Table 1.

Lateral inhibition defects in third instar nota

Genotype*StrongModerateWeakWild typen
N54l9 44.526263.527
Dlrev10 SerRX106 70.521.56251
Dlrev10 1111413727
SerRX106 00010024
Dlrev10+UAS-fng22c 4712.52812.532
Dlrev10 SerRX106+UAS-DlB41 08.5091.524
Dlrev10 SerRX106+UAS-SerIC 00267423
Dlrev10+UAS-SerIC 00010014
UAS-fng22c 00010011
UAS-DlB41 00010020
UAS-SerIC 00010042
neur1 1133.5487.527
neur1 Dlrev10 503515020
neur1SerRX106 33.54719.5036
mib1EY9780 00010018
mib1EY9780 neur1 82.517.50017
mib1EY9780 Dlrev10 404551020
mib1EY9780 SerRX106 00010024
  • Only clones in late larval nota were scored (SOP positions ASC, PSC, ADC, PDC, APA, tr1, PSA, ANP, PNP) (see Huang et al., 1991). n, number of SOP positions scored. No phenotypic preferences were seen depending on the specific SOP position. We therefore grouped all notum SOP positions for the statistical analysis. Some clones must have intersected proneural clusters (rather than wholly encompassing them) – these account for the rare occurrences of weak defects in genotypes known to completely abolish lateral inhibition (e.g. N54l9 and Dlrev10 SerRX106). Additionally, N54l9 clones had a partially penetrant growth defect; as a result some of the very small clones (two to seven cells) that were entirely composed of SOPs were placed in the weak/moderate categories – none of the other genotypes had any growth defects. P-values given in the text refer to pairwise comparisons using a χ-square test.

  • * Genotype refers to the homozygous genotype of mutant clones. UAS transgenes were expressed only within mutant clones usingα tub-Gal4

  • Shown are percentages of SOP positions falling in different categories, which were defined as follows: wild type, one SOP; weak, between one and four SOPs; moderate, between four and eight SOPs; strong, at least eight SOPs

  • Double combinations with mib1EY9780 were generated as mosaic clones of the other allele (neur1, Dlrev10 or SerRX106) in a uniform mib1EY9780 genetic background