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Molecular neuroscience

Fat chance of survival

Nature Reviews Neuroscience volume 8, page 908 (2007)Cite this article

Although VAC14 is expressed throughout the body, the in vivo effects of its loss were restricted to the nervous system. The mice exhibited lesions in several brain regions, including the midbrain, the pons and the medulla. Within these lesions, neuronal cell bodies contained large vacuoles or had completely degenerated. This was accompanied by high levels of apoptosis in these regions. The cortex and hippocampus were not affected; however, when cultured, cells from these regions also became vacuolated.

The authors overexpressed either VAC14 or the gene that encodes phosphatidylinositol-3-phosphate 5-kinase (the enzyme that synthesizes PI(3,5)P2) in fibroblasts that lacked VAC14 (which also became vacuolated in culture). Both manipulations abolished the existing vacuoles and suppressed vacuole formation, confirming that the cellular degeneration resulted from the loss of VAC14 and the subsequent reduction in PI(3,5)P2 levels.

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References

ORIGINAL RESEARCH PAPER

  1. Zhang, Y. et al. Loss of Vac14, a regulator of the signaling lipid phosphatidylinositol 3,5-bisphosphate, results in neurodegeneration in mice. Proc. Natl Acad. Sci. USA 104, 17518–17523 (2007)

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FURTHER READING

  1. Piomelli, D., Astarita, G. & Rapaka, R. A neuroscientist's guide to lipidomics. Nature Rev. Neurosci. 8, 743–754 (2007)

    Article  CAS  Google Scholar 

  2. Chow, C. Y. et al. Mutation of FIG4 causes neurodegeneration in the pale tremor mouse and patients with CMT4J. Nature 448, 68–72 (2007)

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Authors
  1. Katherine Whalley
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Whalley, K. Fat chance of survival. Nat Rev Neurosci 8, 908 (2007). https://doi.org/10.1038/nrn2287

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