Mutation is in the middle of the coiled-coil region.
Nucleotide substitution: C?T.
Amino acid replacement: Q?term.
C14252171T
C?T
Q1181term | mud-PF; Q1181term | mud-PG; Q1181term | mud-PH; Q1181term | mud-PI; Q1181term | mud-PJ; Q1181term | mud-PK; Q1181term | mud-PL
Q?term
Centrosomes are often detached from the spindle poles in mutant neuroblasts. 8% of mutant neuroblasts have disorganised astral microtubules during prophase. Mutant neuroblasts show spindle misorientation, with 20% lacking astral microtubules during metaphase.
mud1 males exhibit enlarged and misshapen mushroom body structures formed by excessive Kenyon cell proliferation.
mud1 females are semi-lethal.
mud1 heterozygous flies demonstrate comparable patterns of landmark orientation, indicating similar responses to visual stimulation in Buridan's paradigm as control flies.
mud1 heterozygous males exhibit reduced activity levels and walk slower than control flies.
Hemizygous males are fully fertile and produce normal numbers of motile sperm.
The Kenyon cell fibres in mud1 mutants do not form a peduncle or lobe system, but instead form a greatly enlarged and misshaped calyx region.
Flies have a number of brain defects, the exact phenotype depending on the genetic background. In the original genetic background in which it was induced, mud1 produces the following phenotype; the calyx is 10 times normal size and misshapen, the peduncle and lobes are absent, the antennal lobe is enlarged, and the central complex is often misshapen. When placed in a Canton S background, the defects are more severe than in the original genetic background.
Semi-lethal.
Late third instar larvae show wild type mushroom bodies but imagos exhibit mutant phenotype: the lobe and stalk system of the mushroom bodies is missing and calyces are enlarged due to failure of the Kenyon cell axons to find their normal way through the central brain neuropil as the neuropil is completely degraded.
Heisenberg.