Scer\GAL4elav.PU-mediated expression of PlexAScer\UAS.cWa results in CNS axon guidance defects - discontinuous, thin or missing CNS longitudinal connectives, and CNS axons abnormally crossing the midline.
Expression of plexAScer\UAS.cWa in embryos under the control of Scer\GAL4elav.PLu causes thick bundles of axons to abnormally cross the midline.
Causes no mutant phenotype in the mushroom bodies when expression is driven by Scer\GAL4.
Embryos expressing plexAScer\UAS.cWa under the control of Scer\GAL4elav.PLu show axon guidance defects in all parts of the motor projection and also in the central nervous system. The dorsal SNa branch splits prematurely into multiple projections in 66% of segments and the dorsal extension of the intersegmental nerve (ISN) defasciculates inappropriately in 25% of segments. The transverse nerve is stalled in 26% of segments, resulting in the 2 halves of the nerve failing to meet. ISNb axons often fail to reach their muscle targets, and the nerve displays a thickened clumped structure, with stalls at choice points 2 and 3. The Fas2-positive longitudinal tracts are less tightly fasciculated than normal and are not always continuous between segments. The outermost Fas2-positive fascicle defasciculates and extends away from the central nervous system.
PlexAUAS.cWa, Scer\GAL4elav.PLu has abnormal neuroanatomy phenotype, enhanceable by PlexAUAS.cWa, Scer\GAL4elav.PLu
PlexAUAS.cWa, Scer\GAL4elav.PU has abnormal neuroanatomy phenotype, suppressible by SelRUAS.cHa, Scer\GAL4elav.PU
PlexAUAS.cWa, Scer\GAL4elav.PLu has abnormal neuroanatomy phenotype, suppressible | partially by Gyc76CKG03723ex173
PlexAUAS.cWa, Scer\GAL4elav.PLu has abnormal neuroanatomy phenotype, suppressible | partially by Gyc76CD945A.UAS.Tag:MYC, Scer\GAL4elav.PLu
PlexAUAS.cWa, Scer\GAL4elav.PLu is an enhancer of abnormal neuroanatomy phenotype of PlexAUAS.cWa, Scer\GAL4elav.PLu
PlexAUAS.cWa, Scer\GAL4elav.PLu has fascicle | ectopic phenotype, enhanceable by PlexAUAS.cWa, Scer\GAL4elav.PLu
PlexAUAS.cWa, Scer\GAL4elav.PU has central nervous system phenotype, suppressible by SelRUAS.cHa, Scer\GAL4elav.PU
PlexAUAS.cWa, Scer\GAL4elav.PLu has fascicle | ectopic phenotype, suppressible | partially by Gyc76CKG03723ex173
PlexAUAS.cWa, Scer\GAL4elav.PLu has fascicle | ectopic phenotype, suppressible | partially by Gyc76CD945A.UAS.Tag:MYC, Scer\GAL4elav.PLu
PlexAUAS.cWa, Scer\GAL4elav.PLu is an enhancer of fascicle | ectopic phenotype of PlexAUAS.cWa, Scer\GAL4elav.PLu
Scer\GAL4elav.PU-mediated expression of SelRScer\UAS.cHa significantly rescues the axon guidance defects seen in SelRScer\UAS.cHa Scer\GAL4elav.PU animals.
A Gyc76CKG03723ex173 background partially suppresses the aberrant axon midline-crossing phenotype of embryos that express plexAScer\UAS.cWa under the control of Scer\GAL4elav.PLu. In contrast, coexpression of Gyc76CScer\UAS.T:Hsap\MYC with plexAScer\UAS.cWa, under the control of Scer\GAL4elav.PLu, enhances the axon guidance phenotype of plexAScer\UAS.cWa-expressing embryos, with many axon bundles crossing the midline. Coexpression of the dominant negative Gyc76CD945A.Scer\UAS.T:Hsap\MYC transgene with plexAScer\UAS.cWa, under the control of Scer\GAL4elav.PLu, results in a partial suppression of the plexAScer\UAS.cWa-induced axon guidance phenotype.
PlexAUAS.cWa/Scer\GAL4elav.PLu partially rescues Df(4)C3
The central nervous system and motor axon guidance defects of homozygous Df(4)C3 embryos are rescued by plexAScer\UAS.cWa expressed under the control of Scer\GAL4elav.PLu.