摘要：SummaryNewts utilize their unique genes to restore missing parts by strategic regulation of conserved signaling pathways. Lack of genetic tools poses challenges to determine the function of such genes. Therefore, we used theDrosophilaeye model to demonstrate the potential of 5 unique newt (Notophthalmus viridescens) gene(s),viropana1-viropana5(vna1-vna5), which were ectopically expressed inL2mutant and GMR-hid, GMR-GAL4 eye.L2exhibits the loss of ventral half of early eye andhead involution defective(hid) triggers cell-death during later eye development. Surprisingly, newt genes significantly restore missing photoreceptor cells both inL2and GMR>hidbackground by upregulating cell-proliferation and blocking cell-death, regulating evolutionarily conserved Wingless (Wg)/Wnt signaling pathway and exhibit non-cell-autonomous rescues. Further, Wg/Wnt signaling acts downstream of newt genes. Our data highlights that unique newt proteins can regulate conserved pathways to trigger a robust restoration of missing photoreceptor cells inDrosophilaeye model with weak restoration capability.Graphical abstractDisplay OmittedHighlights•Newt proteins regulate wingless/Wnt pathway to rescue eye mutant(s) inDrosophila•These proteins non-cell-autonomously rescue missing tissue inDrosophilaeye•Promotes cell proliferation and downregulates cell death inDrosophilaeye mutant(s)•These newt genes may have significant bearing on our understanding of regenerationBiological sciences; Cell biology; Developmental biology
