filzkorper | embryonic stage | maternal effect (with tsl2)
filzkorper | embryonic stage | maternal effect (with tsl3)
filzkorper | embryonic stage | maternal effect (with tsl4)
filzkorper | embryonic stage | maternal effect (with tsl5)
telson | embryonic stage | maternal effect (with tsl2)
telson | embryonic stage | maternal effect (with tsl3)
telson | embryonic stage | maternal effect (with tsl4)
telson | embryonic stage | maternal effect (with tsl5)
Late embryos from tslΔ/tsl2 tslΔ/tsl3, tslΔ/tsl4, tslΔ/tsl5 transheterozygous and tslΔ homozygous mothers exhibit a fully penetrant "terminal class mutant" phenotype, in which some terminal structures are missing (including head structures, abdominal segment 8, telson, and filzkorper), as compared to controls; late embryos from tslΔ/tsl4, tslΔ/tsl5 transheterozygous and tslΔ homozygous mothers also exhibit an increasingly highly penetrant posterior-ventral cuticle hole phenotype, as compared to controls.
Gastrulating embryos from tslΔ homozygous mothers present an elongated, irregular and often incomplete ventral furrow, associated with delayed and patchy apical constriction, misaligned apical edges and apical mis-positioning of the nucleus in ventral domain cells, as compared to controls; these defects are more pronounced at the posterior region of the embryo, which frequently shows a complete failure in apical constriction. These gastrulating embryos also present failed posterior midgut invagination, leaving the pole cells and a large field of Twist-positive mesodermal tissue exposed at the dorsal surface, as compared to controls.
tslΔ mutant females are sterile, laying embryos that fail to specify terminal cell fate.
tslΔ mutant homozygotes show a significant delay of 26 hours to reach pupariation compared with heterozygous controls. The L2-L3 transition is delayed by ~7 hours. tslΔ mutant adult flies are 28% smaller than heterozygous controls and larvae are also noticeably smaller both at the wandering stage and throughout the third instar larval stage.
Wing cell density is significantly higher in tslΔ mutant flies compared with controls, indicating that cell size is reduced. Adult wings are also smaller than controls.
tslΔ/tsl5 mutant transheterozygotes are significantly delayed in reaching pupariation compared with controls.
tslΔ has abnormal developmental rate phenotype, enhanceable by torrv66
tslΔ has abnormal size phenotype, non-suppressible by torrv66
tslΔ is an enhancer of abnormal developmental rate phenotype of torrv66
tslΔ is an enhancer of abnormal size phenotype of PtthUASp.Tag:HA, Scer\GAL4phtm.PO
tslΔ is a suppressor of abnormal size phenotype of torrv66
tslΔ is a non-suppressor of abnormal developmental rate phenotype of PtthUASp.Tag:HA, Scer\GAL4phtm.PO
tslΔ has embryonic/larval cuticle | embryonic stage | ventral | maternal effect phenotype, enhanceable by RhoGEF2[+]/RhoGEF24.4
tslΔ has embryonic/larval cuticle | embryonic stage | ventral | maternal effect phenotype, non-enhanceable by fogUASp.cJa/Scer\GAL4VP16.nanos.UTR
tslΔ/tslΔ is a suppressor | partially of embryonic/larval cuticle | maternal effect | embryonic stage phenotype of Scer\GAL4VP16.nanos.UTR, fogUASp.cJa
tslΔ is a non-suppressor of embryo phenotype of PtthUASp.Tag:HA, Scer\GAL4VP16.nanos.UTR
The ventral cuticle defects displayed by late embryos from tslΔ homozygous mothers are strongly enhanced by heterozygosity for RhoGEF24.4, leading to fully penetrant absence of ventral cuticle.
Late embryos from mothers both homozygous for tslΔ and expressing fogScer\UAS.P\T.cJa under the control of Scer\GAL4nos.UTR.T:Hsim\VP16 exhibit cuticle defects more similar to those of embryos from mothers only homozygous for tslΔ (i.e. some missing terminal structures and ventral-posterior cuticle hole) than those of embryos from mothers only expressing fogScer\UAS.P\T.cJa under the control of Scer\GAL4nos.UTR.T:Hsim\VP16 (i.e. only small amounts of recognizable cuticle remaining).
tslΔ torrv66 double mutants show a dramatically extended larval period compared to either mutant alone, with flies pupating 83 hours after controls. Double mutant adult flies are similar in size to tslΔ mutants alone.
A tslΔ mutant background does not suppress the advanced pupariation phenotype seen in flies expressing PtthScer\UAS.P\T.T:Ivir\HA1 under the control of Scer\GAL4phm.PO. The decrease in male body size is further enhanced. The embryonic patterning defects seen when PtthScer\UAS.P\T.T:Ivir\HA1 is expressed under the control of Scer\GAL4nos.UTR.T:Hsim\VP16 are also not suppressed.
tslΔ is rescued by tslUAS.cJa/Scer\GAL4da-BG00643
tslΔ is not rescued by tslUAS.cJa/Scer\GAL4phtm.PO
The following defects exhibited by embryos from tslΔ mothers are partially rescued by one copy of tslT:Ivir\HA1 : the ventral cuticle hole, but not the "terminal class mutant" phenotype, in late embryos; both the irregularities/gaps in the ventral furrow and the exposure of mesodermal tissue (Twist-positive) at the dorsal surface, but not the elongated ventral furrow or the exposure of pole cells at the dorsal surface, in gastrulating embryos.
The expression of tslScer\UAS.T:Hsap\MYC,T:Avic\GFP-EGFP under the control of Scer\GAL4slbo.2.6 fully rescues the ventral cuticle hole and head defects, and partially rescues the patterning and cuticle defects exhibited by embryos from tslΔ mothers.
Expression of tslScer\UAS.cJa under the control of Scer\GAL4da-BG00643 rescues the delay in pupariation seen in tslΔ mutants. Expression of tslScer\UAS.cJa under the control of Scer\GAL4phm.PO is unable to rescue the phenotype.
Expression of tslT:Ivir\HA1 completely rescues the developmental delay and reduction in size seen in tslΔ mutant flies. The defect in terminal embryonic patterning is not rescued.