Mutation within the salm coding region, introduction of a stop codon.
abdominal lateral pentascolopidial chordotonal organ lch5 & scolopidial dendritic cap cell | supernumerary (with Df(2L)32FP-5)
abdominal lateral pentascolopidial chordotonal organ lch5 & scolopidial ligament cell (with Df(2L)32FP-5)
abdominal lateral pentascolopidial chordotonal organ lch5 & scolopidial neuron | supernumerary (with Df(2L)32FP-5)
abdominal lateral pentascolopidial chordotonal organ lch5 & scolopidial sheath cell | supernumerary (with Df(2L)32FP-5)
abdominal lateral pentascolopidial chordotonal organ lch5 & scolopidium | supernumerary (with Df(2L)32FP-5)
Homozygous embryos lack between one to three peripheral glial cells from the peripheral nervous system in approximately 50% of hemisegments.
salm3/Df(2L)32FP-5 embryos have a normal number of glial cells, although they have a less regular distribution and are more rounded than normal. Neuronal and glial cells in the brain and nerve cord of early stage 16 salm3/Df(2L)32FP-5 embryos are loosely attached or widely separated by an enlargement of the extracellular space (at this stage neuronal cell bodies are tightly packed in wild-type tissue). The cytoplasm of the neuronal and glial cells contains membrane "whorls", autophagosomes and other membranous profiles typical of neurodegenerative processes. The lacunar spaces between the cell bodies and neuronal fibres in the neuropil contain large amounts of extracellular membranous material, mostly in the form of vacuoles which vary greatly in size (the largest approaching the size of whole cell bodies). These vacuoles appear empty, or contain smaller vacuoles, but do not contain organelles or cytoplasmic remnants. There is no increase in apoptotic cell death compared to wild type. Axonal calibre is reduced and filopodia which emanate from the growth cones are often clumped. This phenotype is not seen in the peripheral nerves. The central nervous system of late stage 16 or stage 17 salm3/Df(2L)32FP-5 embryos shows an almost normal organisation. At this stage, most of the extracellular membranous material seen at early stage 16 has disappeared and the neuronal cell bodies are almost as tightly packed as in wild type animals.
Mutant embryos lack oenocytes. Extra lateral chordotonal organs are formed with the number of lateral chordotonal organs in the cluster frequently being 6 or 7 (instead of the wild type 5). The extra chordotonal organs are restricted to the lateral cluster with the other abdominal chordotonal organs (V'ch1, VchAB) remaining wild-type in number. Some of the lateral chordotonal organ arrays are displaced dorsally and frequently point ventrally.
The lch5 sensory organs show misplacement (they are in a dorsal position in approximately 70% of cases) and have 1-3 supernumerary neurons in salm3/Df(2L)32FP-5 embryos, while the thoracic dch3 organ does not show any detectable abnormality. The supernumerary neurons seen in the lch5 organs are associated with supernumerary sheath and cap cells. More than one neuron inserting into a single sheath cell is never seen. All the cells in each scolopidium have a normal ultrastructure, indicating that the supernumerary scolopidia are fully differentiated. Supernumerary glial cells are observed in the position where the ligament cells of the lch5 organ are expected to be. At least 5 ligament cells are always seen, excluding the possibility that the supernumerary neurons are derived from transformed ligament cells. Late stage embryos have an average of 0.4 oenocytes per hemisegment (compared to 5.8-5.9 per oenocytes hemisegment in controls).
Lateral and ventral structures of the tracheal system are not affected. However the dorsal trunk is not properly assembled. Dorsal trunk cells migrate predominantly in a dorsal direction. Sporadic horizontal branches are formed but they occur at ectopic dorsal positions of tracheal metameres. Mutant embryos do not fail to specify the dorsal trunk homotip cells, and show no increased cell death. Mutants develop three ectopic tracheal placodes, Tr-1, Tr0 and Tr11, in addition to the ten wild type placodes. The sizes of Tr-1 and Tr11 are reduced with respect to wild type.
Mitotic clones in the wing cause size reduction and vein displacement.
salm3 rhounspecified double mutant embryos lack all oenocytes. The number of chordotonal organs in the lch5 cluster is reduced from 5 to 3, as is seen in rhounspecified single mutants.
salm3 spi1 double mutant embryos have an average of 3 +/- 0.08 neurons per lch5 organ, similar to spi1 single mutant embryos. The embryos show misplacement of the lch5 organ along the dorsoventral axis comparable to the phenotype seen in salm single mutants. salm3 SIIN double mutant embryos have an average of 3.05 +/- 0.20 neurons per lch5 organ, similar to SIIN single mutant embryos. The embryos show misplacement of the lch5 organ along the dorsoventral axis comparable to the phenotype seen in salm single mutants.
salm3 is rescued by salmC20-sal26
Anderson.
