rawdcp-1 homozygotes show protection against (injury-induced) Wallerian degeneration in third instar larval motor neurons, which is not significantly suppressed by the expression of bskK53R.UAS under the control of Scer\GAL4tey-5053A; in these double mutants, injured axons exhibit severely decreased new growth/sprouting compared to controls, as well as varicosities.
Co-expression of egrUAS.cUa and bskK53R.UAS under the control of Scer\GAL4rn-GAL4-5 (in combination with tub-Gal80[ts] to restrict expression to early stages of third instar larvae) does not lead to ectopic wings compared to controls.
The co-expression of bskK53R.Scer\UAS suppresses the tumor phenotype and tissue disorganization resulting from the expression of dlg1HMS01954, but not from the expression of aPKCΔN.Scer\UAS, under the control of Scer\GAL4Bx-MS1096.
The synaptic overgrowth phenotype (increase in bouton number) seen at the neuromuscular junction in larvae derived from homozygous SkpAGD65 females is partially suppressed by expression of bskK53R.Scer\UAS under the control of Scer\GAL4elav.PU.
The co-expression of bskK53R.Scer\UAS does not suppressed the following defects resulting from the expression of biScer\UAS.cBa in third instar larval wing discs: long distance cell migration and scattering, from expression either under the control of Scer\GAL4dpp.PU or in clones under the control of Scer\GAL4Act5C.PI; and the basal delamination of cells, resulting from the expression under the control of Scer\GAL4C-765.
Co-expression of CskdsRNA.Scer\UAS and Sin3AKK100700 (with Dcr-2Scer\UAS.cDa) results in a much stronger wing disc cell migration phenotype than is seen when either transgene is expressed alone. Upon co-expression of bskK53R.Scer\UAS, massive overgrowth is seen, but the invasion phenotype is suppressed.
Co-expression of PvrCA.Scer\UAS and bskK53R.Scer\UAS in 3-5 day old adult flies, under the control of Scer\GAL4esg-NP5130 and Scer\GAL80ts.αTub84B phenocopies the proliferation of Scer\GAL4esg-NP5130>GFP-positive cells observed upon expression of PvrCA.Scer\UAS alone.
The disruption of the actin cytoskeleton that is seen in the wing imaginal discs of animals expressing Vps4DN.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4Bx-MS1096-KE is partially suppressed by co-expression of bskK53R.Scer\UAS.
Co-expression of bskK53R.Scer\UAS and sggA81T.Scer\UAS pan-neuronally under the control of Scer\GAL4elav-C155 severely and significantly reduces synapse size compared to synapses in Scer\GAL4elav-C155-sggA81T.Scer\UAS flies.
Expression of bskK53R.Scer\UAS (under the control of Scer\GAL4BG380) suppresses the hiwND8 synaptic phenotype, reducing the number of synaptic boutons and branches and increasing bouton size and the intensity of synaptic vesicle markers.
Ectopic expression of bskK53R.Scer\UAS, under the regulatory control of Scer\GAL4Ddc.PL in hep1 mutants restores the morphology of dorsomedial dopaminergic neuron. The thoracic cleft formation observed in parkScer\UAS.T:Hsap\MYC overexpression mutants (Scer\GAL4ap-md544) and bskK53R.Scer\UAS mutants is mutually enhanced by their co-expression.
Downregulation of JNK signaling in clones of scribunspecified mutant tissue by overexpression of bskK53R.Scer\UAS suppresses apoptosis (from 16.6% to wild-type levels of 25%) and increases the overgrowth of the tissue, even compared to wild-type, resulting in scribunspecified bskK53R.Scer\UAS clones contributing over 70% of the tissue in third instar eye imaginal discs.
The enlarged wing disc posterior compartment observed upon exposure to ionizing radiation of individuals expressing BacA\p35UAS.cHa alone, or in combination with either okrKK107487 or mei-41GD4258, is suppressed by the additional co-expression of bskK53R.UAS.
The additional co-expression of bskK53R.UAS suppresses the longer DNA damage response to an exposure to ionizing radiation (assessed by phospho-H2Av immunostaining) in the wing disc posterior compartment observed in individuals co-expressing BacA\p35UAS.cHa and either okrKK107487 or mei-41GD4258 under the control of Scer\GAL4en.PU.