Robo signalling controls pancreatic progenitor identity by regulating Tead transcription factors

Sophie Escot, David Willnow, Heike Naumann, Silvia Francescantonio and Francesca M. Spagnoli ()
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Sophie Escot: Max-Delbrueck Center for Molecular Medicine
David Willnow: Max-Delbrueck Center for Molecular Medicine
Heike Naumann: Max-Delbrueck Center for Molecular Medicine
Silvia Francescantonio: Max-Delbrueck Center for Molecular Medicine
Francesca M. Spagnoli: Max-Delbrueck Center for Molecular Medicine

Nature Communications, 2018, vol. 9, issue 1, 1-12

Abstract: Abstract A complex interplay of intrinsic factors and extrinsic signalling pathways controls both cell lineage commitment and maintenance of cell identity. Loss of defined cellular states is the cause of many different cancers, including pancreatic cancer. Recent findings suggest a clinical role for the conserved SLIT/ROBO signalling pathway in pancreatic cancer. However, whilst this pathway has been extensively studied in many processes, a role for Slit and Robo genes in pancreas cell identity and plasticity has not been established yet. Here, we identify Slit/Robo signalling as a key regulator of pancreatic progenitor identity. We find that Robo1 and Robo2 are required for preserving pancreatic cell identity shortly after fate induction and, subsequently, for expansion of the pancreatic progenitor pool in the mouse. Furthermore, we show that Robo receptors control the expression of Tead transcription factors as well as its downstream transcriptional activity. Our work identifies an interplay between Slit/Robo pathway and Tead intrinsic regulators, functioning as gatekeeper of pancreatic cell identity.

Date: 2018
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DOI: 10.1038/s41467-018-07474-6

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