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Protection or restoration of pancreatic β-cell mass as a therapeutic treatment for type 1 diabetes requires understanding of the mechanisms that drive the specification and development of pancreatic endocrine cells. Septins are filamentous small GTPases that function in the regulation of cell division, cytoskeletal organization and membrane remodeling, and are involved in various tissue-specific developmental processes. However, their role in pancreatic endocrine cell differentiation remains unknown. Here we show by functional manipulation techniques in transgenic zebrafish lines that suppression of  sept7b , the zebrafish ortholog of human  SEPT7 , profoundly increases the number of endocrine progenitors but limits their differentiation, leading to reduction in β- and α-cell mass. Furthermore, we discovered that  shh  ( sonic hedgehog ) expression in the endoderm, essential for the development of pancreatic progenitors of the dorsal pancreatic bud, is absent in larvae depleted of  sept7b . We also discovered that  sept7b  is important for the differentiation of ventral pancreatic bud-derived cells:  sept7b- depleted larvae exhibit downregulation of Notch receptors  notch1a  and  notch1b  and show precocious differentiation of  NeuroD -positive endocrine cells in the intrapancreatic duct and gut epithelium. Collectively, this study provides a novel insight into the development of pancreatic endocrine progenitors, revealing an essential role for  sept7b  in endocrine progenitor differentiation.

sept7b is required for the differentiation of pancreatic endocrine progenitors