anterior fascicle & synapse, with Scer\GAL4elav-C155
Border follicle cell clusters in homozygous females show significantly reduced net cluster movement compared to wild type in the early (but not in the late) phase of posterior migration. The cells show increased tumbling in the early phase of posterior migration. The number of cellular extensions from the front of the border cell cluster is reduced compared to wild type in the early phase of posterior migration.
Border cells are motile but much less directional in a Pvf1EP1624 mutant background. Migration is delayed for about 95% of border cell clusters in Pvf1EP1624 mutants.
Mutants show mild defects in posterior migration of border follicle cells towards the oocyte.
13% of Pvf1EP1624 egg chambers show border cell migration defects.
Males show rotated external terminalia. The phenotype shows variable penetrance and expressivity, both of which increase at higher temperatures. Direction of rotation of spermiduct is unaffected, though the sperm pump lies on the left rather than the wild type right. There is some degree of pupal lethality and adults show reduced fertility. Individuals occasionally show a failure of dorsal closure.
Border follicle cells show migration defects in homozygous Pvf1EP1624 stage 10 egg chambers; in 81% of egg chambers they have migrated 76-100% the normal distance, in 8% they have migrated 51-75% the normal distance, in 6% they have migrated 26-50% the normal distance and in 5% they have migrated 0-25% the normal distance. Pvf1EP1624 has little effect on the border cell migration phenotype seen in egg chambers expressing one of copy of Pvf1Scer\UAS.cMa under the control of Scer\GAL4Act5C.PI in anterior follicle cell clones. If the egg chambers are also heterozygous or homozygous for Pvf1EP1624, in 80% of cases the border cell clusters migrate normally to the oocyte.
Mutant larvae show no obvious defects in blood cell counts. Mutant pupae show 40-60% lethality.
Homozygotes exhibit a weak border cell migration phenotype.
Mutant larvae expressing Pvf1EP1624 under the control of Scer\GAL4elav-C155 have reduced or abnormal synapses. Mutant larvae expressing Pvf1EP1624 under the control of Scer\GAL4elav-C155 have ISN neuron pathfinding defects.
Pvf1EP1624, Scer\GAL4ptc-559.1 is a suppressor of radiation resistant | cell non-autonomous phenotype of E2f1RNAi.UAS.cJa, Scer\GAL4ptc-559.1
Df(3L)Krn-27-7-B, Pvf1EP1624, spi1 has sterile phenotype
Df(3L)Krn-27-7-B, Pvf1EP1624, spi1 has partially lethal phenotype
Pvf1EP1624, Scer\GAL4slbo.2.6 has border follicle cell phenotype, enhanceable by EgfrUAS.cBa, Scer\GAL4slbo.2.6
Pvf1EP1624 has border follicle cell phenotype, enhanceable by hepAct.UAS/Scer\GAL4slbo.2.6
Pvf1EP1624 has border follicle cell phenotype, non-enhanceable by Df(3L)Krn-27-7-B
Pvf1EP1624 has border follicle cell phenotype, non-enhanceable by spi1
Pvf1EP1624, Scer\GAL4slbo.2.6 is an enhancer of border follicle cell phenotype of EgfrUAS.cBa, Scer\GAL4slbo.2.6
Pvf1EP1624, Scer\GAL4slbo.2.6 is an enhancer of border follicle cell phenotype of EgfrDN.UAS, Scer\GAL4slbo.2.6
Pvf1EP1624, Scer\GAL4ptc-559.1 is a suppressor of wing disc | cell non-autonomous phenotype of E2f1RNAi.UAS.cJa, Scer\GAL4ptc-559.1
Pvf1EP1624, Scer\GAL4ey.3.5.Exel is a suppressor of eye phenotype of Scer\GAL4ey.3.5.Exel, kayFbz.UAS
Pvf1EP1624, grkHF, spi1 has egg chamber phenotype
Pvf1EP1624, tai[+]/tai61G1 has border follicle cell phenotype
Pvf1EP1624, tai61G1 has border follicle cell phenotype
One copy of Pvf1EP1624 attenuates the protective effect on surrounding cells seen when cell death is initiated through expression of E2f1dsRNA.Scer\UAS.cJa under the control of Scer\GAL4ptc-559.1.
The effect on border cell cluster migration of expressing PvrScer\UAS.T:Avic\GFP under the control of Scer\GAL4c522 in a single border follicle cell in a EgfrdsRNA.slbo Pvf1EP1624 background (to remove endogenous guidance information) has been studied. These clusters are dynamic and display disordered movement including cluster tumbling. In those border cell clusters where the single PvrScer\UAS.T:Avic\GFP-expressing cell is located at the front of the cluster, the cluster on average moves forward, when the PvrScer\UAS.T:Avic\GFP-expressing cell is in the back, the cluster on average moves relatively more backwards and when the PvrScer\UAS.T:Avic\GFP-expressing cell is on the side of the cluster, border cell migration is unaltered compared to control clusters without a PvrScer\UAS.T:Avic\GFP-expressing cell.
Expression of Pvf1EP1624 suppresses the small eye phenotype associated with kayFbz.Scer\UAS, when both are expressed under the control of Scer\GAL4ey.3.5.Exel.
Expression of hepAct.Scer\UAS under the control of Scer\GAL4slbo.2.6 enhances the severity of the posterior migration defects seen in Pvf1EP1624 mutant border follicle cells.
Pvf1EP1624; Df(3L)Krn-27-7-B double mutant egg chambers show no enhancement of the border cell migration defects seen in Pvf1EP1624 single mutants. Likewise, no enhancement is seen in Pvf1EP1624; spi1 double mutants.
Pvf1EP1624; spi1; Df(3L)Krn-27-7-B triple mutants are poorly viable or sterile.
The egg chambers of Pvf1EP1624; spi1; grkHF females do not develop normally.
About 6% of Pvf1EP1624 tai61G1 double heterozygous egg chambers have border cell migration defects.
The combination of Pvf1EP1624, and EgfrDN.Scer\UAS (driven by Scer\GAL4slbo.2.6) leads to strong effect. Border cells are not able to reach the oocyte by stage 10, and they also show a low level of "off track" migration.
The effect on border cell cluster migration of expressing Pvr::Hsap\EGFRhE-P.Scer\UAS.T:Avic\GFP under the control of Scer\GAL4c522 in a single border follicle cell in a EgfrdsRNA.slbo Pvf1EP1624 background (to remove endogenous guidance information) has been studied. Overall disordered, or tumbling border cell movements are seen in these clusters. In those border cell clusters where the single Pvr::Hsap\EGFRhE-P.Scer\UAS.T:Avic\GFP-expressing cell is located at the front of the cluster, the cluster on average moves forward, when the Pvr::Hsap\EGFRhE-P.Scer\UAS.T:Avic\GFP-expressing cell is in the back, the cluster on average moves relatively more backwards.
Excision of the P{EP} element reverts the mutant phenotype.