Dataset Information


Pancreatic Islet-Autonomous Signals Modulate Identity Changes of Glucagon+ α-Cells

ABSTRACT: The mechanisms restricting regeneration and maintaining cell identity upon injury are poorly characterized in higher vertebrates. Upon β-cell loss, 1-2% of the glucagon-producing α-cells spontaneously engage insulin production in mice. Here we explore the mechanisms of this plasticity. We show that the adaptive α-cell identity changes are constrained by intra-islet Insulin- and Smoothened-mediated signaling, among others. Combining β-cell loss, or insulin signaling inhibition, with Smoothened inactivation in α- or δ-cells, stimulates insulin production in more α-cells. These findings suggest that removing constitutive “brake signals” is crucial for neutralizing the refractoriness to adaptive cell-fate changes. It appears that cell identity maintenance is an active process mediated by repressive signals curbing an intrinsic trend of differentiated cells to change. Overall design: RNA-Seq analyses on five purified cells namely, mature α-cells, mature β-cells, α-cells 30 days after DT, α-cells ectopically expressing PDX1 and α-cells expressing PDX1

INSTRUMENT(S): Illumina HiSeq 2000 (Mus musculus)

SUBMITTER: Simone Gupta  

PROVIDER: GSE109285 | GEO | 2018-06-18



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