Amino acid replacement: E164K.
Nucleotide substitution: G810A.
Revision of data reported in FBrf0111813.
G16269911A
G810A
C12157416T
E164K | Khc-PA
E164K
Reported base location of mutation is relative to noncoding strand.
Results in larval posterior paralysis in combination with a null Khc allele.
Both anterograde and retrograde flux of axonal mitochondria is inhibited in Khc23/Khc27 larvae.
45% of eggs from females containing homozygous germline clones show defects in dorsal appendage morphology; 38% have fused dorsal appendages, 5% have reduced dorsal appendages and 2% have missing dorsal appendages.
The velocity of ooplasmic streaming in stage 10B oocytes is dramatically reduced in mutant females compared to wild type.
Approximately 85% of Khc23 mutants are embryonic lethal, with the remaining 15% lethal in the larval/pupal stages. Endosomes in Khc23 stage 9 embryos exhibit saltations, but no not exhibit slow-streaming currents and have an approximate 1.7-fold reduction in mean velocity compared to wild-type. In stage 10B-11 Khc23 oocytes, saltation and some short, individual dsiplacements occur, although concerted fast currents are rare, occuring in a small region of only one out of nine oocytes. Khc23 endosomes move at a mean velocity approximately 11-fold less than wild-type.
Hemizygotes do not survive to adulthood.
Based on the ability of the allele to compromise Khc function, the following alleles can be ranked from strongest to weakest as follows: Khc27 > Khc23 = Khc17.