Dpp signaling participates in the balance between proliferation and differentiation of the Outer Proliferation Centre in Drosophila melanogaster larval Optic Lobe

The balance between the proliferative state of undifferentiated cells and relative quiescence of their progeny is a prerequisite for a correct development of the tissues during morphogenesis. Affected processes can give rise to tumor formation or, at the converse, to hypotrophy. This is also the case for the Optic Lobe (OL) in the 3rd instar larval brain of Drosophila melanogaster, that develops from undifferentiated cells in a structure called neuroepithelium (NE). In particular, the Outer Proliferation Centre (OPC) of the NE undergoes proliferation and gives rise to the neuroblasts (NB) of the medulla and lamina. Recent works have shown that the Hippo and the Notch/Serrate pathways are involved in and coordinate the differentiative wave of proliferation/differentiation of the OPC into NBs, with the latter involving a subset of the Subperineurial Glia (SpG), cells lying along the furrow between the OPC and the Lamina Proliferation Centre (LPC), called OL-associated cortex glia. Here we show that the Dpp signaling is involved in OPC proliferation/transition to NBs. Our data indicate that Dpp is expressed in the OL-associated glia, adjacent to the distal, undifferentiated region of the OPC expressing the type I Dpp receptor Tkv and one of its indirect target genes, diminutive (dm), encoding the oncoprotein Myc. Overexpression of Dpp or Tkv in the OPC led to NE expansion and increased Myc expression, while clones overexpressing the negative Dpp effector Dad shut Myc off, whose lack induced ectopic Dpn expression. NE and clonal dpp interference showed no phenotypes, further indicating that the Dpp source is external to the OPC. Indeed, when we overexpressed Dpp in glial cells (repo-Gal4) or directly in Dpp expressing cells (dpp-Gal4), we observed the expansion of the NE and of the Myc+ region at the expense of NBs Dpn+ compartment with supernumerary OL-associated glia, while the opposite phenotype is obtained by interfering dpp expression.