The rhinoceros gene of drosophila restricts cell fate specification in the developing eye

Abstract

Inductive signaling between cells in the developing eye of Drosophila is very important for establishing the correct number and identity of cell fates. Among the signaling pathways that regulate cell fate determination in the developing eye, RTK/Ras/MAPK is among the most important. One effect of RTK/Ras/MAPK signaling is to downregulate the transcription factor Yan, thus allowing differentiation. A previous genetic screen identified modifiers of YanACT, a constitutively active isoform of Yan. From this screen, two alleles of Enhancer of YanAC, 3-5 (EY3-5) were identified as enhancers. A genetic screen was conducted to isolate new EY3-5 alleles for genetic and molecular characterization. The conclusion is reached that the defining phenotype of EY3-5 is a multigenic effect caused by large deletions present in the two founding alleles of EY3-5. These studies led to the investigation of the roles of three genes in signal transduction. The strongest enhancer of YanACT among these three genes, called hidden clones, appears to be necessary for growth and is involved in early cell fate decisions in the eye. Also described here is the role of the rhinoceros (rno) gene in regulating eye cell fates. Mutation of mo causes the overproduction of eye cell fates and inhibits apoptosis. These phenotypes are similar to those seen when EGFR is hyperactivated in argos mutants. Tests between argos and rno alleles show a strong genetic interaction. Furthermore, mo mutant tissue shows reduced production of Argos ligand. These data suggest a role for rno in the inhibition of EGFR by regulating expression of argos.

(cont.) Alleles of mo also display a general delay in the expression of differentiation markers in photoreceptors and cone cells. The rno gene encodes a nuclear, PHD zinc finger protein, implying that it functions as a transcription factor. Lastly, described here is the genetic analysis of nurf301, that encodes the largest subunit of the Nucleosome Remodeling Factor complex. In nurf301 mutants, heat shock transcription and expression of homeotic genes is impaired. Lastly, blood cells are overproduced in nurf301 larvae. This phenotype and genetic interactions suggest a role for the NURF complex as an antagonist of the JAK/STAT signaling pathway.