Deletion of part of the coding region (Mulligan et al., Mol Cell Biol 8: 1481-1488).
2 kb deletion
otu17 heterozygotes show a rare and mild ovary 'germline tumor' phenotype; homozygotes lack germline cells.
Ovaries contain tumorous egg cysts.
Spermatogenesis normal but mating behaviour fails because wild type females refuse to react to the courtship attempts of mutant males. Effect is not absolute, and depends on allele (there is a strong correlation between male sterility and severity of impairment in the female phenotype) and varies between affecting 6.7% (otu14) and 86.6% (otu12) of mutant males.
92% of homozygous ovarioles have quiescent oogonia, and 8% have tumorous oogonia.
Quiescent allele; homozygous and hemizygous ovarioles usually contain vitellaria that lack developing follicles, 8% or less of the oogonia are tumour-generating.
quiescent; ovarioles lack germ cells
otu17 has neoplasia | oogenesis | dominant phenotype, enhanceable by Scer\GAL4VP16.nanos.UTR/CG15930UAS.cPa
Sxlf4/Sxlf2, otu17 has female sterile | dominant phenotype
otu17 has germarium phenotype, enhanceable by Scer\GAL4VP16.nanos.UTR/CG15930UAS.cPa
otu17 has ovary phenotype, enhanceable by Scer\GAL4VP16.nanos.UTR/CG15930UAS.cPa
otu17 dominantly suppresses the ability of Wolbachia to suppress Sxlf4 defects in oogenesis.
Almost no Sxlf2/Sxlf4 females make eggs if they also carry otu17/+. Most egg chambers in these females are tumorous.
The phenotype of a reduction in recombination across the y-sn interval on the X chromosome that is seen in SxlM1,f3/Sxlfs3 females is enhanced by otu17/+ ; there is a further reduction in map distance in the double mutants. In addition, the rate of X chromosome nondisjunction is increased eightfold.
SxlM1,f3, otu17 double heterozygotes show reduced recombination across the y-sn interval on the X chromosome compared to wild type, with the reduction being stronger than the weak reduction seen in SxlM1,f3 single heterozygotes.
Rescued by otu+t5.4 : fertility, normal ovarian development and normal 3.2kb message expressed in ovaries is restored.
Digan.
Mutation reduces the ability of SxlcF1.otu to induce female Sxl+ RNA splicing in the male germline: number of autoregulatory cysts in testes is much reduced.
Quiescent (QUI) class allele. The ovarian phenotype of flies transheterozygous for otu17 and a number of other otu mutations has been analysed.
One of QUI class of alleles.
Likely to be a null mutation.
Shows a dominant interaction with ovoD2 and ovoD3 : more extreme mutant phenotype as assayed by reduction in number of egg chambers at stage 10 or further developed. There is no apparent correlation with strength of otu allele and its interaction with the ovo alleles.
QUI class of otu allele. P{otu-98} fails to restore detectable levels of fertility, P{otu-104} completely restores fertility.