Decoding a Cell's Fate: How Notch and receptor tyrosine kinase signals specify the Drosophila R7 photoreceptor.

Abstract

The process by which the Drosophila R7 photoreceptor is specified has become a classic model for understanding how cell-cell signals direct cell fates. In the R7 precursor cell, both the Notch and receptor tyrosine kinase (RTK) signaling pathways are active, and the information they encode directs the specification of the R7 photoreceptor identity. In this process, Notch performs three distinct functions: it both opposes and promotes the actions of the RTK pathway to specify the photoreceptor fate, and it determines the type of photoreceptor that is specified. The RTK pathway drives transcription of phyl - a gene expression necessary for photoreceptor specification. We show that Notch activity induces transcription of the yan gene which encodes a transcriptional repressor of phyl. This defines an antagonism between the two pathways, with RTK promoting and Notch opposing phyl transcription. We previously showed that Notch activity supplies Sevenless to the R7 precursor to allow the RTK pathway hyperactivation required to overcome the Notch repression, and we now identify the regulation of Yan activity as a site of integration of RTK and Notch signaling pathways. Once the cell is specified as a photoreceptor, the third Notch function then prevents seven-up (svp) transcription. The Svp transcription factor directs the R1/6 photoreceptor fate, and the prevention of its expression ensures the default R7 specification.