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. 2003 Apr 14;161(1):55–66. doi: 10.1083/jcb.200301026

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Copyright © 2003, The Rockefeller University Press

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Figure 3. — Gross analysis of KIF5A conditional mutant mice (KIF5A ^nul ^l/KIF5A^flox; Cre^synapsin). (A) Western blot analysis to measure KIF5A protein levels in the brains of KIF5A^null/KIF5A^flox; Cre^synapsin mice. Equal amounts of brain homogenate from 3-wk-old mutant and control (KIF5A^flox/KIF5A^WT) littermates were loaded; actin was used as a loading control. Each marked number represents the ratio between the mutant band and control band after normalizing with the actin band. (B and C) KIF5A excision by Cre^synapsin transgene in DRG (B) and spinal cord motor neurons (C) of KIF5A^null/KIF5A^flox; Cre^synapsin mutant. Tissue sections from ∼3-wk-old mutant and control littermates were stained with KIF5A-specific antibody. Spinal cord sections were also double stained with an anti-BIP antibody to visualize the motor neuron cell bodies. Note the decreased or lack of KIF5A staining in some neurons (arrowheads). Bar, 100 μm. (D) A comparison of body weight (mean ± SD) among 3-wk-old littermates with different genotypes. Note the obvious low body weight in the KIF5A^null/KIF5A^flox; Cre^synapsin mutant group, n = 4 for each group. *, P < 0.01. (E) Most KIF5A^null/KIF5A^flox; Cre^synapsin mutant mice died around 3 wk of age. Postnatal survival curve of a group of mice (142 total, 113 control and 29 mutant) is shown here. The rate of survival of the different genotypes was plotted against age. (F) Abnormal hind limb posture in an older KIF5A^null/KIF5A^flox; Cre^synapsin mutant mouse. Two 7.5-mo-old littermates (control and KIF5A^null/KIF5A^flox) are shown.

Figure 3. — Gross analysis of KIF5A conditional mutant mice (KIF5A ^nul ^l/KIF5A^flox; Cre^synapsin). (A) Western blot analysis to measure KIF5A protein levels in the brains of KIF5A^null/KIF5A^flox; Cre^synapsin mice. Equal amounts of brain homogenate from 3-wk-old mutant and control (KIF5A^flox/KIF5A^WT) littermates were loaded; actin was used as a loading control. Each marked number represents the ratio between the mutant band and control band after normalizing with the actin band. (B and C) KIF5A excision by Cre^synapsin transgene in DRG (B) and spinal cord motor neurons (C) of KIF5A^null/KIF5A^flox; Cre^synapsin mutant. Tissue sections from ∼3-wk-old mutant and control littermates were stained with KIF5A-specific antibody. Spinal cord sections were also double stained with an anti-BIP antibody to visualize the motor neuron cell bodies. Note the decreased or lack of KIF5A staining in some neurons (arrowheads). Bar, 100 μm. (D) A comparison of body weight (mean ± SD) among 3-wk-old littermates with different genotypes. Note the obvious low body weight in the KIF5A^null/KIF5A^flox; Cre^synapsin mutant group, n = 4 for each group. *, P < 0.01. (E) Most KIF5A^null/KIF5A^flox; Cre^synapsin mutant mice died around 3 wk of age. Postnatal survival curve of a group of mice (142 total, 113 control and 29 mutant) is shown here. The rate of survival of the different genotypes was plotted against age. (F) Abnormal hind limb posture in an older KIF5A^null/KIF5A^flox; Cre^synapsin mutant mouse. Two 7.5-mo-old littermates (control and KIF5A^null/KIF5A^flox) are shown.