"In unc-104 animals, GFP-tagged synaptobrevin (Nonet, 1999; and Figure 8B) and other synaptic vesicle components were restricted to cell bodies (Nonet et al., 1993, 1997, 1998), and fluorescence was distributed within the intracellular space."
This RNAi was able to suppress the locomotion phenotypes found in L-AChR(gf) animals. L-AChR(gf) enhances synaptic activation of muscles by increasing L-AChR function.
This RNAi was able to suppress the locomotion phenotypes found in L-AChR(gf) animals. L-AChR(gf) enhances synaptic activation of muscles by increasing L-AChR function.
This RNAi was able to suppress the locomotion phenotypes found in L-AChR(gf) animals. L-AChR(gf) enhances synaptic activation of muscles by increasing L-AChR function.
This RNAi was able to suppress the locomotion phenotypes found in L-AChR(gf) animals. L-AChR(gf) enhances synaptic activation of muscles by increasing L-AChR function.
This RNAi was able to suppress the locomotion phenotypes found in L-AChR(gf) animals. L-AChR(gf) enhances synaptic activation of muscles by increasing L-AChR function.
"To quantify the synaptic decrease of the L-AChRs in emc-6(kr150), we generated a knock-in strain carrying the unc-29 L-AChR subunit endogenously tagged with tagRFP using the MosTIC technique (46). Consistent with immunostaining of LAChRs, we observed an 82% decrease of the amount of L-AChR at the NMJ (Fig. 3 D and E). The remaining L-AChRs still formed synaptic clusters in emc-6(kr150) mutants."