Hs2std267 mutant ovarioles show an increase in the number of stalk cells.
Hs2std267 mutant testes are smaller than those of wild-type. There is a loss of investment cones, which are characteristic for elongated spermatids, suggesting that maturation of male germ cells fail in Hs2std267 mutant testes.
Hs2std267 mutants exhibit defects in wing disc tracheoblasts.
Hs2std267 mutants do not exhibit ectopic wing vein material.
Hs2std267 has increased mortality during development phenotype, enhanceable by Hsepid12
Hs2std267, Hs6std770 has partially lethal - majority die phenotype
Hs2std267 has stalk follicle cell phenotype, non-suppressible by Hsepid12
Hs2std267, Hs6stGD3078, Hsepid12, Scer\GAL4btl.PS has imaginal tracheoblast | temperature conditional phenotype
Hs2std267, Hs6stGD3078, Scer\GAL4btl.PS has imaginal tracheoblast | temperature conditional phenotype
Hs2std267, Hs6stRNAi.UAS.cKa, Scer\GAL4btl.PS has imaginal tracheoblast phenotype
Hs2std267, Hs6std770 has tracheal precursor cell phenotype
Hs2std267, Hs6std770 has adult tracheal air sac phenotype
Hs2std267 Hsepid12 double mutants exhibit an ovariole stalk cell phenotype similar to that in Hs2std267 single mutants.
Tracheoblasts from Hs2std267 Hsepid12 double mutants are indistinguishable from wild-type.
Hs2std267 Hsepid12 double mutants do not exhibit ectopic wing vein material, indicating that Hs2std267 suppresses the ectopic posterior cross vein phenotype found in Hsepid12 mutants.
Knockdown of Hs6st through expression of Hs6stGD3078 under the control of Scer\GAL4btl.PS at 25[o]C in a Hs2std267 mutant background severely interferes with tracheoblast formation.
Knockdown of Hs6st through expression of Hs6stGD3078 under the control of Scer\GAL4btl.PS at 25[o]C in a Hs2std267 Hsepid12 double mutant background severely interferes with tracheoblast formation.
Embryos that are maternal and zygotic mutant for Hs6std770 and Hs2std267 are partial lethal during development. However, significant fractions of these null mutants survive to the adult stage without visible phenotypes.
Hs2std267/Hs6std770 zygotic double mutants are completely lethal. Although invagination seems to occur normally in Hs2std267/Hs6std770 embryos, they exhibit several characteristic defects in branching morphogenesis. First, mutant tracheal precursor cells fail to migrate to form the primary branches. Second, clusters of mutant tracheal cells tend to extend dorsally and ventrally, forming long, skinny sacs of tracheal precursor cells of various sizes. Finally, approximately 16% of mutant embryos show fusion of the tracheal sacs to those in the neighboring segments.
Expression of Hs6stdsRNA.IR.Scer\UAS.K in btl-expressing (tracheal) cells (through the control of Scer\GAL4btl.PS in a Hs2std267 homozygous mutant background completely blocks the formation of the tracheoblast. No such effect is observed when Hs6stdsRNA.IR.Scer\UAS.K is expressed in bnl expressing (non-tracheal) cells (through Scer\GAL4bnl-NP2211) in the same mutant background.
