Cytoplasmic FMR1-Interacting Protein 2 Is a Major Genetic Factor Underlying Binge Eating

Kirkpatrick, Stacey L; Goldberg, Lisa R.; Yazdani, Neema; Babbs, R.K.; Wu, Jiayi; Reed, Eric; Jenkins, D. Graham; Bolgioni, Amanda F.; Landaverde, Kelsey I.; Luttik, Kimberly; Mitchell, Karen S.; Kumar, Vivek; Johnson, W. Evan; Mulligan, Megan K.; Cottone, Pietro; Bryant, Camron D.

doi:10.1016/j.biopsych.2016.10.021

Cited by 71 publications

(165 citation statements)

References 74 publications

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“…Distinct floor texture squares on each side of the apparatus differentiated the two sides (Plaskolite Inc., Columbus, OH, USA). For SPF conditioning, a small, porcelain dish was secured to the floor texture via adhesive putty in the far corner of each side of the chamber (Kirkpatrick et al ., 2016). Experiments were recorded using a security camera system (Swann Communications, Melbourne, Australia) and used for tracking analysis (Anymaze, Stoelting, Wood Dale, IL, USA).…”

Section: Methodsmentioning

confidence: 99%

“…We recently described a procedure for assessing sweetened palatable food (SPF) consumption and CPP (SPF-CPP) (Kirkpatrick et al ., 2016). Briefly, we assessed mice for initial preference for the SPF-paired side on D1 and then trained mice for seven, 30-min SPF training sessions (D2,4,9,11,16,18,23) and six 30-min “No-SPF” training sessions (D3,5,10,12,17,19).…”

Section: Methodsmentioning

confidence: 99%

“…To account for individual and sex differences in body weight, we quantified SPF consumption as percent body weight. To investigate possible differences in escalation in SPF intake over time, regression analyses were conducted in GraphPad Prism 7.01 (GraphPad Software, La Jolla, CA, USA) as previously reported (Babbs et al ., 2013, Kirkpatrick et al ., 2016). …”

Section: Methodsmentioning

confidence: 99%

“…We collected striatum punches from naïve female and male Csnk1e KO and WT littermates (Kirkpatrick et al ., 2016, Yazdani et al ., 2015, Yazdani et al ., 2016). We habituated mice to the dissection room for at least 90-min prior to sacrifice and collected brain tissue between 1300 h and 1700 h. Brains were rapidly removed and sectioned with a brain matrix to obtain a 3 mm thick section from which a 2.5 mm diameter punch of the striatum was collected (dorsal striatum, Bregma 2.90 to − 0.10 mm, dorsal-ventral 2 - 4.5 mm).…”

Section: Methodsmentioning

confidence: 99%

“…Based on the proposed negative regulatory role for Csnk1e in the locomotor stimulant properties of drugs of abuse (Bryant et al ., 2009a, Bryant et al ., 2012), in the present study, we tested the hypothesis that Csnk1e negatively regulates opioid and psychostimulant reward as well as changes in the consummatory and rewarding behaviors induced by limited, intermittent access to sweetened palatable food ( SPF ) (Kirkpatrick et al ., 2016)– a naturally rewarding stimulus. Consumption of highly palatable foods induces the release of endogenous opioids (Difeliceantonio et al ., 2012, Nathan & Bullmore, 2009) and dopamine that activate the mesolimbic dopamine system (Bello & Hajnal, 2010) and reinforce eating behavior, leading to escalated consumption.…”

Section: Introductionmentioning

confidence: 99%

See 4 more Smart Citations

Casein kinase 1‐epsilon deletion increases mu opioid receptor‐dependent behaviors and binge eating1

Goldberg

Kirkpatrick

Yazdani

et al. 2017

Genes Brain and Behavior

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Genetic and pharmacological studies indicate that casein kinase-1 epsilon (Csnk1e) contributes to psychostimulant, opioid, and ethanol motivated behaviors. We previously used pharmacological inhibition to demonstrate that Csnk1e negatively regulates the locomotor stimulant properties of opioids and psychostimulants. Here, we tested the hypothesis that Csnk1e negatively regulates opioid and psychostimulant reward using genetic inhibition and the conditioned place preference assay in Csnk1e knockout mice. Similar to pharmacological inhibition, Csnk1e knockout mice showed enhanced opioid-induced locomotor activity with the mu opioid receptor agonist fentanyl (0.2 mg/kg i.p.) as well as enhanced sensitivity to low-dose fentanyl reward (0.05 mg/kg). Interestingly, female knockout mice also showed a markedly greater escalation in consumption of sweetened palatable food – a behavioral pattern consistent with binge eating that also depends on mu opioid receptor activation. No difference was observed in fentanyl analgesia in the 52.5°C hot plate assay (0–0.4 mg/kg), naloxone conditioned place aversion (4 mg/kg), or methamphetamine conditioned place preference (0–4 mg/kg). To identify molecular adaptations associated with increased drug and food behaviors in knockout mice, we completed transcriptome analysis via mRNA sequencing of the striatum. Enrichment analysis identified terms associated with myelination and axon guidance and pathway analysis identified a differentially expressed gene set predicted to be regulated by the Wnt signaling transcription factor, Tcf7l2. To summarize, Csnk1e deletion increased mu opioid receptor-dependent behaviors, supporting previous studies indicating an endogenous negative regulatory role of Csnk1e in opioid behavior.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Casein kinase 1‐epsilon deletion increases mu opioid receptor‐dependent behaviors and binge eating1

Goldberg

Kirkpatrick

Yazdani

et al. 2017

Genes Brain and Behavior

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Loss of cytoplasmic FMR1‐interacting protein 2 (CYFIP2) induces browning in 3T3‐L1 adipocytes via repression of GABA‐BR and activation of mTORC1

Manigandan

Yun

2022

J of Cellular Biochemistry

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Obesity and related metabolic disorders are epidemic diseases. Promoting thermogenesis and a functional increase in the browning of white adipocytes may counteract obesity. On the other hand, the molecular mechanism that regulates brown and beige fat-mediated thermogenesis is unclear. This article reports a molecular network led by cytoplasmic FMR1-interacting protein 2 (CYFIP2) that negatively regulates adipocyte browning in white adipocytes. Although the function of CYFIP2 in Fragile X Syndrome (FXS) and autism have been reported, its physiological roles in adipocytes remain elusive. Therefore, this study examined the physiological consequences of its deprivation in cultured 3T3-L1 white adipocytes using loss-of-function studies. Combined real-time quantitative reverse-transcription polymerase chain reaction and immunoblot analysis showed that the loss of CYFIP2 induces fat browning, as evidenced by the gene and protein expression levels of the brown fat-associated markers. A deficiency of CYFIP2 promoted mitochondrial biogenesis and significantly enhanced the expression of the core set beige fat-specific genes (Cd137, Cidea, Cited1, Tbx1, and Tmem26) and proteins (PGC-1α, PRDM16, and UCP1). In addition, a CYFIP2 deficiency promoted lipid catabolism and suppressed adipogenesis, lipogenesis, and autophagy. A mechanistic study showed that the loss of CYFIP2 induces browning in white adipocytes, independently via the activation of mTORC1 and suppression of the GABA-BR signaling pathway. The present data revealed a previously unidentified mechanism of CYFIP2 in the browning of white adipocytes and emphasized the potential of CYFIP2 as a pharmacotherapeutic target for treating obesity and other metabolic disorders.

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Adenosine‐to‐Inosine RNA Editing in Mouse and Human Brain Proteomes

et al. 2019

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Proteogenomics is based on the use of customized genome or RNA sequencing databases for interrogation of shotgun proteomics data in search for proteome‐level evidence of genome variations or RNA editing. In this work, the products of adenosine‐to‐inosine RNA editing in human and murine brain proteomes are identified using publicly available brain proteome LC‐MS/MS datasets and an RNA editome database compiled from several sources. After filtering of false‐positive results, 20 and 37 sites of editing in proteins belonging to 14 and 32 genes are identified for murine and human brain proteomes, respectively. Eight sites of editing identified with high spectral counts overlapped between human and mouse brain samples. Some of these sites have been previously reported using orthogonal methods, such as α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionic acid (AMPA) glutamate receptors, CYFIP2, coatomer alpha. Also, differential editing between neurons and microglia is demonstrated in this work for some of the proteins from primary murine brain cell cultures. Because many edited sites are still not characterized functionally at the protein level, the results provide a necessary background for their further analysis in normal and diseased cells and tissues using targeted proteomic approaches.

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Cytoplasmic FMR1-Interacting Protein 2 Is a Major Genetic Factor Underlying Binge Eating

Cited by 71 publications

References 74 publications

Casein kinase 1‐epsilon deletion increases mu opioid receptor‐dependent behaviors and binge eating1

Casein kinase 1‐epsilon deletion increases mu opioid receptor‐dependent behaviors and binge eating1

Loss of cytoplasmic FMR1‐interacting protein 2 (CYFIP2) induces browning in 3T3‐L1 adipocytes via repression of GABA‐BR and activation of mTORC1

Adenosine‐to‐Inosine RNA Editing in Mouse and Human Brain Proteomes

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