The expression of lolaL.Scer\UAS results in third instar larval class I abdominal dorsal multidendritic ddaD and ddaE neurons exhibiting a reduced dendritic tree (expression under the control of Scer\GAL4221) and class IV abdominal dorsal multidendritic ddaC neurons exhibiting a significant decrease in the number of dendrite branch terminals (expression under the control of Scer\GAL4ppk.PG), as compared to controls.
MARCM-mediated expression of lolaL.Scer\UAS, using Scer\GAL4GH146, results in strong targeting defects in antero-dorsal projection neuron (adPN) and lateral (lPN) neuroblast clones. Phenotypes often include a large increase in wandering dendrites in the antennal lobe (AL) and some degree of loss of targeting and ectopic targeting. Often dendrites appear to be largely restricted to one region of the AL, such as dorsal or lateral, and have wandering dendrites through this region in many glomeruli, but fail to innervate normal targets or extend any dendrites into other regions of the AL.
MARCM-mediated expression of lolaL.Scer\UAS, using Scer\GAL4GH146, results in weak phenotypes in vPN neuroblast clones.
The DL1 dendrites are targeted correctly with MARCM-mediated expression of lolaL.Scer\UAS, using Scer\GAL4GH146, but frequently show a large increase in dendritic mass outside of DL1, wandering throughout the AL. In axons, lolaL.Scer\UAS overexpression often results in an increase in branching in mushroom body and lateral horn regions.
MARCM clones simultaneously mutant for lolae76 and lolaL.Scer\UAS, induced using Scer\GAL4GH146, exhibit: i) cell loss and lack of dendritic extensions in adPN and lPN neuroblast clones; ii) a strong reduction of VA1lm and DA1 targeting in vPN clones, with the pan-AL neuron often showing little dendritic process elaboration and only rare innervation of much of the AL.
DL1 MARCM clones simultaneously mutant for lolae76 and lolaL.Scer\UAS, induced using Scer\GAL4GH146 innervate DL1 in addition to having extensive dendritic innervation in the rest of the AL. Axonal defects range from a failure to extend or elaborate branches in the LH to an increase in ectopic branching.