title: Stop and go: antagonistic signals in the specification of the Drosophila R7 photoreceptor viewed from an evolutionary perspective.
abstract: The Drosophila R7 photoreceptor precursor is directed to its fate by signals from adjacent cells that activate its Receptor Tyrosine Kinase (RTK) and Notch (N) signaling pathways. Counter-intuitively, the N activity both promotes and inhibits the photoreceptor fate in the R7 precursor. We offer an evolutionary perspective for this in which earlier ommatidia had fewer photoreceptors and used N to inhibit the addition of any more. When additional photoreceptors were added by evolution, an RTK signal was used to overcome the N inhibition in these cells, and these new additions potently activated N in their neighboring cells, preventing them from also responding to the RTK signal. The R7 precursor also receives this block, and requires robust RTK activation for it to become a photoreceptor. This is achieved by N transcriptionally activating a new RTK, one that is potently activated in the R7 precursor and sufficing to overcome the N inhibition. The unusually high RTK signal in R7 requires additional transduction components not needed when the signal is mild; in R7 the small GTPases Ras and Rap are both required to transduce the signal, but in other photoreceptors Ras alone suffices.
authors.affiliation: Genetics and Development, College of Physicians and Surgeons, Columbia University, New York, NY, USA.
authors.forename: Yannis Emmanuel
authors.initials: YE
authors.lastname: Mavromatakis
authors.forename: Andrew
authors.initials: A
authors.lastname: Tomlinson
mesh_terms: D000818:Animals; D002454:Cell Differentiation; D004330:Drosophila / Q000254:growth & development / Q000378:metabolism*; D019143:Evolution, Molecular; D017956:Photoreceptor Cells, Invertebrate / Q000378:metabolism*; D020794:Receptor Protein-Tyrosine Kinases / Q000378:metabolism; D051880:Receptors, Notch / Q000378:metabolism; D015398:Signal Transduction
chemical_list: D051880:Receptors, Notch; D020794:Receptor Protein-Tyrosine Kinases