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Cited by 26Eating Disorders and BehaviorsRegulation of Appetite and ObesityGenetics and Neurodevelopmental Disorders

Cyfip1 Haploinsufficiency Increases Compulsive-Like Behavior and Modulates Palatable Food Intake in Mice: Dependence on Cyfip2 Genetic Background, Parent-of Origin, and Sex

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Babbs, Richard K, Beierle, Jacob A, Ruan, Qiu T, Kelliher, Julia C, Chen, Melanie M, Feng, Ashley X, Kirkpatrick, Stacey L, Benitez, Fabiola A +6 more·2019·G3 Genes|Genomes|Genetics
DOI 10.1534/g3.119.400470PMC PMC6723122

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Abstract

Binge eating (BE) is a heritable trait associated with eating disorders and involves episodes of rapid, large amounts of food consumption. We previously identified cytoplasmic FMR1-interacting protein 2 (Cyfip2) as a genetic factor underlying compulsive-like BE in mice. CYFIP2 is a homolog of CYFIP1 which is one of four paternally-deleted genes in patients with Type I Prader-Willi Syndrome (PWS), a neurodevelopmental disorder whereby 70% of cases involve paternal 15q11-q13 deletion. PWS symptoms include hyperphagia, obesity (if untreated), cognitive deficits, and obsessive-compulsive behaviors. We tested whether Cyfip1 haploinsufficiency (+/−) would enhance compulsive-like behavior and palatable food (PF) intake in a parental origin- and sex-dependent manner on two Cyfip2 genetic backgrounds, including the BE-prone C57BL/6N (Cyfip2N/N) background and the BE-resistant C57BL/6J (Cyfip2J/J) background. Cyfip1+/− mice showed increased compulsive-like behavior on both backgrounds and increased PF intake on the Cyfip2N/N background. In contrast, maternal Cyfip1 haploinsufficiency on the BE-resistant Cyfip2J/J background induced a robust escalation in PF intake in wild-type Cyfip1J/J males while having no effect in Cyfip1J/- males. Notably, induction of behavioral phenotypes in wild-type males following maternal Fmr1+/− has previously been reported. In the hypothalamus, there was a paternally-enhanced reduction in CYFIP1 protein whereas in the nucleus accumbens, there was a maternally-enhanced reduction in CYFIP1 protein. Nochange in FMR1 protein (FMRP) was observed in Cyfip1+/− mice, regardless of parental origin. To summarize, Cyfip1 haploinsufficiency increased compulsive-like behavior and induced genetic background-dependent, sex-dependent, and parent-of-origin-dependent effects on PF consumption and CYFIP1 expression that could have relevance for neurodevelopmental and neuropsychiatric disorders.

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  • Because CYFIP1 is deleted or imprinted in patients with type I Prader-Willi syndrome, an NDD defined by extreme hyperphagia and a hyperresponsive reward system to food-associated cues, the shared biological functions of CYFIP1 and 2 might be associated with maladaptive feeding in humans.

    “Because CYFIP1 is deleted or imprinted in patients with type I Prader–Willi syndrome, an NDD defined by extreme hyperphagia and a hyperresponsive reward system to food-associated cues, the shared biological functions of CYFIP1 and 2 might be associated with maladaptive feeding in humans177,178.”

    From The WAVE complex in developmental and adulthood brain disorders (2025) · cites this paper as [178]

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  • Maternally inherited Cyfip1 haploinsufficient mice have reduced Cyfip1 gene expression in the nucleus accumbens and an increase in compulsive-like behaviours.

    “In animals, Babbs et al. [75] found that maternally inherited Cyfip1 haploinsufficient mice have reduced Cyfip1 gene expression in the nucleus accumbens and an increase in compulsive-like behaviours.”

    From Linking haploinsufficiency of the autism- and schizophrenia-associated gene Cyfip1 with striatal-limbic-cortical network dysfunction and cognitive inflexibility (2024) · cites this paper as [75]

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Authors
Babbs, R. K., Beierle, J. A., Ruan, Q. T., Kelliher, J. C., Chen, M. M., Feng, A. X., Kirkpatrick, S. L., Benitez, F. A., Rodriguez, F. A., Pierre, J. J., Anandakumar, J., Kumar, V., Mulligan, M. K., & Bryant, C. D.
Affiliations
  • Laboratory of Addiction Genetics, Department of Pharmacology and Experimental Therapeutics and Psychiatry
  • Boston University (US)
  • Jackson Laboratory (US)
  • University of Tennessee Health Science Center (US)
Corresponding author
Bryant, Camron D
ORCID
Venue
G3 Genes|Genomes|Genetics
Publisher
Oxford University Press (OUP)
Published
2019-09-01
Volume
9
Issue
9
Pages
3009-3022
ISSN
2160-1836 (ISSN-L)
DOI
10.1534/g3.119.400470
PMC
PMC6723122
OpenAlex
W2962857843
Cited by
26
References
70
Citations by year
2026: 2 · 2025: 3 · 2024: 3 · 2023: 4 · 2022: 3 · 2021: 4 · 2020: 5 · 2019: 2
FWCI
4.09
Type
journal article
Language
en
Open access
Licence
Locations
  • G3 Genes Genomes Genetics (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
  • The Mouseion at the JAXlibrary (Jackson Laboratory) (submittedVersion)
Funders
  • Wellcome Trust
  • National Institutes of Health (1s10od023663-01)
  • National Institute on Drug Abuse (U01DA041668, R01DA039168, R21DA038738)
  • National Institute of General Medical Sciences (T32GM008541)
Topics
  • Social Sciences › Psychology › Clinical Psychology › Eating Disorders and Behaviors
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
Keywords
CYFIP1, haploinsufficiency, CYFIP2, binge eating, compulsive-like behavior, palatable food intake, parent-of-origin effects, sex differences, Prader-Willi syndrome, 15q11-q13 deletion, FMRP, hypothalamus, nucleus accumbens, genetic background, compulsive eating
MeSH terms
Animals, Antigens, Neoplasm, Appetite Regulation, Behavior, Animal, Compulsive Behavior, Female, Hypothalamus, Male, Mice, Inbred C57BL, Proteins, Reward, Mice, Knockout, Intracellular Signaling Peptides and Proteins, Adaptor Proteins, Signal Transducing, Fragile X Messenger Ribonucleoprotein 1, Haploinsufficiency, Intrinsically Disordered Proteins

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