Liyne Nogay

Quantifications, bioinformatic analysis, and statistics For all quantifications of imaging data, control and experimental samples were processed together and imaged in parallel, using the same confocal settings. Images were processed, analyzed, and quantified using tools in Fiji (ImageJ 2.9.0) [107]. Extreme care was taken to apply consistent methods (i.e., number of projected sections, thresholding methods, processing) for image analysis.

Abstract Tissue damage and inflammation trigger systemic signals that induce catabolic breakdown and nutrient release in distant organs, a process well-characterized in the context of tumor cachexia. While mechanisms allowing tumors to circumvent these systemic growth restrictions are known, the physiological processes that overcome inflammation-induced growth restrictions to support tissue repair and regeneration remain largely unexplored.

Yki and EGF cooperate to drive compensatory proliferation in response to non-inflammatory damage To investigate which of these signaling pathways may truly be required for compensatory proliferation, we systematically analyzed sufficiency and necessity of Hippo/Yki and Ras/ERK signaling in hid-expressing disc. We first asked if Hippo/Yki or Ras/ERK activation alone were sufficient to induce accelerated EdU incorporation.