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. Author manuscript; available in PMC: 2015 Jul 28.
Published in final edited form as: J Neurochem. 2011 Jan 19;116(4):659–668. doi: 10.1111/j.1471-4159.2010.07158.x

Fig. 2. Lithium reduces the accumulation of LC3 dots resulting from CLN3 mutation.

Fig. 2

(A) Photomicrograph showing the effect of CLN3 deletion on LC3 dot formation. SH-SY5Y-LC3 cells were transiently transfected with pcDNA, pCLN3Δ1 (1– 153), pCLN3Δ2 (1–263), pCLN3Δ3 (154–438), pCLN3 AS or pCLN3 for 24 h and then examined for LC3 dot formation. (B) Inhibition of LC3 dot formation by lithium. SH-SY5Y-LC3 cells were transiently transfected as in (A) and then treated with 10 mM NaCl or 10 mM LiCl for 24 h. The formation of GFP-LC3-positive dots was assessed using a fluorescence microscope. Bars indicate means ± S.D. (n > 30 cells). Asterisks indicate significant difference from control (p < 0.05). (C) SH-SY5Y cells were transiently cotransfected with mCherry-GFP-LC3 and either pcDNA, pCLN3Δ1 (1–153), pCLN3Δ2 (1–263), pCLN3Δ3 (154–438), pCLN3 AS or pCLN3 for 24 h and then left untreated (Mock) or treated with 10 mM LiCl for 24 h. The numbers of cells showing only red fluorescence were counted under a confocal microscope as described in Materials and methods. Bars indicate means ± S.D. (n > 30 cells). Asterisks indicate significant difference from control (p < 0.05)