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on was not affected.Together with spatially GSK525762A restricted somatic Tai expression this supplies evidence that the ecdysone co activator Taiman can act as cell speci c co activator of ecdysone signalling in niche and ECs.To determine speci c cellular processes regulated by the ecdysone pathway in somatic cells proximal to the ovarian stem cell niche,we downregulated ecdysone signalling employing transgenic UAS tai RNAi,UAS EcR RNAi and UAS ab lines crossed to ovarian somspeci c drivers combined with the temperature sensitive Gal80 method to avoid the lethality brought on by down regulation of ecdysone pathway components throughout developmental stages.When the co activator of ecdysone signalling Tai was downregulated or the co repressor Abrupt overexpressed in soma,mutant germaricontained several SSCs,this mutant phenotype became even more pro nounced over time resembling older ecd1ts also as JAKSTAT mutant germaria.
Similar phenotypes were observed when EcR RNAi ies were kept at the restrictive temperature,the development of germline cysts was retarded,and the ratio of fusome containing cysts GSK525762A to SSCs was reduced 2 3 times.Down regulation of EcR for longer periods led to an increase within the number of SSCs.In addition,in proximity to undeveloped cysts mutant germaricontained extrsomatic cells,most likely improperly differentiated ECs.These datprovide evidence that the somspeci c disrup tion of the ecdysone pathway is causing germline differentition defects,indicating cell non autonomous role of this steroid hormone signalling.
Ecdysone signalling regulates turnover of cell adhesion proteins In order to analyse how mutant somatic cells trigger block in germline cyst maturation,we TCID used an FRT recombination method to Messenger RNA evaluate ecdysone pathway de cient and wild variety somatic TCID cells within 1 germarium.Detailed analysis of tai mutant ESCs and their progeny showed that they lose their squamous shape,and type layer resembling columnar epithelium.Interestingly,these mutant cells expressed higher levels of the cell adhesion molecules b CateninArmadillo,DE Cadherin and cytoskeleton com ponent Adducin.DE Cadherin was also upregulated in abnormal somatic cells resulting from somatic overexpression of Abrupt or down regulation of EcR pointing towards possible defects in cell cell contacts,shape rearrangement and signalling transduction processes.
These datimply that in our method the ecdysone pathway has speci c role in EC differentiation viregultion of cell adhesion complexes that are essential for establishment of correct germline somcommunications.Perhaps,when connections amongst germline cysts and surrounding somare perturbed,signalling cascades GSK525762A that initiate germline differentiation are also perturbed causing developmental delay.Ecdysone signalling controls the stem cell niche formation One more process within the germarium that must need really accurate regulation of cell adhesion would be the niche establish ment.If ecdysone signalling is essential to control this process also,we would expect to determine abnormalities in niche formation in ecdysone pathway mutants.Recall that mutant tai animals indeed had enlarged niches and extrGSCs,phenotype not noticed in other instances analysed here.
This discrepancy may be explained by the time throughout the animals development when the mutation was introduced.Within the tai experiment,animals were tai de cient throughout all developmental stages,including TCID the per iod of niche establishment.In other instances in this study the ecdysone pathway was misregulated throughout adulthood immediately after the niche was already formed and CpCs had stopped division.Also,in tai heterozygouts both the somand the germline were mutant and the germline can impact viNotch signalling the size of the niche.To prove that the niche expansion is somoriginated phenotype,we knocked down tai in somatic pre adult cells that contribute to niches employing the FRTbab1Gal4UASFlp method that enables to induce mutant CpC clones throughout niche formation.
As expected,germariwith tai clonal CpCs had substantially enlarged niches,which supplies evidence that the ecdysone GSK525762A pathway co activator Tai is essential throughout devel opmental stages speci cally within the pre niche cells to control the GSC niche assembly.Possibly in tai mutant somatic cells within the larval ovary,like in ECs in adults,increased levels of cell adhesion molecules enable them to adhere greater to germline cells and obtain much more signalling which makes them adopt the niche cell fate.To con rm that the niche enlargement is an ecdysone signalling reliant phenotype and is not related with Tai independent function,we introduced other ecdysone pathway component mutations throughout the period TCID of niche development.As a lot of the tested mutant combinations affected viability,we could disrupt ecdysone signalling throughout development only viinduction of single cell clones employing the actoCD2oGal4,hsFlp method and viEcR overexpression.Mutant single somatic clonal cells expressing UAS ab or UAS EcR RNAi resembled niche cells by their shape a