ArticlePLoS genetics2016
The Drosophila ETV5 Homologue Ets96B: Molecular Link between Obesity and Bipolar Disorder.
Article in PLoS genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 26 citations in OpenAlex.
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- MIGGRI: A multi-instance graph neural network model for inferring gene regulatory networks for Drosophila from spatial expression images.PLoS computational biology · 2023Article
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- Genetic Associations with Weight Gain among South Africans who Initiated Dolutegravir-Containing and Tenofovir-Containing Regimens.Journal of acquired immune deficiency syndromes (1999) · 2021Article
- Transient Administration of Dopaminergic Precursor Causes Inheritable Overfeeding Behavior in YoungBrain sciences · 2020Article
- Exposure to the environmental pollutant bisphenol A diglycidyl ether (BADGE) causes cell over-proliferation in Drosophila.Environmental science and pollution research international · 2020Article
- Shared Genetic Loci Between Body Mass Index and Major Psychiatric Disorders: A Genome-wide Association Study.JAMA psychiatry · 2020Article
- CCAP regulates feeding behavior via the NPF pathway inProceedings of the National Academy of Sciences of the United States of America · 2020Article
- Human iPSC-Derived Neuronal Cells FromFrontiers in neuroscience · 2020Article
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- Evidence that genes involved in hedgehog signaling are associated with both bipolar disorder and high BMI.Translational psychiatry · 2019Article
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Several reports suggest obesity and bipolar disorder (BD) share some physiological and behavioural similarities. For instance, obese individuals are more impulsive and have heightened reward responsiveness, phenotypes associated with BD, while bipolar patients become obese at a higher rate and earlier age than people without BD; however, the molecular mechanisms of such an association remain obscure. Here we demonstrate, using whole transcriptome analysis, that Drosophila Ets96B, homologue of obesity-linked gene ETV5, regulates cellular systems associated with obesity and BD. Consistent with a role in obesity and BD, loss of nervous system Ets96B during development increases triacylglyceride concentration, while inducing a heightened startle-response, as well as increasing hyperactivity and reducing sleep. Of notable interest, mouse Etv5 and Drosophila Ets96B are expressed in dopaminergic-rich regions, and loss of Ets96B specifically in dopaminergic neurons recapitulates the metabolic and behavioural phenotypes. Moreover, our data indicate Ets96B inhibits dopaminergic-specific neuroprotective systems. Additionally, we reveal that multiple SNPs in human ETV5 link to body mass index (BMI) and BD, providing further evidence for ETV5 as an important and novel molecular intermediate between obesity and BD. We identify a novel molecular link between obesity and bipolar disorder. The Drosophila ETV5 homologue Ets96B regulates the expression of cellular systems with links to obesity and behaviour, including the expression of a conserved endoplasmic reticulum molecular chaperone complex known to be neuroprotective. Finally, a connection between the obesity-linked gene ETV5 and bipolar disorder emphasizes a functional relationship between obesity and BD at the molecular level.
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