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. 1999 Aug 1;19(15):6446–6456. doi: 10.1523/JNEUROSCI.19-15-06446.1999

Fig. 3.

Fig. 3.

Bcl-2 overexpression increases the number of motor and sensory axons in mutant NF-L (Pro) mice to above wild-type levels. Axon counts from L5 motor (A) and sensory (B) roots are indicated for the various mouse genotypes at ages of 2, 3, 4, 8, 16, 24, and 60 weeks.A, NF-L (Pro) mutant mice have considerably fewer motor axons than wild-type mice do. Overexpression of Bcl-2 alone results in mice with many more axons than in wild type. Bcl-2 overexpression in mutant NF-L (Pro) mice restores the total number of axons to greater than wild-type levels at all ages examined. Counts are averages from three to five mice of each genotype and age with the exception of the 15-month-old animals (n = 2). B, Sensory axons are relatively spared from mutant NF-L (Pro) transgene–mediated killing. Overexpression of Bcl-2 may increase the numbers of NF-L (Pro) axons early in life, but a common final number of axons is reached in NF-L (Pro) mutants regardless of Bcl-2 expression levels. Counts are averages from three to five mice of each genotype and age with the exception of the 15-month-old animals (n = 2). Error bars represent the SD of the data.