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The transcription factor MafB plays an essential role in  β -cell differentiation during the embryonic stage in rodents. Although MafB disappears from  β -cells after birth, it has been reported that MafB can be evoked in  β -cells and is involved in insulin +β -cell number and islet architecture maintenance in adult mice under diabetic conditions. However, the underlying mechanism by which MafB protects  β -cells remains unknown. To elucidate this, we performed RNA sequencing using an inducible diabetes model ( A0B Δpancmice) that we previously generated. We found that the deletion of  Mafb  can induce  β -cell dedifferentiation, characterized by the upregulation of dedifferentiation markers,  Slc5a10  and  Cck,  as well as several  β -cell-disallowed genes, and by the downregulation of mature  β -cell markers,  Slc2a2  and  Ucn3 . However, there is no re-expression of well-known progenitor cell markers,  Foxo1  and  Neurog3 . Further, the appearance of ALDH1A3 +  cells and the disappearance of UCN3 +  cells also verify the  β -cell dedifferentiation state. Collectively, our results suggest that MafB can maintain  β -cell identity under certain pathological conditions in adult mice, providing novel insight into the role of MafB in  β -cell identity maintenance.

MafB Maintains β -Cell Identity under MafA-Deficient Conditions