nurse cell (with CSN5ex13)
nurse cell (with CSN5ex21)
6.3% of egg chambers in CSN5ex21/CSN5L4032 flies raised at 18oC have twice the normal number of germ cells (n>500). Oogenesis is normal in CSN5L4032/+ flies. 10.1% of egg chambers in CSN5ex13/CSN5L4032 flies raised at 18oC have twice the normal number of germ cells (n>500). In germaria carrying CSN5L4032 germ-line clones, the fusome is often less branched, and sometimes there were more individual fusomes than in wild-type germaria. These germaria contain unbranched fusomes and spherical spectrosomes (fusome precursors) not only at the anterior, but also more posteriorly. Both M-phase and S phase markers can be seen much more posteriorly in these germaria than in wild-type.
Females carrying homozygous germline clones lay eggs with a range of abnormal phenotypes that are affected by temperature. Flies raised at 25oC lay eggs with phenotypes closest to normal. At 18oC, many of the defective eggs have fused dorsal appendages. At 29oC, there is an increasing frequency of properly separated, but short, dorsal appendages and dorsalised eggs. Some eggs have an unusually weak eggshell. Somatic clones induced in the ovary do not result in eggshell defects. At 29oC, homozygotes die during early development and less than 1% of the mutant larvae become prepupae. At 18oC. 90% of mutant larvae pupariate and 1-2% escape as adults. The number of pole cells is often reduced in embryos derived from homozygous female germline clones and in some cases the pole cells are not tightly clustered but are found in a loose, non-contiguous group near, but not tightly associated with the posterior end of the embryo. 5-15% of eggs laid by CSN5ex21/CSN5L4032 females have fused dorsal appendages.
A few embryos are recovered from females containing homozygous germ-line clones. These embryos cannot undergo the cell movements required for gastrulation.
Homozygous mutant embryos hatch normally and proceed through first and second larval instars without any apparent defect. Developmental retardation was apparent during the middle of the third larval instar. 10-30% of larvae become increasingly sluggish and flaccid and do not reach pupariation. The majority of larvae pupate but cease to develop, less than 10% reach pharate adult stage. No adults eclose. No cuticular abnormalities are apparent these adults.
CSN5L4032/CSN5ex21 has increased cell number | oogenesis phenotype, suppressible by CycEAR95/CycE[+]
CSN5L4032/CSN5ex21 has increased cell number | oogenesis phenotype, suppressible by CycE[+]/CycE05206
CSN5L4032, Rpn6k00103 has increased occurrence of cell division | oogenesis phenotype
CSN4k08018, CSN5L4032 has increased cell death | oogenesis phenotype
CSN4k08018, CSN5L4032 has increased occurrence of cell division | oogenesis phenotype
CSN5L4032/CSN5ex21 has nurse cell phenotype, suppressible by CycEAR95/CycE[+]
CSN5L4032/CSN5ex21 has nurse cell phenotype, suppressible | partially by CycE[+]/CycE05206
CSN5L4032/CSN5ex13 has nurse cell phenotype, suppressible | partially by CycE[+]/CycE05206
CSN5L4032/CSN5ex21 has dorsal appendage phenotype, suppressible by mei-41unspecified/mei-41unspecified
CSN5L4032/CSN5[+] is an enhancer of female germline stem cell | germline clone phenotype of slmb2
CSN5L4032/CSN5[+] is an enhancer of dorsal appendage phenotype of grkHF
CSN5L4032/CSN5[+] is an enhancer of dorsal appendage phenotype of Egfrf2
CSN5L4032/CSN5[+] is an enhancer of dorsal appendage phenotype of grk2B6
CSN5L4032, slmb2 has germarium | germline clone phenotype
CSN5L4032/CSN5[+], slmb2 has germarium | germline clone phenotype
CSN4k08018, CSN5L4032 has ovary phenotype
CSN4k08018, CSN5L4032 has nurse cell phenotype
CSN4k08018/CSN4[+], CSN5L4032 has egg chamber phenotype
CSN5L4032, Rpn6[+]/Rpn6k00103 has nurse cell phenotype
CSN5L4032, Rpn6[+]/Rpn6k00103 has egg chamber phenotype
CSN5L4032, Rpn6k00103 has nurse cell phenotype
CSN5L4032, Rpn6k00103 has egg chamber phenotype
CSN4k08018, CSN5L4032 has egg chamber phenotype
CSN5L4032/CSN5[+], Rpn6k00103 has nurse cell phenotype
CSN5L4032/CSN5[+], Rpn6k00103 has egg chamber phenotype
CSN4k08018, CSN5L4032/CSN5[+] has ovary phenotype
CSN4k08018, CSN5L4032/CSN5[+] has nurse cell phenotype
CSN4k08018, CSN5L4032/CSN5[+] has egg chamber phenotype
CSN4k08018/CSN4[+], CSN5L4032 has ovary phenotype
CSN4k08018/CSN4[+], CSN5L4032 has nurse cell phenotype
The number of egg chambers with twice the normal number of germ cells in CSN5ex21/CSN5L4032 flies, is reduced to 0.6% by CycEAR95/+. The number of egg chambers with twice the normal number of germ cells in CSN5ex13/CSN5L4032 flies, is reduced to 3.4% by CycE05206/+. (n>500) The ovaries of CSN5L4032/CSN4k08018 transheterozygotes exhibit apoptosis and extra cell division of nurse cells, as well as fused egg chambers. The penetrance of these phenotypes can exceed 50%. Unlike either single heterozygote, nurse cells in CSN5L4032; Rpn6k00103 transheterozygous females exhibit ectopic apoptosis, incorrect numbers of mitotic divisions and fusions of neighbouring egg chambers.
The fused dorsal appendage phenotype of eggs laid by grk2B6/+ females is enhanced if the females are also heterozygous for CSN5L4032. The fused dorsal appendage phenotype of eggs laid by grkHF/+ females is enhanced if the females are also heterozygous for CSN5L4032. The fused dorsal appendage phenotype of eggs laid by Egfrf2/+ females is weakly enhanced if the females are also heterozygous for CSN5L4032.
Excision of the P{lacW} can be associated with a reversion to wild-type.
Reversion analysis proved that the P{lacW} is responsible for the lethal phenotype.
Precise excision of the P{lacW} element reverts the mutant phenotype.