title: The ETS domain transcriptional repressor Anterior open inhibits MAP kinase and Wingless signaling to couple tracheal cell fate with branch identity.
abstract: Cells at the tips of budding branches in the Drosophila tracheal system generate two morphologically different types of seamless tubes. Terminal cells (TCs) form branched lumenized extensions that mediate gas exchange at target tissues, whereas fusion cells (FCs) form ring-like connections between adjacent tracheal metameres. Each tracheal branch contains a specific set of TCs, FCs, or both, but the mechanisms that select between the two tip cell types in a branch-specific fashion are not clear. Here, we show that the ETS domain transcriptional repressor anterior open (aop) is dispensable for directed tracheal cell migration, but plays a key role in tracheal tip cell fate specification. Whereas aop globally inhibits TC and FC specification, MAPK signaling overcomes this inhibition by triggering degradation of Aop in tip cells. Loss of aop function causes excessive FC and TC specification, indicating that without Aop-mediated inhibition, all tracheal cells are competent to adopt a specialized fate. We demonstrate that Aop plays a dual role by inhibiting both MAPK and Wingless signaling, which induce TC and FC fate, respectively. In addition, the branch-specific choice between the two seamless tube types depends on the tracheal branch identity gene spalt major, which is sufficient to inhibit TC specification. Thus, a single repressor, Aop, integrates two different signals to couple tip cell fate selection with branch identity. The switch from a branching towards an anastomosing tip cell type may have evolved with the acquisition of a main tube that connects separate tracheal primordia to generate a tubular network.
authors: Institute of Molecular Life Sciences and PhD Program in Molecular Life Sciences, University of Zurich, Winterthurer Str. 190, CH-8057 Zurich, Switzerland. sara.caviglia@imls.uzh.ch
authors: Sara
authors: S
authors: Caviglia
authors: Stefan
authors: S
authors: Luschnig
mesh_terms: D000818:Animals; D030801:Animals, Genetically Modified; D002454:Cell Differentiation / Q000235:genetics; D019070:Cell Lineage / Q000235:genetics; D015536:Down-Regulation / Q000235:genetics; D029721:Drosophila Proteins / Q000037:antagonists & inhibitors / Q000737:chemistry* / Q000235:genetics / Q000378:metabolism* / Q000502:physiology*; D004331:Drosophila melanogaster / Q000196:embryology / Q000235:genetics; D004625:Embryo, Nonmammalian; D005136:Eye Proteins / Q000737:chemistry* / Q000235:genetics / Q000502:physiology*; D018507:Gene Expression Regulation, Developmental; D020935:MAP Kinase Signaling System / Q000235:genetics; D009024:Morphogenesis / Q000235:genetics; D017434:Protein Structure, Tertiary / Q000235:genetics / Q000502:physiology; D050783:Proto-Oncogene Proteins c-ets / Q000737:chemistry; D012097:Repressor Proteins / Q000737:chemistry* / Q000235:genetics / Q000502:physiology*; D015398:Signal Transduction / Q000235:genetics; D014132:Trachea / Q000166:cytology / Q000196:embryology* / Q000378:metabolism; D051155:Wnt1 Protein / Q000037:antagonists & inhibitors / Q000378:metabolism*
chemical_list: C076188:AOP protein, Drosophila; D029721:Drosophila Proteins; D005136:Eye Proteins; D050783:Proto-Oncogene Proteins c-ets; D012097:Repressor Proteins; D051155:Wnt1 Protein; C074622:wg protein, Drosophila