A647V | mei-41-PA
Position of mutation on reference sequence inferred by FlyBase curator. Reported nucleotide change is not consistent with amino acid change.
Amino acid replacement: A384V.
In addition to the A384V amino acid replacement, which may cause the mutant phenotype, a number of additional amino acid changes are present compared to the U34925 mei-41 GenBank sequence (these "common" mutations are also present in other mei-41 mutant alleles, possibly due to variability present in the mutagenised population).
Nucleotide substitution: T3768A.
Nonsense mutation at codon 42, resulting in a stop six codons later.
56% of eggs derived from mei-41D3/mei-41D3 ; armi1/armi72.1 double mutant females have normal dorsal appendages, but the fraction of embryos with normal dorsal appendages increases to 83% if the females are fed caffeine.
Mutant larvae do not show efficient G2 arrest after exposure to 500Rad or 4000Rad irradiation. The mutant larvae do not show a reduction in BrdU incorporation after a 4000Rad irradiation exposure, in contrast to wild-type larvae.
In mei-41D3;pr-set720 double mutants, the mitotic index, significantly reduced in pr-set720 mutants, is rescued to be similar to that observed in wild-type and the homozygous mei-41D3 mutant. The number of prophase cells is reduced compared with the number observed in pr-set720 homozygotes and becomes similar to wild-type and pr-set720 mutants. The ratio of anaphase/telophase cells with lagging chromatids is increased when the DNA damage checkpoint is abolished in the double homozygous mei-41D3;pr-set720 mutant, indicating that the defect in chromomsome condensation is independent of checkpoint activation and that, in the absence of the checkpoint, the severity of the chromosome condensation defect is enhanced.
mei-41D3/mei-41RT1 partially suppresses the dorsal appendage defects of mus301094 homozygotes; 70% of eggs derived from double mutant females have wild-type dorsal appendages, 21% have fused dorsal appendages and 9% have no dorsal appendages. mei-41D3/mei-41RT1 partially suppresses the dorsal appendage defects of eggs derived from spn-Bunspecified females.
20% of embryos derived from homozygous mei-41D3 females cellularise if they are carrying one copy of wee+tPa, and 50% cellularise if they are carrying two copies of wee+tPa (and some develop to adulthood in this case). The incompletely penetrant syncytial arrest phenotype of embryos derived from homozygous weeDS1 females is enhanced if the females also carry mei-41D3, so that only 39% of the embryos cellularise if the females carry one copy of mei-41D3 and only 29% of the embryos cellularise if the females carry two copies of mei-41D3.
The eggshell patterning defects of eggs derived from spn-BBU/spn-BBU females are suppressed if the females also carry mei-41D3/+ or mei-41D3/mei-41RT1. The eggshell patterning defects of eggs derived from mus301D4/mus301094 females are suppressed if the females also carry mei-41D3/+ or mei-41D3/mei-41D3. The eggshell patterning defects of eggs derived from vasRG53/vasPH165 females are not suppressed if the females also carry mei-41D3/mei-41D3.
mei-41D3 grpfsA4 double heterozygous larvae are more sensitive to methyl methanesulfonate than single heterozygous larvae. If mei-41D3/mei-41D5 females are also heterozygous for grpfsA4, the hatch rates are reduced to 1% and 23% at 25oC and 20oC respectively. The lethality of embryos derived from mei-41D3/mei-41D5 females is partly rescued if the females are also heterozygous for either CycAunspecified or CycBunspecified, and greater rescue is seen if the females are also heterozygous for both CycAunspecified and CycBunspecified.