Expression of Scer\GAL4^GMR.PU>Hsap\TARDBP^{N345K.Scer\UAS.T:Avic\GFP-YFP} leads to age- and dose-dependent neurodegeneration as indicated by depigmentation in the eye.

Expression of Hsap\TARDBP^{N345K.Scer\UAS.T:Avic\GFP-YFP} in motor neurons under the control of Scer\GAL4^D42 results in nuclear morphology defects and smaller synapses compared with wild-type. This anatomical phenotype is accompanied by an impairment in locomotor function, as indicated by a significant increase in larval turning time compared with controls.

Expression of Hsap\TARDBP^{N345K.Scer\UAS.T:Avic\GFP-YFP} in glial cells under the control of Scer\GAL4^repo.PU affects nuclear shape.

Compared with controls, expression of Hsap\TARDBP^{N345K.Scer\UAS.T:Avic\GFP-YFP} in glial cells under the control of Scer\GAL4^repo.PU results in significantly smaller neuromuscular junctions (NMJs) with a decreased number of synaptic boutons. When tested for their ability to turn, larvae expressing the transgene in glia also exhibit a significant impairment in locomotor function.

Hsap\TARDBP^{N345K.Scer\UAS.T:Avic\GFP-YFP}-expression leads to a mismatch of pre- and post-synaptic areas. Expression of Hsap\TARDBP^{N345K.Scer\UAS.T:Avic\GFP-YFP} in motor neurons leads to a significant increase in the area of pre-synaptic active zones, while its expression in glia results in reduction in the size of post-synaptic areas.

Both motor neuron and glial expression of Hsap\TARDBP^{N345K.Scer\UAS.T:Avic\GFP-YFP} can lead to alterations in adult locomotion and sleep patterns.