Mis-expression of aretScer\UAS.P\T.cFa in female germline stem cells (GSCs) and their immediate descendants under the control of Scer\GAL4nos.UTR.T:Hsim\VP16 results in a progressive decline in GSC numbers per germarium within two weeks after eclosion.
In wild-type animals, all the primordial germ cells (PGCs) carry a single spherical fusome (spectrosome) or two dividing spherical fusomes at late third instar. However, all the Scer\GAL4nos.UTR.T:Hsim\VP16>aretScer\UAS.P\T.cFa-overexpressing gonads contain PGCs with branched fusomes indicative of precocious cell differentiation.
Ovarioles of aretScer\UAS.P\T.cFa; Scer\GAL4nos.UTR.T:Hsim\VP16 flies have a range of germ cell replication defects: In some cases no oocyte develops and endoreplication of the nurse cells fails. In other cases egg chambers have 31 nurse cells, and one oocyte with 5 ring canals instead of 4. In rare cases (<5%) these egg chambers form with a mislocalised oocyte, or with two oocytes. Fused egg chambers also occasionally form. aretScer\UAS.P\T.cFa; Scer\GAL4nos.UTR.T:Hsim\VP16 flies lay fewer eggs than wild-type. Of the eggs that are laid, approximately 5% are clearly ventralised, as assessed by absence or fusion of dorsal appendages. Eggs also occasionally form a posterior micropyle. About 15% of the resulting embryos have cuticles with a typical posterior group phenotype.
Scer\GAL4VP16.nanos.UTR, bru1UASp.cFa has increased occurrence of cell division | oogenesis phenotype, non-suppressible by vasαTub67C.GFP/Scer\GAL4VP16.nanos.UTR
Scer\GAL4VP16.nanos.UTR, bru1UASp.cFa has decreased occurrence of cell division | oogenesis phenotype, non-suppressible by vasαTub67C.GFP/Scer\GAL4VP16.nanos.UTR
Scer\GAL4VP16.nanos.UTR, bru1UASp.cFa has increased occurrence of cell division | oogenesis phenotype, non-suppressible by oskfs(1)K10.3'UTR.UAS/Scer\GAL4VP16.nanos.UTR
Scer\GAL4VP16.nanos.UTR, bru1UASp.cFa has decreased occurrence of cell division | oogenesis phenotype, non-suppressible by oskfs(1)K10.3'UTR.UAS/Scer\GAL4VP16.nanos.UTR
Scer\GAL4VP16.nanos.UTR, bru1UASp.cFa has abnormal cell polarity | oogenesis phenotype, non-suppressible by vasαTub67C.GFP/Scer\GAL4VP16.nanos.UTR/grk2B6/grk[+]
Scer\GAL4VP16.nanos.UTR, bru1UASp.cFa has female germline stem cell | progressive phenotype, enhanceable by enokK1293/enok[+]
Scer\GAL4VP16.nanos.UTR, bru1UASp.cFa has nurse cell | ectopic phenotype, non-suppressible by vasαTub67C.GFP
Scer\GAL4VP16.nanos.UTR, bru1UASp.cFa has nurse cell phenotype, non-suppressible by vasαTub67C.GFP
Scer\GAL4VP16.nanos.UTR, bru1UASp.cFa has oocyte | ectopic phenotype, non-suppressible by vasαTub67C.GFP
Scer\GAL4VP16.nanos.UTR, bru1UASp.cFa has oocyte phenotype, non-suppressible by vasαTub67C.GFP
Scer\GAL4VP16.nanos.UTR, bru1UASp.cFa has ring canal | ectopic phenotype, non-suppressible by vasαTub67C.GFP
Heterozygosity for enokK1293 exacerbates the female germline stem cell loss elicited by Scer\GAL4nos.UTR.T:Hsim\VP16>aretScer\UAS.P\T.cFa overexpression.
aptScer\UAS.P\T.cFa or vasαTub67C.T:Avic\GFP do not suppress the germ cell replication defects seen in Scer\GAL4nos.UTR.T:Hsim\VP16; aretScer\UAS.P\T.cFa ovarioles. In contrast oskScer\UAS.P\T.cFa or osk3'UTR.Scer\UAS.P\T can fully suppress these phenotypes, although oskfs(1)K10.3'UTR.Scer\UAS can not. grk3'UTR.Scer\UAS.P\T partially suppresses these phenotypes. Heterozygosity for grk2B6 enhances the penetrance of dorsal appendage loss or fusion phenotypes in eggs laid by Scer\GAL4nos.UTR.T:Hsim\VP16; aretScer\UAS.P\T.cFa females from 5% to 90%. This phenotype still shows over 90% penetrance in eggs laid by Scer\GAL4nos.UTR.T:Hsim\VP16; aretScer\UAS.P\T.cFa; grk2B6/+; vasαTub67C.T:Avic\GFP flies.
The early arrest phenotype seen in aretQB mutant ovaries is rescued by aretScer\UAS.P\T.cFa; Scer\GAL4nos.UTR.T:Hsim\VP16.