LGALS4 and amyotrophic lateral sclerosis: In view of the loss-of-function phenotype of the locomotive ability of flies with whole-body knockout of dTDP expression (Fig. 1; [23]) and the disease phenotypes caused by overexpression of human hTDP-43 in Drosophila[19], we have tested whether the pathway(s) leading to ALS disease pathology was conserved in the fruit flies by knockdown or overexpression of dTDP in the motor neurons of Drosophila. We first used the motor neuron-specific driver (D42-GAL4) to knockdown the endogenous dTDP in the motor neurons.