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Background  Adult echinoderms can completely regenerate major parts of their central nervous system even after severe injuries. Even though this capacity has long been known, the molecular mechanisms that drive fast and complete regeneration in these animals have remained uninvestigated. The major obstacle for understanding these molecular pathways has been the lack of functional genomic studies on regenerating adult echinoderms.    Results  Here, we employ RNA interference-mediated gene knockdown to characterize the role of  Myc  during the early (first 48 hours) post-injury response in the radial nerve cord of the sea cucumber  Holothuria glaberrima . Our previous experiments identified  Myc  as the only pluripotency-associated factor, whose expression significantly increased in the wounded CNS. The specific function(s) of this gene, however, remained unknown. Here we demonstrate that knockdown of  Myc  inhibits dedifferentiation of radial glia and programmed cell death, the two most prominent cellular events that take place in the regenerating sea cucumber nervous system shortly after injury.    Conclusions  In this study, we show that  Myc  overexpression is required for proper dedifferentiation of radial glial cells and for triggering the programmed cell death in the vicinity of the injury.  Myc  is thus the first transcription factor, whose functional role has been experimentally established in echinoderm regeneration.    Electronic supplementary material  The online version of this article (doi:10.1186/s12861-015-0071-z) contains supplementary material, which is available to authorized users.

Myc regulates programmed cell death and radial glia dedifferentiation after neural injury in an echinoderm