simaKG07607/+ mutants have a significantly greater reduction in adult eclosion under hypoxic conditions, relative to normoxic conditions, compared to controls, as well as a significant reduction in adult survival of 14 h hypoxia (1 percent oxygen).
simaKG07607 mutants are significantly more likely to die from Serratia marcescens infection than their wild-type counterparts.
simaKG07607 homozygote and heterozygote adults display similar robust response to acute hypoxia as wild-type controls: large proportion of hearts (40-60%) become asystolic (stop beating), those that continue to beat show increased heart period due to increased diastolic interval during hypoxic conditions compared to during re-oxygenation, systolic interval does not significantly change either in wild-type or in simaKG07607 mutants. However, the cardiac contractility (measured as fractional shortening) observed during hypoxia is much lower in simaKG07607 homozygotes than in wild-type (heterozygotes show intermediate phenotype). Unlike wild-type, simaKG07607 mutants display increased diastolic diameters during acute hypoxia and their fractional shortening and systolic diameters recover almost completely to preexposure values following reoxygenation.
Majority of simaKG07607 homozygote hearts fail to beat following a sustained 18 hr under hypoxic conditions (1% O[[2]]), simaKG07607 heterozygote hearts continue to beat but show increased susceptibility to sustained hypoxia compared to wild-type: the decrease in their heart period (increased rate) is more pronounced and they show significant decrease (rather than increase as seen in wild-type) in systolic interval after prolonged hypoxia. Their cardiac contractility is also more reduced as simaKG07607/+ hearts do not shorten as much as in wild-type.
Chronic moderate hypoxia (3 weeks in 4% O[[2]]) leads to significantly reduced heart period (simaKG07607 mutants show lower diastolic as well as systolic intervals) and cardiac contractility (primarily due to lower diastolic diameter) in simaKG07607/+ compared to wild-type.
simaKG07607 mutants exhibit a significant reduction in survival under hypoxic conditions, as compared to controls.
Approximately 99% of flies homozygous for simaKG07607 are non-viable. The few escapers lay few eggs (less than two per female) and complete ovarian degeneration is observed within two to four days after females hatched.
Clusters containing homozygous somatic clones of simaKG07607 display defects during border follicle cell migration. First, the mutant cells are always detected in the leading cell in the cluster. In wild-type cells, there is alternative, competing leadership among the cells of a cluster. Furthermore, in cases in which there is more than one simaKG07607-mutant cell within the same border cell cluster, only one mutant cell is detected to lead the cluster, whereas the other mutant cell is migrating with the rear of the cluster. During stage 9 of oogenesis, 80-90% of border cell clusters with simaKG07607-mutant cells migrate faster than the corresponding anterior follicle cells, reaching the nurse cell and oocyte border prematurely. Moreover, simaKG07607-mutant leading cells appear to be pulling the clusters forward more efficiently than wild-type leading cells, because there is an extension of the actin network between the leading simaKG07607-mutant cell and the following cell. In contrast, the predominant phenotype observed during stage 10 of oogenesis is a delay of migration.
simaKG07607 homozygous embryos show a strongly suppressed pentrance of tracheal phenotypes induced by hypoxia treatment at either stage 11 or stage 15, compared to wild type.
Homozygous embryos can survive up to and through the pupal phase.
Homozygous simaKG07607 flies behave as wild-type flies when subjected to anoxia/reoxygenation stress.
Homozygous embryos develop without any obvious morphological defects compared to controls and the first instar larvae look healthy and motile under normoxia conditions.
Only a small proportion of homozygotes reach the pupal stage under hypoxic conditions.
sima[+]/simaKG07607 is a suppressor | partially of lethal phenotype of agoΔ3-7/ago3
sima[+]/simaKG07607 is a suppressor | partially of lethal phenotype of agoΔ3-7
sima[+]/simaKG07607 is a suppressor | partially of lethal phenotype of agoΔ3-7/ago1
sima[+]/simaKG07607 is a suppressor of lethal phenotype of Scer\GAL4btl.PS, VhlRNAi.UAS.cMa
sima[+]/simaKG07607 is a suppressor of tracheole | cell non-autonomous phenotype of Scer\GAL4tey-5053A, agoΔF.UAS
sima[+]/simaKG07607 is a suppressor of tracheole | increased number phenotype of agoΔ3-7/ago1
sima[+]/simaKG07607 is a suppressor of tracheole phenotype of agoΔ3-7/ago1
sima[+]/simaKG07607 is a suppressor of larval lateral H tracheal branch phenotype of agoΔ3-7/ago1
sima[+]/simaKG07607 is a suppressor of larval lateral H tracheal branch phenotype of agoΔ3-7/ago3
sima[+]/simaKG07607 is a suppressor of tracheole | increased number phenotype of agoΔ3-7/ago3
sima[+]/simaKG07607 is a suppressor | partially of embryonic/larval tracheal section phenotype of Scer\GAL4btl.PS, VhlRNAi.UAS.cMa
simaKG07607/simaKG07607 is a suppressor of embryonic/larval tracheal section phenotype of Scer\GAL4btl.PS, VhlRNAi.UAS.cMa
The increase in the number of tracheal branches that terminate on ventrolateral body wall muscle 12 caused by expression of agoΔF.Scer\UAS under the control of Scer\GAL4tey-5053A is suppressed by simaKG07607/+.
simaKG07607 dominantly delays the lethal phase of agoΔ3-7 homozygotes and of agoΔ3-7/ago1 and agoΔ3-7/ago3 transheterozygotes.
simaKG07607 dominantly suppresses the excess and overlapping terminal tracheal branching seen in agoΔ3-7/ago1 larvae.
simaKG07607 dominantly suppresses the increase in number of terminal branches per lateral LH cell seen in ago3/agoΔ3-7 larvae.
simaKG07607/+ significantly reduces the penetrance of Scer\GAL4btl.PS VhldsRNA.Scer\UAS tracheal defects, while simaKG07607/simaKG07607 further suppresses these defects to background levels.
simaKG07607/+ completely suppresses the pupal lethality of Scer\GAL4btl.PS VhldsRNA.Scer\UAS.
Hph1 simaKG07607 double homozygotes are indistinguishable from controls, both in terms of pupal weight and the duration of larval development. Under normoxia conditions, the double homozygotes can survive to adulthood, although 76% of the animals fail to eclose from the pupal case, and those that do emerge look weak and frequently die shortly after eclosion.
Precise excision of the insertion reverts the hypoxia-dependent lethality.