The genomic response of the Drosophila embryo to JNK signaling

Dev Cell. 2001 Oct;1(4):579-86. doi: 10.1016/s1534-5807(01)00045-4.

Abstract

During Drosophila development, the Jun N-terminal kinase signal transduction pathway regulates morphogenetic tissue closure movements that involve cell shape changes and reorganization of the actin cytoskeleton. We analyzed the genome-wide transcriptional response to activation of the JNK pathway in the Drosophila embryo by serial analysis of gene expression (SAGE) and identified loci encoding cell adhesion molecules and cytoskeletal regulators as JNK responsive genes. The role of one of the upregulated genes, chickadee (chic), encoding a Drosophila profilin, in embryogenesis was analyzed genetically. chic-deficient embryos fail to execute the JNK-mediated cytoskeletal rearrangements during dorsal closure. This study demonstrates a transcriptional mechanism of cytoskeletal regulation and establishes SAGE as an advantageous approach for genomic experiments in the fruitfly.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Actins / metabolism
  • Animals
  • Cell Adhesion / physiology
  • Contractile Proteins*
  • Cytoskeleton / metabolism
  • Drosophila Proteins
  • Drosophila melanogaster / embryology*
  • Embryo, Nonmammalian / embryology
  • Gene Expression Regulation, Developmental
  • JNK Mitogen-Activated Protein Kinases*
  • MAP Kinase Kinase 4
  • Microfilament Proteins / genetics
  • Microfilament Proteins / metabolism
  • Mitogen-Activated Protein Kinase Kinases / genetics
  • Mitogen-Activated Protein Kinase Kinases / metabolism*
  • Profilins
  • Signal Transduction / genetics*
  • Transcription, Genetic / physiology

Substances

  • Actins
  • Contractile Proteins
  • Drosophila Proteins
  • Microfilament Proteins
  • Profilins
  • chic protein, Drosophila
  • JNK Mitogen-Activated Protein Kinases
  • MAP Kinase Kinase 4
  • Mitogen-Activated Protein Kinase Kinases