TABLE 1.
Class | Allele | Origina | Morphogenetic phenotypec | Light-induced degeneration | Molecular defect |
---|---|---|---|---|---|
I | sdtEH681 | EH | No | No | Stop codon in exon 3g |
sdtXH21 | HK | No | No | No mutation found | |
sdtM120 | HK | No | Nof | Stop codon in exon 3 | |
sdt7D22 | W | Yes | Nof | ND | |
II | sdtXP96 | W | Yesd | Weak | Stop codon at the end of exon 6g |
III | sdtN5 | Wb | Noe | Yes | Stop codon in L27Ng |
IV | sdtK70 | HK | Yes | Yes | No mutation found |
sdtK85 | HK | Yes | Yes | Stop codon in L27N | |
sdtE195 | HK | Yes | Yes | Stop codon in L27C |
EH, Eberl and Hilliker (1988); W, Wieschaus et al. (1984); HK, T. Hummel and C. Klämbt (unpublished data).
This allele is also named sdtNO5 (Eberl and Hilliker 1988) or sdtXNO5 (Hong et al. 2001). The identity of these alleles was verified by sequence analysis.
Revealed in the light microscope as defects in the shape of the rhabdomeres.
Stalk membranes of mutant PRCs are reduced by 40% (Hong et al. 2003).
Stalk membranes of mutant PRCs are reduced by 50% (see Figure 2).
Occasionally, one PRC per ommatidium was absent.