All Nhe2null exons have been excised.
Scer\FRT-mediated recombination between the two progenitor insertions has resulted in the deletion of the genomic sequence between them. All exons of Nhe2 have been removed.
Nhe2null homozygous females lay significantly fewer eggs compared to controls. Their germaria show frequent defects including cyst encapsulation defects and/or disorganized follicular epithelium, and loss of germline stem cells, as compared to controls. When stalks were present in the ovarioles, stalk cells exhibited signs of differentiation defects, illustrated by ectopic expression of Eya and a mostly rounded morphology, as compared to controls.
Retinal architecture in homozygous Nhe2null mutant flies is organized and regular, resembling wild type. In third instar larval eye discs tissue morphology is indistinguishable from wild type but there are fewer proliferative cells than in wild type. In pupal eyes, the secondary pigment cells are thicker than in wild type and cell shapes and cell contacts are irregular.
The intracellular pH (pHi) in Nhe2null eye discs is significantly lower than in controls, but is unchanged from wild type by the pupal stages.
Nhe2null, RafUAS.F179, Scer\GAL4GMR.PU has cell lethal phenotype
Nhe2null, Scer\GAL4GMR.PU is an enhancer of retina phenotype of RafUAS.F179, Scer\GAL4GMR.PU
Nhe2null, Scer\GAL4GMR.PU is an enhancer of rhabdomere phenotype of RafUAS.F179, Scer\GAL4GMR.PU
Expression of phlScer\UAS.F179 under the control of Scer\GAL4GMR.PU in a Nhe2null mutant background results in synthetic cell lethality. Externally, the adult eye phenotype is identical to expression of phlScer\UAS.F179 alone, except that eye colour is lighter, but internally there is loss of tissue architecture and cell structure with coagulative necrosis, including loss of rhabdomere morphology, absence of distinct cell membranes and diffusion of pigment granules.
Nhe2null suppresses the tissue morphology defects and hyperproliferation seen in third instar larval eye disc when phlScer\UAS.F179 is expressed under the control of Scer\GAL4GMR.PU. Neuronal cell fates appear unaffected.
Nhe2null enhances the morphological defects seen in the retina of pupal expressing phlScer\UAS.F179 under the control of Scer\GAL4GMR.PU. All cell types appear smaller and more cells have abnormal morphologies. More ommatidia have extra cone cells. Cell death is seen that is not detected in either mutant alone.
In contrast to either mutant alone, the intracellular pH (pHi) in eye discs expressing phlScer\UAS.F179 under the control of Scer\GAL4GMR.PU in a Nhe2null mutant background is similar to wild type. However, the pHi is reduced compared to wild type by the pupal stages.
Nhe2null is rescued by Scer\GAL4Mef2.PR/Nhe2UAS.cGa
Nhe2null is not rescued by Scer\GAL4elav.PU/Nhe2UAS.cGa
The semi-lethality of Nhe2null flies is rescued by expression of Nhe2Scer\UAS.cGa using the muscle-specific Scer\GAL4Mef2.PR driver, but not using the neuronal Scer\GAL4elav.PU driver.