Fig 3.

Pancreas-specific knockout of Mst1/2 leads to architectural defects in the exocrine and endocrine compartments yet has negligible effect on glucose homeostasis. (A) Mst1/2 knockout offspring lack the ordered arrangement of acinar cells observed in wild-type controls (both aged 6 weeks). Amylase positivity was detected in cells thought to be duct-like (arrows). Compared to controls, insulin-positive cells are highly dispersed in the Mst1/2 KOs. (B) Endocrine cell populations were characterized using immunofluorescent costaining of insulin and glucagon. Control mice contained normally appearing islets consisting of an insulin-positive interior surrounded by glucagon-positive exterior. Mst1/2 KO offspring harbored smaller islets consisting of cell clusters oftentimes expressing only a single hormone. (C) Ratios of insulin- to glucagon-expressing cells remained unchanged between control and knockout offspring (blue, insulin; red, glucagon). (D) Resting blood glucose levels reveal no significant difference between Mst1/2 KOs and controls (P = 0.35). (E) Fasting Mst1/2 KOs respond equally as well as controls following glucose challenge (red, Mst1/2 KO; blue, control). Scale bar, 50 μm.