Slit signaling promotes the terminal asymmetric division of neural precursor cells in the Drosophila CNS

B. Mehta, K. M. Bhat

Research output: Contribution to journalArticle

21 Citations (Scopus)

Abstract

The bipotential Ganglion Mother Cells, or GMCs, in the Drosophila CNS asymmetrically divide to generate two distinct post-mitotic neurons. Here, we show that the midline repellent Slit (Sli), via its receptor Roundabout (Robo), promotes the terminal asymmetric division of GMCs. In GMC-1 of the RP2/sib lineage, Slit promotes asymmetric division by down regulating two POU proteins, Nubbin and Mitimere. The down regulation of these proteins allows the asymmetric localization of Inscuteable, leading to the asymmetric division of GMC-1. Consistent with this, over-expression of these POU genes in a late GMC-1 causes mis-localization of Insc and symmetric division of GMC-1 to generate two RP2s. Similarly, increasing the dosage of the two POU genes in sli mutant background enhances the penetrance of the RP2 lineage defects whereas reducing the dosage of the two genes reduces the penetrance of the phenotype. These results tie a cell-non-autonomous signaling pathway to the asymmetric division of precursor cells during neurogenesis.

Original languageEnglish (US)
Pages (from-to)3161-3168
Number of pages8
JournalDevelopment
Volume128
Issue number16
StatePublished - 2001
Externally publishedYes

Fingerprint

Penetrance
Drosophila
POU Domain Factors
Asymmetric Cell Division
Gene Dosage
Neurogenesis
Ganglia
Stem Cells
Down-Regulation
Phenotype
Gene Expression
Neurons
Genes
Proteins

Keywords

  • Asymmetric division
  • Cell signaling
  • Drosophila melanogaster
  • Ganglion mother cells
  • Neurogenesis
  • Roundabout
  • Slit

ASJC Scopus subject areas

  • Anatomy
  • Cell Biology

Cite this

Slit signaling promotes the terminal asymmetric division of neural precursor cells in the Drosophila CNS. / Mehta, B.; Bhat, K. M.

In: Development, Vol. 128, No. 16, 2001, p. 3161-3168.

Research output: Contribution to journalArticle

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