Nucleotide substitution: G2779A. This alters the splice acceptor site of exon 6a.
Lesion disrupts the splice acceptor site for the exon specific for the 104kD isoform.
Nucleotide substitution: G2779A. This alters the 3' splice acceptor site at the 5' end of the exon 6a from the invariant AG dinucleotide, which is required for splice acceptor site function, to AA.
G8487383A
G2779A
G to A substitution in the splice acceptor for exon 6a.
nurse cell & nuclear chromosome (with otu11)
otu13/otu13 females are sterile. otu13/+ females are fertile, but nurse cells in egg chambers in these females exhibit the 5-blob phenotype - a failure of nurse cell chromosome dispersal from stage 6 onwards, with the major chromosome arms remaining condensed, in contrast to wild type, but egg chambers do not exhibit any defects in oocyte polarization.
The ring canals are devoid of fusome material and have inner rims that are indistinguishable from wild-type in homozygous females. Ring canals lacking both fusomes and an inner ring are also seen in these females and a number of ring canals that are a fraction of wild-type size are occasionally seen. Fusomes contain actin filaments, and are generally linear or unbranched.
Tumorous phenotype.
ONC class allele.
Tumorous ovaries. Mutant phenotype can be suppressed by SxlM1, and some egg cysts show partial fertility and fecundity. otu11/otu13 females are completely sterile, producing small ovaries containing mostly tumorous egg cysts. Transheterozygotes with otu2 or otu10 produce ovaries containing predominantly 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.
Homozygous and hemizygous females have tumorous ovaries.
Oncogenic allele; approximately half of homozygous and hemizygous ovarioles contain tumour-generating oogonia. Substantial numbers of differentiated cystocytes are also produced.
oncogenic; cystocytes continue dividing and produce tumors
otu13 has female sterile phenotype, non-suppressible by SxlM1
SxlM1, otu11/otu13 has female fertile phenotype
otu13 has nurse cell phenotype, enhanceable by Df(2R)Exel7130/+
otu13 has chromatin phenotype, enhanceable by Df(2R)Exel7130/+
otu13 has nurse cell phenotype, enhanceable by pea[+]/pea1
Df(2R)Exel7130/+ or pea1/+ enhances the nurse cell chromatin defects seen in otu13/+ females.
One or two copies of P{hs-otu.N} causes substantial morphological suppression but only partial suppression of sterility.
Mohler.
Oncogenic (ONC) class allele. The ovarian phenotype of flies transheterozygous for otu13 and a number of other otu mutations has been analysed.
Oncogenic class (ONC) of otu allele.
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.