggression. Such acts are often associated with ethanol consumption. The Drosophila melanogaster model system, which has long been used to study how ethanol affects the nervous system and behavior, has also been used to study the molecular origins of aggression. In addition, ethanol-induced aggression has been demonstrated in flies. Recent publications show that ethanol stimulates Drosophila aggression in 2 ways: the odor of ethanol and the consumption of ethanol both make males more aggressive. These ethanol effects occur at concentrations that flies likely experience in the wild. A picture emerges of males arriving on their preferred reproductive site—fermenting plant matter—and being stimulated by ethanol to fight harder to secure the site for their own use. Fly fighting assays appear to be a suitable bioassay for studying how low doses of ethanol reshape neural signaling.
Alcohol‐induced aggression in Drosophila
Addiction Biology · 2021 · 13 citations
Senior authorCorresponding- Medicine
- Psychology
- Biology
Alcohol-induced aggression is a destructive and widespread phenomenon associated with violence and sexual assault. However, little is understood concerning its mechanistic origin. We have developed a Drosophila melanogaster model to genetically dissect and understand the phenomenon of sexually dimorphic alcohol-induced aggression. Males with blood alcohol levels of 0.04-mg/ml BAC were less aggressive than alcohol-naive males, but when the BAC had dropped to ~0.015 mg/ml, the alcohol-treated males showed an increase in aggression toward other males. This aggression-promoting treatment is referred to as the post-ethanol aggression (PEA) treatment. Females do not show increased aggression after the same treatment. PEA-treated males also spend less time courting and attempt to copulate earlier than alcohol-naive flies. PEA treatment induces expression of the FruM transcription factor (encoded by a male-specific transcript from the fruitless gene), whereas sedating doses of alcohol reduce FruM expression and reduce male aggression. Transgenic suppression of FruM induction also prevents alcohol-induced aggression. In male flies, alcohol-induced aggression is dependent on the male isoform of the fruitless transcription factor (FruM). Low-dose alcohol induces FruM expression and promotes aggression, whereas higher doses of alcohol suppress FruM and suppress aggression.
Author response for "Alcohol-induced Aggression"
2021-11-01
peer-reviewOpen access1st authorCorrespondingAuthor response: Alcohol potentiates a pheromone signal in flies
2020-08-28
peer-reviewOpen accessSenior authorFor Drosophila melanogaster, the scent of alcohol—normally associated with preferred egg-laying sites—potentiates a male pheromone signal, thereby increasing the aggressive competition between males for the reproductive resource.
Alcohol potentiates a pheromone signal in flies
eLife · 2020 · 9 citations
Senior authorCorresponding- Biology
- Zoology
- Neuroscience
on alcohol-containing food sources. Although fruit flies are a common laboratory model organism of choice, there is relatively little understood about the ethological relationship between flies and ethanol. In this study, we find that when male flies inhabit ethanol-containing food substrates they become more aggressive. We identify a possible mechanism for this behavior. The odor of ethanol potentiates the activity of sensory neurons in response to an aggression-promoting pheromone. Finally, we observed that the odor of ethanol also promotes attraction to a food-related citrus odor. Understanding how flies interact with the complex natural environment they inhabit can provide valuable insight into how different natural stimuli are integrated to promote fundamental behaviors.
Recent grants
Homeostatic Regulation of Neuronal Ion Channel Expression
NSF · $391k · 2007–2011
NIH · $701k · 2011
Epigenetic dissection of functional ethanol tolerance and dependence
NIH · $338k · 2008–2019
Epigenetic dissection of functional ethanol tolerance and dependence
NIH · $3.0M · 2008–2022
NIH · $443k · 2005
Frequent coauthors
- 25 shared
Anita K. Hopper
- 21 shared
Alfredo Ghezzi
University of Puerto Rico at Río Piedras
- 12 shared
Harish R. Krishnan
University of Illinois Chicago
- 10 shared
Sukant Khurana
- 9 shared
Annie Park
University of Oxford
- 9 shared
Brooks G. Robinson
Oregon Health & Science University
- 8 shared
Kuei-Shu Tung
National Taiwan University
- 8 shared
H M Traglia
Pennsylvania State University
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