Amino acid replacement: E321K.
Amino acid replacement: E?K.
G2602494A
E321K | Klp3A-PA; E321K | Klp3A-PB
E321K
Nucleotide substitution thought to be responsible for mutant phenotype. Other differences thought to be polymorphic variants.
T2601629C
I609T | Klp3A-PA; I609T | Klp3A-PB
I609T
Likely to be polymorphism. Other observed change in mutant thought to be responsible for mutant phenotype.
The total meiotic exchange frequency for chromosome arm 2L shows little deviation from that of wild-type for homozygous and Klp3Amei-352/Df(1)ED6579 females, but the distribution of exchanges along the chromosome arm is altered. Klp3Amei-352 shows reduced female fertility both as a homozygote (3.7% of eggs hatch) and in transheterozygous combination with other Klp3A mutants (% eggs hatching given in each case); Df(1)ED6579 (2.02%), Klp3A1 (1.90%), Klp3A6 (1.46%) and Klp3A2 (10.29%). The majority of embryos derived from homozygous, Klp3Amei-352/Klp3A2, Klp3Amei-352/Klp3A1 or Klp3Amei-352/Klp3A6 females appear to arrest very early, with only one small nucleus plus a mass of polar body chromatin.
Homozygous larval brain ganglia have a reduced ability to synthesise DNA after exposure to N-acetoxy-2-acetylaminofluorene compared to wild-type.
Elevates meiotic exchange in the proximal euchromatin of the X chromosome.
Hemizygous male larvae are not sensitive to HN2 and MMS.
Mutants are weakly recombination defective. Mutants do not show sensitivity to UV light, γ rays or X rays. Homozygotes and hemizygotes do not show an increased frequency of spontaneous chromosome aberrations in neuroblast metaphases compared to wild-type larvae.
Klp3Amei-352 mutation increases mitotic chromosome instability approximately three-fold.
Klp3Amei-352 females show exchange between the normally achiasmate fourth chromosomes.
Homozygous females are more sterile than can be accounted for by the observed frequencies of aneuploid ova. <up>FlyBase curator comment: FBrf0187654 demonstrates that the semisterility of mutant females is due to maternal-effect lethality, and that both the reduced fertility and the exchange phenotype are the consequence of the same mutational lesion.</up>
FBrf0023919 noted that homozygous females have a more severe defect in fertility than would be predicted given the frequency of nondisjunction seen among surviving progeny and did not determine whether the meiotic and semisterility phenotypes were due to a single mutation or to mutations in two separate loci on the X chromosome. FBrf0187654 demonstrates that the semisterility is a consequence of maternal effect lethality an that both the meiotic and semisterility phenotypes of Klp3Amei-352 mutants are due to a single lesion, in the Klp3A locus.