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Cajal–Retzius (CR) cells are essential for cortical development and lamination. These pioneer neurons arise from distinct progenitor sources, including the cortical hem and the ventral pallium at pallium–subpallium boundary (PSB). CXCR4, the canonical receptor for the chemokine CXCL12, controls the superficial location of hem-derived CR cells. However, recent studies showed that CXCR7, a second CXCL12 receptor, is also expressed in CR cells at early developmental stages. We thus investigated the role of CXCR7 during CR cell development using multiple loss-of-function approaches.  Cxcr7  gene inactivation led to aberrant localization of Reelin-positive cells within the pallium. In addition,  Cxcr7  −/−  mice were characterized by significant accumulation of ectopic CR cells in the lateral part of the dorsal pallium compared with  Cxcr4  knockout mice. Loss-of-function approaches, using either gene targeting or pharmacological receptor inhibition, reveal that CXCR7 and CXCR4 act both in CR positioning. Finally, conditional  Cxcr7  deletion in cells derived from  Dbx1 -expressing progenitors indicates an essential role of CXCR7 in controlling the positioning of a subpopulation of PSB-derived CR cells. Our data demonstrate that CXCR7 has a role in the positioning of hem and PSB-derived CR cells, CXCL12 regulating CR cell subpial localization through the combined action of CXCR4 and CXCR7.

CXCR7 Receptor Controls the Maintenance of Subpial Positioning of Cajal–Retzius Cells