Functional Synergy between Cholecystokinin Receptors CCKAR and CCKBR in Mammalian Brain Development

Nishimura, Sadako; Bilgüvar, Kaya; Ishigame, Keiko; Šestan, Nenad; Günel, Murat; Louvi, Angeliki

doi:10.1371/journal.pone.0124295

Cited by 35 publications

(28 citation statements)

References 131 publications

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“…CCK1R in nodose and dorsal root ganglia are known to play vital roles in satiety and other peripheral sensations ( Broberger et al, 2001 ; Li et al, 2011 ; Kaczynska and Szereda-Przestaszewska, 2015 ). Highly localized CCK1R expression in the mouse hippocampus and defined extracortical sites are also well-recognized ( Nishimura et al, 2015 ). Third ventricular ependymal cell CCK1R is known to be important for infant mouse satiety ( Ozaki et al, 2013 ).…”

Section: Discussionmentioning

confidence: 99%

Cholecystokinin 1 Receptor – A Unique G Protein-Coupled Receptor Activated by Singlet Oxygen (GPCR-ABSO)

Jiang

et al. 2018

Front. Physiol.

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Plasma membrane-delimited generation of singlet oxygen by photodynamic action with photosensitizer sulfonated aluminum phthalocyanine (SALPC) activates cholecystokinin 1 receptor (CCK1R) in pancreatic acini. Whether CCK1R retains such photooxidative singlet oxygen activation properties in other environments is not known. Genetically encoded protein photosensitizers KillerRed or mini singlet oxygen generator (miniSOG) were expressed in pancreatic acinar tumor cell line AR4-2J, CCK1R, KillerRed or miniSOG were expressed in HEK293 or CHO-K1 cells. Cold light irradiation (87 mW⋅cm-2) was applied to photosensitizer-expressing cells to examine photodynamic activation of CCK1R by Fura-2 fluorescent calcium imaging. When CCK1R was transduced into HEK293 cells which lack endogenous CCK1R, photodynamic action with SALPC was found to activate CCK1R in CCK1R-HEK293 cells. When KillerRed or miniSOG were transduced into AR4-2J which expresses endogenous CCK1R, KillerRed or miniSOG photodynamic action at the plasma membrane also activated CCK1R. When fused KillerRed-CCK1R was transduced into CHO-K1 cells, light irradiation activated the fused CCK1R leading to calcium oscillations. Therefore KillerRed either expressed independently, or fused with CCK1R can both activate CCK1R photodynamically. It is concluded that photodynamic singlet oxygen activation is an intrinsic property of CCK1R, independent of photosensitizer used, or CCK1R-expressing cell types. Photodynamic singlet oxygen CCK1R activation after transduction of genetically encoded photosensitizer in situ may provide a convenient way to verify intrinsic physiological functions of CCK1R in multiple CCK1R-expressing cells and tissues, or to actuate CCK1R function in CCK1R-expressing and non-expressing cell types after transduction with fused KillerRed-CCK1R.

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Section: Discussionmentioning

confidence: 99%

Cholecystokinin 1 Receptor – A Unique G Protein-Coupled Receptor Activated by Singlet Oxygen (GPCR-ABSO)

Jiang

et al. 2018

Front. Physiol.

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“…It has been demonstrated as a central regulator of neuronal circuits. It plays vital roles in the gastrointestinal system, satiation, memory, anxiety-related behaviors, and other neuropsychiatric disorders [Lee and Soltesz, 2011;Zwanzger et al, 2012;Nishimura et al, 2015;Washington et al, 2016]. Finally, we identified LGI2 (OMIM 608301) as another candidate gene.…”

Section: Discussionmentioning

confidence: 99%

A Rare de novo Interstitial Duplication at 4p15.2 in a Boy with Severe Congenital Heart Defects, Limb Anomalies, Hypogonadism, and Global Developmental Delay

Liang

Xie²,

Shen³

et al. 2016

Cytogenet Genome Res

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Proximal 4p deletion syndrome is a relatively rare genetic condition characterized by dysmorphic facial features, limb anomalies, minor congenital heart defects, hypogonadism, cafe-au-lait spots, developmental delay, tall and thin habitus, and intellectual disability. At present, over 20 cases of this syndrome have been published. However, duplication of the same region in proximal 4p has never been reported. Here, we describe a 2-year-5-month-old boy with severe congenital heart defects, limb anomalies, hypogonadism, distinctive facial features, pre- and postnatal developmental delay, and mild cognitive impairments. A de novo 4.5-Mb interstitial duplication at 4p15.2p15.1 was detected by chromosomal microarray analysis. Next-generation sequencing was employed and confirmed the duplication, but revealed no additional pathogenic variants. Several candidate genes in this interval responsible for the complex clinical phenotype were identified, such as RBPJ, STIM2, CCKAR, and LGI2. The results suggest a novel contiguous gene duplication syndrome.

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“…To create a thalamusspecific postnatal knockout of Tcf7l2 we first crossed Tcf7l2 +/tm1a mice with transgenic animals that expressed flippase and then with mice that expressed CRE recombinase from the Cholecystokinin (Cck) gene promoter. Cck is upregulated postnatally and is expressed specifically in the thalamus and pallium (Allen Brain Atlas, 2011;Nishimura et al, 2015). In the resulting Cck Cre :Tcf7l2 fl/fl mice, TCF7L2 was absent in most thalamic nuclei in adult, but was maintained in the medial habenula ( Fig.…”

Section: Generation Of Mice With the Complete And Conditional Knockoumentioning

confidence: 99%

TCF7L2 regulates postmitotic differentiation programs and excitability patterns in the thalamus

Lipiec

Koziński

Zajkowski

et al. 2019

Preprint

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StatementThe study describes a role of TCF7L2 in neuronal differentiation of thalamic glutamatergic neurons at two developmental stages, highlighting its involvement in the postnatal establishment of critical thalamic electrophysiological features. AbstractNeuronal phenotypes are controlled by terminal selector transcription factors in invertebrates, but few examples of such regulators have been provided in vertebrates. TCF7L2 has been identified as a regulator of efferent outgrowth in the thalamus and habenula. We used a complete and conditional knockout of Tcf7l2 in mice to investigate the hypothesis that TCF7L2 plays a dual role in thalamic neuron differentiation and functions as a terminal selector. Connectivity and cell clustering was disrupted in the thalamo-habenular region in Tcf7l2 -/embryos. The expression of subregional thalamic and habenular transcription factors was lost and region-specific cell migration and axon guidance genes were downregulated. In mice with postnatal Tcf7l2 knockout, the induction of genes that confer terminal electrophysiological features of thalamic neurons was impaired. Many of these genes proved to be TCF7L2 direct targets. The role of TCF7L2 in thalamic terminal selection was functionally confirmed by impaired firing modes in thalamic neurons in the mutant mice.These data corroborate the existence of master regulators in the vertebrate brain that maintain regional transcriptional network, control stage-specific genetic programs and induce terminal selection.of the mice colony, and Kacper Posyniak for assistance with sample staining and acquisition.

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Functional Synergy between Cholecystokinin Receptors CCKAR and CCKBR in Mammalian Brain Development

Cited by 35 publications

References 131 publications

Cholecystokinin 1 Receptor – A Unique G Protein-Coupled Receptor Activated by Singlet Oxygen (GPCR-ABSO)

Cholecystokinin 1 Receptor – A Unique G Protein-Coupled Receptor Activated by Singlet Oxygen (GPCR-ABSO)

A Rare de novo Interstitial Duplication at 4p15.2 in a Boy with Severe Congenital Heart Defects, Limb Anomalies, Hypogonadism, and Global Developmental Delay

TCF7L2 regulates postmitotic differentiation programs and excitability patterns in the thalamus

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