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Inhibition of SoxB2 or HDACs suppresses Hydractinia head regeneration by affecting blastema formation

Regeneration has long been known to occur in the cnidarian Hydractinia. This process refers to its ability to regrow structures, i.e a head, lost by injury, a phenomenon that depends on the migration of proliferative cells to the site of injury, and the formation of a blastema, a mass of undifferent...

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Detalles Bibliográficos
Autores principales: Flici, Hakima, Frank, Uri
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6067865/
https://www.ncbi.nlm.nih.gov/pubmed/30083285
http://dx.doi.org/10.1080/19420889.2018.1450032
Descripción
Sumario:Regeneration has long been known to occur in the cnidarian Hydractinia. This process refers to its ability to regrow structures, i.e a head, lost by injury, a phenomenon that depends on the migration of proliferative cells to the site of injury, and the formation of a blastema, a mass of undifferentiated cells that will restore the missing head tissues. In our study, we showed that members of SoxB transcription factors and HDACs are involved in the regulation of Hydractinia neurogenesis in tissue homeostasis and regeneration. Particularly, we revealed that knockdown of SoxB2 or Hdac2 (a class I HDAC) knockdown, or inhibition of HDAC activity, suppress head regeneration. Here, we show that SoxB2 knockdown, or the inhibition of HDACs activity by TSA, a HDAC Class I and II inhibitor, interfere with head regeneration by affecting the migration of proliferative cells and the formation of a proliferative blastema.