Table 1.
Summary of the structural defects caused by the eight RNAi lines
| Gene | Control/HU (P)* | Expression rank† | RNAi line | Structural defects with OK107‡ |
Structural defect with CS§ |
Gene ontology/human homolog | ||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|
| MBs, % (n) | Als, % (n) | OLs, % (n) | No. of brains | MBs, % (n) | ALs, % (n) | OLs, % (n) | No. of brains | |||||
| CG9296 | 1.771 (0.008) | A | 9296R-3 | 25 (5) | 0 (0) | 75 (15) | 20 | 7 (1) | 0 (0) | 0 (0) | 15 | Signaling: cGMP-specifc phosphodiesterase/PDE6D |
| CG6083 | 1.686 (0.045) | D | 6083R-1 | 35 (7) | 0 (0) | 0 (0) | 20 | 10 (2) | 0 (0) | 0 (0) | 20 | Metabolic enzyme: aldehyde reductase/AKR1B1 |
| CG4853 | 1.664 (0.020) | C | 4853R-1 | 24 (4) | 6 (1) | 0 (0) | 17 | 5 (1) | 0 (0) | 0 (0) | 20 | Signaling: Ras gualyl-nucleotide exchange factor/RASGEF1C |
| CG6372 | 2.026 (0.018) | C | 6372R-2 | 43 (6) | 0 (0) | 0 (0) | 14 | 13 (2) | 0 (0) | 0 (0) | 15 | Proteolysis and peptidolysis: leucyl aminopeptidase/LAP3 |
| Itp-r83A | 1.699 (0.028) | B | 1063R-2 | 24 (5) | 5 (1) | 0 (0) | 21 | 13 (2) | 0 (0) | 0 (0) | 16 | Signaling: inositol-1,4,5-triphosphate receptor/ITPR1 |
| Hr46 | 3.489 (0.022) | A | 11823R-4 | 30 (19) | 0 (0) | 0 (0) | 64 | 0 (0) | 0 (0) | 0 (0) | 20 | Transcription: ligand-dependent nuclear receptor/RORB |
| CG17221 | 1.786 (0.010) | B | 17221R-1 | 30 (6) | 0 (0) | 0 (0) | 20 | 10 (2) | 0 (0) | 0 (0) | 21 | Metabolic enzyme: zinc-containing alchohol dehydrogenase/RTN4IP1 |
| CG12301 | 2.095 (0.020) | B | 12301R-2 | 30 (6) | 0 (0) | 0 (0) | 20 | 11 (2) | 0 (0) | 0 (0) | 18 | Other function: Utp14 protein domain/UTP14A |
*Control/HU signal ratio in microarray experiments (see Table 2).
†Expression rank by in situ hybridization (see Table 3).
‡Anatomical brain defects in UAS-RNAi flies crossed with OK107. See Table 4 for specific description of the MB phenotypes. RNAi for CG4853 and Itp-r83A caused weak AL defects in single brains. Only CG9296 RNAi caused OL degeneration.
§Anatomical brain defects in UAS-RNAi flies crossed with Canton S. MB defects were rare in these control flies, and only weak β -lobe fusion was observed. Similarly, only weak β -lobe fusion was observed in 8.3% (5 of 60) of the progeny of OK107 crossed with Canton S. No abnormality was detected for ALs and OLs. Flies were raised at 28°C to stimulate the Gal4 activity. Note that β -lobe fusion is less frequent at 25°C (1 of 60 for OK107/Canton S).