| First Author | Mogul AS | Year | 2021 |
| Journal | eNeuro | PubMed ID | 34326065 |
| Mgi Jnum | J:308449 | Mgi Id | MGI:6729657 |
| Doi | 10.1523/ENEURO.0252-21.2021 | Citation | Mogul AS, et al. (2021) Cre recombinase driver mice reveal lineage-dependent and -independent expression of Brs3 in the mouse brain. eNeuro :ENEURO.0252-21.2021 |
| abstractText | Bombesin receptor subtype-3 (BRS3) is an orphan receptor that regulates energy homeostasis. We compared Brs3 driver mice with constitutive or inducible Cre recombinase activity. The constitutive BRS3-Cre mice show reporter signal (Cre-dependent tdTomato) in the adult brain due to lineage tracing in the dentate gyrus, striatal patches, and indusium griseum, in addition to sites previously identified in the inducible BRS3-Cre mice (including hypothalamic and amygdala subregions, and parabrachial nucleus). We detected Brs3 reporter expression in the dentate gyrus at day 23 but not at postnatal day one or five months of age. Hypothalamic sites expressed reporter at all three time points, and striatal patches expressed Brs3 reporter at one day but not five months. Parabrachial nucleus Brs3 neurons project to the preoptic area, hypothalamus, amygdala, and thalamus. Both Cre recombinase insertions reduced Brs3 mRNA levels and BRS3 function, causing obesity phenotypes of different severity. These results demonstrate that driver mice should be characterized phenotypically and illustrate the need for knock-in strategies with less effect on the endogenous gene.Significance StatementBombesin receptor subtype-3 (BRS3) expression is a marker for selected neurons that regulate body temperature and energy metabolism, among other functions. BRS3-Cre recombinase driver mice allow investigation of these neurons, demonstrating discrete populations with stable (including hypothalamic and amygdala subregions, parabrachial nucleus) and with developmentally transient expression (dentate gyrus, striatal patches). These mice also illustrate the need for knock-in strategies having less effect proper expression of the endogenous gene. |
