An Evolutionarily Conserved SoxB-Hdac2 Crosstalk Regulates Neurogenesis in a Cnidarian

Cell Reports

R. Cathriona Millane¹  Hakima Flici¹  Uri Frank¹  Graham Govinden¹  Amy Houlihan¹  Andreas D. Baxevanis²  Sanbing Shen³  Stephanie D. Boomkamp³  Christine E. Schnitzler⁴ 

[1] Centre for Chromosome Biology (CCB), School of Natural Sciences, National University of Ireland, Galway H91 CF50, Ireland;Computational and Statistical Genomics Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892-8002, USA;Regenerative Medicine Institute (REMEDI), National University of Ireland, Galway, Galway H91 CF50, Ireland;Whitney Laboratory for Marine Bioscience, University of Florida, St. Augustine, FL 32080, USA;

关键词: nervous system;    regeneration;    transcription factor;    SoxB;    histone deacetylase;    Hdac2;    Hydractinia;    evolution;    cnidaria;    neurogenesis;   

DOI  :  10.1016/j.celrep.2017.01.019

来源: DOAJ

【 摘 要 】

SoxB transcription factors and histone deacetylases (HDACs) are each major players in the regulation of neurogenesis, but a functional link between them has not been previously demonstrated. Here, we show that SoxB2 and Hdac2 act together to regulate neurogenesis in the cnidarian Hydractinia echinata during tissue homeostasis and head regeneration. We find that misexpression of SoxB genes modifies the number of neural cells in all life stages and interferes with head regeneration. Hdac2 was co-expressed with SoxB2, and its downregulation phenocopied SoxB2 knockdown. We also show that SoxB2 and Hdac2 promote each other’s transcript levels, but Hdac2 counteracts this amplification cycle by deacetylating and destabilizing SoxB2 protein. Finally, we present evidence for conservation of these interactions in human neural progenitors. We hypothesize that crosstalk between SoxB transcription factors and Hdac2 is an ancient feature of metazoan neurogenesis and functions to stabilize the correct levels of these multifunctional proteins.

【 授权许可】

Unknown