Trithorax regulates systemic signaling during drosophila imaginal disc regeneration

Andrea Skinner, Sumbul Jawed Khan, Rachel K. Smith-Bolton

Research output: Contribution to journalArticlepeer-review


Although tissue regeneration has been studied in a variety of organisms, from Hydra to humans, many of the genes that regulate the ability of each animal to regenerate remain unknown. The larval imaginal discs of the genetically tractable model organism Drosophila melanogaster have complex patterning, wellcharacterized development and a high regenerative capacity, and are thus an excellent model system for studying mechanisms that regulate regeneration. To identify genes that are important for wound healing and tissue repair, we have carried out a genetic screen for mutations that impair regeneration in the wing imaginal disc. Through this screen we identified the chromatin-modification gene trithorax as a key regeneration gene. Here we show that animals heterozygous for trithorax are unable to maintain activation of a developmental checkpoint that allows regeneration to occur. This defect is likely to be caused by abnormally high expression of puckered, a negative regulator of Jun N-terminal kinase (JNK) signaling, at the wound site. Insufficient JNK signaling leads to insufficient expression of an insulin-like peptide, dILP8, which is required for the developmental checkpoint. Thus, trithorax regulates regeneration signaling and capacity.

Original languageEnglish (US)
Pages (from-to)3500-3511
Number of pages12
JournalDevelopment (Cambridge)
Issue number20
StatePublished - Oct 15 2015


  • Chromatin
  • JNK signaling
  • Regeneration

ASJC Scopus subject areas

  • Molecular Biology
  • Developmental Biology


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