Taranis Protects Regenerating Tissue from Fate Changes Induced by the Wound Response in Drosophila

• Regenerative signaling in Drosophila can induce aberrant cell fate changes
• These fate changes are caused by JNK-induced misregulation of engrailed
• Taranis stabilizes engrailed expression and prevents these cell fate changes
• Taranis is not required for these cell fates during normal development

SummaryRegenerating tissue must replace lost structures with cells of the proper identity and function. How regenerating tissue establishes or maintains correct cell fates during regrowth is an open question. We have identified a gene, taranis, that is essential for maintaining proper cell fate in damaged and regenerating Drosophila wing imaginal discs but that is dispensable for these fates in normal wing development. In regenerating tissue with reduced levels of Taranis, expression of the posterior selector gene engrailed is silenced through an autoregulatory silencing mechanism that requires the PRC1 component polyhomeotic, resulting in a transformation of posterior tissue into anterior tissue late in regeneration. An essential component of the wound response, JNK signaling, induces this misregulation of engrailed expression. Taranis can suppress these JNK-induced cell fate changes without interfering with JNK signaling activity. Thus, taranis protects regenerating tissue from deleterious side effects of wound healing and regeneration.

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