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. Author manuscript; available in PMC: 2012 Apr 1.
Published in final edited form as: Eur J Cell Biol. 2010 Dec 10;90(4):291–300. doi: 10.1016/j.ejcb.2010.10.014

Fig. 6. Knockdown of Tmod2 and Tmod1 impact distinct aspects of neurite initiation and extension.

Fig. 6

N2a cells were plated on Poly-L-Lysine coated coverslips and transfected with vectors co-expressing GFP and Tmod2 shRNA (A-C), or GFP and Tmod1 shRNA (D-F). As control, vectors co-expressing GFP and a respective shRNA mismatch construct were used. Cells were induced to differentiate by serum reduction and the addition of 40 μM retinoic acid. Shown are the percent of GFP-positive cells bearing neurites (A, D), the number of neurites per cell (excluding cells not bearing neurites; B, E) and the mean length of primary neurites (C, F). The decrease in endogenous Tmod2 leads to about a 1.8-fold (p < 0.01) increase in numbers of neurite-bearing cells (A) and about a 1.6 fold (p < 0.05) increase in the mean length of neurites (C), without effect on numbers of neurites per cell (p < 0.4) (B). The decrease in endogenous Tmod1 levels leads to about a 1.3-fold (p < 0.05) increase in neurite numbers per cell (E) and a 10% decrease in the mean length of neurites (p < 0.04) (F), without effect on percentages of neurite-bearing cells (p < 1.0) (D). Results are means ± s.e.m. across experiments for three independent experiments. Asterisks indicate significant differences compared to control at (*) p < 0.05 or (**) p < 0.01 (t-Test, paired, two tailed).