| First Author | Estivill-Torrús G | Year | 2008 |
| Journal | Cereb Cortex | Volume | 18 |
| Issue | 4 | Pages | 938-50 |
| PubMed ID | 17656621 | Mgi Jnum | J:174115 |
| Mgi Id | MGI:5051901 | Doi | 10.1093/cercor/bhm132 |
| Citation | Estivill-Torrus G, et al. (2008) Absence of LPA1 signaling results in defective cortical development. Cereb Cortex 18(4):938-50 |
| abstractText | Lysophosphatidic acid (LPA) is a simple phospholipid with extracellular signaling properties mediated by specific G protein-coupled receptors. At least 2 LPA receptors, LPA(1) and LPA(2), are expressed in the developing brain, the former enriched in the neurogenic ventricular zone (VZ), suggesting a normal role in neurogenesis. Despite numerous studies reporting the effects of exogenous LPA using in vitro neural models, the first LPA(1) loss-of-function mutants reported did not show gross cerebral cortical defects in the 50% that survived perinatal demise. Here, we report a role for LPA(1) in cortical neural precursors resulting from analysis of a variant of a previously characterized LPA(1)-null mutant that arose spontaneously during colony expansion. These LPA(1)-null mice, termed maLPA(1), exhibit almost complete perinatal viability and show a reduced VZ, altered neuronal markers, and increased cortical cell death that results in a loss of cortical layer cellularity in adults. These data support LPA(1) function in normal cortical development and suggest that the presence of genetic modifiers of LPA(1) influences cerebral cortical development. |
