Analysis Tools
mortality/aging
growth/size/body
nervous system
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• at P25, brains are smaller than those of wild-type controls
• however, brain structures including the hippocampus appear grossly normal
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• in vitro, cultured hippocampal neurons from E16.5 embryos exhibit polarity defects at at day 6 (DIV6): about half of them generate multiple axons, ranging from 2 to 4, as assessed by immunostaining for axon markers; however, the density of synapsin-positive puncta per axon length is normal at DIV14, suggesting normal axon and dendrite differentiation despite multiple axon formation
• in vivo, a few pyramidal neurons stained by the Golgi method at P6 (cingulate cortex) or P8 (anterior cortex) exhibit multiple axon-like processes rather than a single axon extending from the soma towards the ventricular side of the cortex, unlike in wild-type cortex
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• in vitro, cultured hippocampal neurons from E16.5 embryos exhibit polarity defects at DIV6: about half of them generate multiple axons, ranging from 2 to 4, as assessed by immunostaining for axon markers
• transfection of hippocampal neurons with alphaTAT1-specific siRNA at DV1 to deplete alpha-tubulin acetyltransferase-1 (key enzyme for tubulin acetylation) abolishes supernumerary axon formation
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digestive/alimentary system
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• at P21 in absorptive cells located at the lateral walls of villi the apicobasal orientation of microtubules seen in wild-type controls is absent with many microtubules showing a wavy appearance
• total microtubule density is also decreased in absorptive cells located at the lateral walls of villi
• disordered nuclear positioning, reduced cell height and abnormal positioning of other organelles (Golgi complex, mitochondria) at P21 in absorptive cells located at the lateral walls of villi
• however, apicobasolateral membrane polarity and cell junctions appear similar to controls
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cellular
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• at DIV6, cultured hippocampal neurons exhibit supernumerary axons, along with an increased number of neurites having nocodazole-resistant/acetylated microtubules relative to wild-type neurons
• transfection of hippocampal neurons with alphaTAT1-specific siRNA at DV1 to deplete alpha-tubulin acetyltransferase-1 (key enzyme for tubulin acetylation) abolishes supernumerary axon formation
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