(Downloading may take up to 30 seconds.
If the slide opens in your browser, select File -> Save As to save it.)

Click on image to view larger version.


Figure 1


Fig. 1. Loss of sad-1 and nab-1 functions lead to polarity defects in various neurons. (A) L1-stage sad-1 and nab-1 animals have DD polarity defects. Arrowheads indicate the ectopic dorsal SNB-1::GFP (juIs1) or UNC-49B::GFP (oxIs22) signal. A schematic diagram of the normal connectivity of DD neurons in L1 is shown on the left of the images. (B) sad-1 and nab-1 mutations lead to a decreased number of DD synapses in adult-stage C. elegans. The number of juIs1 puncta on the dorsal nerve cord of nab-1;lin-5, lin-5;sad-1 and nab-1;lin-5;sad-1 animals was compared with lin-5 animals (n>15 animals, P< 0.001 by Tukey-Kramer multiple comparison test). (C) Polarity defects in a DA8 cholinergic motoneuron of sad-1 and nab-1 shown by SNB-1::GFP (wdIs20). sad-1 and nab-1 animals show SNB-1::GFP puncta in the dendritic region of the neuron (arrowheads). *DA8 cell body. (D) ASI chemosensory neurons are visualized using the Pstr-3 SNB-1::GFP vesicle marker (kyIs105). Wild-type animals shows discrete vesicle clusters along the axon, but none in the dendritic process (arrowhead). Both sad-1 and nab-1 animals show puncta in the dendritic and axonal processes. *ASI-neuron cell body. Scale bar: 5 µm in C.