@article{TEXTUAL,
      recid = {10005},
      author = {Adams, Melissa T. and Dwulet, Jaeann M. and Briggs,  Jennifer K. and Reissaus, Christopher A. and Jin, Erli and  Szulczewski, Joseph M. and Lyman, Melissa R. and Sdao,  Sophia M. and Kravets, Vira and Nimkulrat, Sutichot D. and  Ponik, Suzanne M. and Merrins, Matthew J. and Mirmira,  Raghavendra G. and Linnemann, Amelia K. and Benninger,  Richard K. P. and Blum, Barak},
      title = {Reduced synchroneity of intra-islet  ca<sup>2+</sup> oscillations in vivo in  <i>Robo</i>-deficient β cells},
      journal = {eLife},
      address = {2021-07-07},
      number = {TEXTUAL},
      abstract = {The spatial architecture of the islets of Langerhans is  hypothesized to facilitate synchronized insulin secretion  among β cells, yet testing this in vivo in the intact  pancreas is challenging. Robo βKO mice, in which the genes  Robo1 and Robo2 are deleted selectively in β cells, provide  a unique model of altered islet spatial architecture  without loss of β cell differentiation or islet damage from  diabetes. Combining Robo βKO mice with intravital  microscopy, we show here that Robo βKO islets have reduced  synchronized intra-islet Ca<sup>2+</sup> oscillations among  β cells in vivo. We provide evidence that this loss is not  due to a β cell-intrinsic function of Robo, mis-expression  or mis-localization of Cx36 gap junctions, or changes in  islet vascularization or innervation, suggesting that the  islet architecture itself is required for synchronized  Ca<sup>2+</sup> oscillations. These results have  implications for understanding structure-function  relationships in the islets during progression to diabetes  as well as engineering islets from stem cells.},
      url = {http://knowledge.uchicago.edu/record/10005},
}