The entire CSN5 transcriptional unit is deleted.
CSN5N mutant female germline stem cell(GSC) clones are lost from the niche much more quickly than wild type controls. No dramatic increase in apoptosis is seen in GSCs or cysts compared to controls fewer CSN5N mutant GSCs are undergoing mitosis (BrdU staining). The remaining GSCs fail to differentiate and accumulate as cystoblasts.
Females carrying CSN5N germ-line clones generated using the produced by using the dominant-female-sterile - FLP/FRT technique, lay a few eggs during a short period of time starting 5-6 days after heat shock-induced recombination. The first eggs are morphologically normal and sometimes hatch. Eggs laid in the following day or two are very small and have dorsal appendage defects. After that, no more eggs are laid. Shortly after heat shock these ovaries show a predominance of extra cystocyte divisions. Later they show a reduced number of cystocytes, which are often polyploid. Later still there is a complete arrest of oogenesis at the beginning of germline development, probably before the very first mitotic division. The remaining germ cells often become enormously polyploid and often contain oversized spectrosomes or structures similar to a fragmented fusome. Late clones also sometimes lack a fusome or spectrosome completely. These polyploid, nondividing germ cells may be the germline stem cells: there are never more than three in a germarium, and they retain contact with somatic cells that probably correspond to the basal and terminal filament cells of normal germaria.
Mutants do not survive to third instar stage. When homozygous CSN5N somatic clones are made in the larval developing eye, no cell cycle phenotype is seen.
CSN5N/CSN5[+] is an enhancer of cystoblast | increased number phenotype of bamz3-2884/bamΔ86
CSN5N/CSN5[+], bamΔ86 has cystoblast | increased number phenotype
One copy of CSN5N drastically and significantly enhances the differentiation defect of the bamΔ86/+ mutants. The number of cystoblasts and two cell pairs is significantly increased compared to either heterozygote alone.
One copy of CSN5N drastically enhances the differentiation defects seen in bamz3-2884/bamΔ86 mutant cystoblasts.
CSN5L4032