Literature DB >> 30403723

Structure of the Golgi apparatus is not influenced by a GAG deletion mutation in the dystonia-associated gene Tor1a.

Sara B Mitchell1, Sadahiro Iwabuchi1, Hiroyuki Kawano1, Tsun Ming Tom Yuen1,2, Jin-Young Koh1, K W David Ho1,3, N Charles Harata1,3,4.   

Abstract

Autosomal-dominant, early-onset DYT1 dystonia is associated with an in-frame deletion of a glutamic acid codon (ΔE) in the TOR1A gene. The gene product, torsinA, is an evolutionarily conserved AAA+ ATPase. The fact that constitutive secretion from patient fibroblasts is suppressed indicates that the ΔE-torsinA protein influences the cellular secretory machinery. However, which component is affected remains unclear. Prompted by recent reports that abnormal protein trafficking through the Golgi apparatus, the major protein-sorting center of the secretory pathway, is sometimes associated with a morphological change in the Golgi, we evaluated the influence of ΔE-torsinA on this organelle. Specifically, we examined its structure by confocal microscopy, in cultures of striatal, cerebral cortical and hippocampal neurons obtained from wild-type, heterozygous and homozygous ΔE-torsinA knock-in mice. In live neurons, the Golgi was assessed following uptake of a fluorescent ceramide analog, and in fixed neurons it was analyzed by immuno-fluorescence staining for the Golgi-marker GM130. Neither staining method indicated genotype-specific differences in the size, staining intensity, shape or localization of the Golgi. Moreover, no genotype-specific difference was observed as the neurons matured in vitro. These results were supported by a lack of genotype-specific differences in GM130 expression levels, as assessed by Western blotting. The Golgi was also disrupted by treatment with brefeldin A, but no genotype-specific differences were found in the immuno-fluorescence staining intensity of GM130. Overall, our results demonstrate that the ΔE-torsinA protein does not drastically influence Golgi morphology in neurons, irrespective of genotype, brain region (among those tested), or maturation stage in culture. While it remains possible that functional changes in the Golgi exist, our findings imply that any such changes are not severe enough to influence its morphology to a degree detectable by light microscopy.

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Year:  2018        PMID: 30403723      PMCID: PMC6221310          DOI: 10.1371/journal.pone.0206123

Source DB:  PubMed          Journal:  PLoS One        ISSN: 1932-6203            Impact factor:   3.240


  110 in total

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Review 2.  The functional neuroanatomy of dystonia.

Authors:  Vladimir K Neychev; Robert E Gross; Stephane Lehéricy; Ellen J Hess; H A Jinnah
Journal:  Neurobiol Dis       Date:  2011-02-12       Impact factor: 5.996

3.  Examination of synaptic vesicle recycling using FM dyes during evoked, spontaneous, and miniature synaptic activities.

Authors:  Sadahiro Iwabuchi; Yasuhiro Kakazu; Jin-Young Koh; Kirsty M Goodman; N Charles Harata
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4.  Differential dendritic targeting of AMPA receptor subunit mRNAs in adult rat hippocampal principal neurons and interneurons.

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5.  Golgi tubule traffic and the effects of brefeldin A visualized in living cells.

Authors:  N Sciaky; J Presley; C Smith; K J Zaal; N Cole; J E Moreira; M Terasaki; E Siggia; J Lippincott-Schwartz
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6.  GM130 Regulates Golgi-Derived Spindle Assembly by Activating TPX2 and Capturing Microtubules.

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Journal:  Cell       Date:  2015-07-09       Impact factor: 41.582

7.  An anticholinergic reverses motor control and corticostriatal LTD deficits in Dyt1 ΔGAG knock-in mice.

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Review 8.  The pathophysiological basis of dystonias.

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9.  Subtle microstructural changes of the striatum in a DYT1 knock-in mouse model of dystonia.

Authors:  Chang-Hyun Song; Douglas Bernhard; Caroline Bolarinwa; Ellen J Hess; Yoland Smith; H A Jinnah
Journal:  Neurobiol Dis       Date:  2013-01-19       Impact factor: 5.996

10.  Altered dendritic morphology of Purkinje cells in Dyt1 ΔGAG knock-in and purkinje cell-specific Dyt1 conditional knockout mice.

Authors:  Lin Zhang; Fumiaki Yokoi; Yuan-Hu Jin; Mark P DeAndrade; Kenji Hashimoto; David G Standaert; Yuqing Li
Journal:  PLoS One       Date:  2011-03-29       Impact factor: 3.240

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