2R11 alleles disrupt Notch signaling in the asymmetrically dividing thoracic ESO lineages. (a) Diagram of the asymmetric divisions during development of the ESO lineage; black circles represent Notch signal–receiving cells, white circles represent Notch signal–sending cells. (b) A possible model for Notch signaling in asymmetrically dividing ESO lineages (adopted by Rajan et al., 2009). (c and d) Thoracic y−/− clones of the parental 42Diso chromosome (c) or of the 2R11N8 allele (generated in a Minute background) (d). (e–g′′′) Analysis of different cell type markers of the ESO lineage at 24 h APF; pupal thoraces reveal that mutant ESO cells acquire erroneous cell fates. (e–e′′′) Supernumerary, elav-positive neurons arise in 2R11 negatively marked clones. (f–f′′′) Extra prospero–positive sheath and elav-positive neuron cells develop in 2R11 thoracic clones. (g–g′′′) Su(H)-positive socket cells are absent from 2R11 clones. In e-g′′′, cells of the ESO lineages are marked by Cut. (h–h′′′) Tramtrack-positive pIIa cells are absent from dEHBP1A28 clones within pupal nota at 17 h APF, revealing that Notch signaling is affected within the mutant regions. pIIa and pIIb cells are stained for Sens. Arrows indicate mutant pIIa cells, and the arrowhead points to a wild-type pIIa cell. The alleles used in e–e′′′ and g–g′′′ are dEHBP1O4. The alleles used in f–f′′′ and h–h′′′ are dEHBP1A28. Bars, 10 µm.
