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Publication Detail
Pax6 is expressed in subsets of V0 and V2 interneurons in the ventral spinal cord in mice.
  • Publication Type:
    Journal article
  • Publication Sub Type:
    Journal Article
  • Authors:
    Panayiotou E, Panayi E, Lapathitis G, Francius C, Clotman F, Kessaris N, Richardson WD, Malas S
  • Publication date:
  • Pagination:
    328, 334
  • Journal:
    Gene Expr Patterns
  • Volume:
  • Issue:
  • Status:
  • Country:
  • PII:
  • Language:
  • Keywords:
    Pax6, V0 interneurons, V2 interneurons, Ventral spinal cord, Animals, Body Patterning, Cell Lineage, Eye Proteins, Female, GATA3 Transcription Factor, Gene Expression, Gene Expression Regulation, Developmental, Homeodomain Proteins, Interneurons, Male, Mice, Mice, Transgenic, Neural Stem Cells, PAX2 Transcription Factor, PAX6 Transcription Factor, Paired Box Transcription Factors, Receptors, Notch, Repressor Proteins, Signal Transduction, Spinal Cord
The embryonic spinal cord in mice is organized into eleven progenitor domains. Cells in each domain first produce neurons and then switch to specifying glia. Five of these domains known as p3, pMN, p2, p1 and p0 are located in the ventral spinal cord and each expresses a unique code of transcription factors (TFs) that define the molecular profile of progenitor cells. This code is largely responsible for determining the subtype specification of neurons generated from each domain. Pax6 codes for a homedomain-containing TF that plays a central role in defining the molecular boundaries between the two ventral-most domains, p3 and pMN. Using fate mapping and gene expression studies we show that PAX6, in addition to each patterning function, is expressed in a group of late born interneurons that derive from the p2 and p0 domains. The p2-derived neurons represent a subset of late born V2b interneurons and their specification depends on Notch signaling. The V0 neurons represent V0v ventral neurons expressing Pax2. Our data demonstrate that interneuron diversity in the ventral spinal cord is more complex than originally appreciated and point to the existence of additional mechanisms that determine interneuron diversity, particularly in the p2 domain.
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