title: Expression of p73 and Reelin in the developing human cortex.
abstract: Cajal-Retzius (CR) cells of the developing neocortex secrete Reelin (Reln), a glycoprotein involved in neuronal migration. CR cells selectively express p73, a p53 family member implicated in cell survival and apoptosis. Immunocytochemistry in prenatal human telencephalon reveals a complex sequence of migration waves of p73- and Reln-immunoreactive (IR) neurons into the cortical marginal zone (MZ). At early preplate stages, p73/Reln-IR cells arise in distinct sectors of the telencephalon, including cortical primordium and ganglionic eminences. After the appearance of the cortical plate, further p73/Reln-IR cells originate in the medial periolfactory forebrain. In addition, p73 marks a novel cell population that appears at the choroid-cortical junction or cortical hem before the emergence of the dorsal hippocampus. A pronounced mediolateral gradient in the density of p73/Reln-IR neurons in the neocortical MZ at 8 gestational weeks suggests that a subset of CR cells migrate tangentially from cortical hem and taenia tecta into neocortical territory. This hypothesis is supported by the absence of p73-transcripts in prospective neocortex of p73-/-mice at embryonic day 12 (E12), whereas they are present in cortical hem and taenia tecta. In the p73-/- preplate, Reln is faintly expressed in a calretinin-positive cell population, not present in this form in the E12 wild-type cortex. At P2, Reln-IR CR cells are undetectable in the p73-/- cortex, whereas Reln-expression in interneurons is unchanged. Our results point to a close association between p73 and Reln in CR cells of the developing neocortex, with a partial dissociation in early preplate and basal telencephalon, and to a p73-mediated role of the cortical hem in neocortical development.
authors.affiliation: Department of Anatomy, University La Laguna, 38071 Tenerife, Spain. gmeyer@ull.es
authors.forename: Gundela
authors.initials: G
authors.lastname: Meyer
authors.forename: Carlos Gustavo
authors.initials: CG
authors.lastname: Perez-Garcia
authors.forename: Hajnalka
authors.initials: H
authors.lastname: Abraham
authors.forename: Daniel
authors.initials: D
authors.lastname: Caput
mesh_terms: D000818:Animals; D064032:Calbindin 2; D015816:Cell Adhesion Molecules, Neuronal / Q000276:immunology / Q000378:metabolism*; D004268:DNA-Binding Proteins / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D004848:Epithelium / Q000196:embryology / Q000378:metabolism; D016326:Extracellular Matrix Proteins / Q000276:immunology / Q000378:metabolism*; D015870:Gene Expression; D016147:Genes, Tumor Suppressor; D006801:Humans; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D019579:Neocortex / Q000166:cytology / Q000196:embryology* / Q000378:metabolism*; D009419:Nerve Tissue Proteins; D009687:Nuclear Proteins / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D016548:Prosencephalon / Q000166:cytology / Q000196:embryology / Q000378:metabolism; D012333:RNA, Messenger / Q000096:biosynthesis; D000091042:Reelin Protein; D064030:S100 Calcium Binding Protein G / Q000378:metabolism; D012697:Serine Endopeptidases; D013687:Telencephalon / Q000166:cytology / Q000196:embryology / Q000378:metabolism; D014158:Transcription, Genetic; D000072160:Tumor Protein p73; D025521:Tumor Suppressor Proteins
chemical_list: C576764:CALB2 protein, human; C576511:Calb2 protein, mouse; D064032:Calbindin 2; D015816:Cell Adhesion Molecules, Neuronal; D004268:DNA-Binding Proteins; D016326:Extracellular Matrix Proteins; D009419:Nerve Tissue Proteins; D009687:Nuclear Proteins; D012333:RNA, Messenger; D000091042:Reelin Protein; D064030:S100 Calcium Binding Protein G; C000606460:TP73 protein, human; C000606368:Trp73 protein, mouse; D000072160:Tumor Protein p73; D025521:Tumor Suppressor Proteins; C000717127:RELN protein, human; C000717128:Reln protein, mouse; D012697:Serine Endopeptidases