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MUNC18–1 gene abnormalities are involved in neurodevelopmental disorders through defective cortical architecture during brain development

Overview of attention for article published in Acta Neuropathologica Communications, November 2017
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Title
MUNC18–1 gene abnormalities are involved in neurodevelopmental disorders through defective cortical architecture during brain development
Published in
Acta Neuropathologica Communications, November 2017
DOI 10.1186/s40478-017-0498-5
Pubmed ID
Authors

Nanako Hamada, Ikuko Iwamoto, Hidenori Tabata, Koh-ichi Nagata

Abstract

While Munc18-1 interacts with Syntaxin1 and controls the formation of soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNARE) complex to regulate presynaptic vesicle fusion in developed neurons, this molecule is likely to be involved in brain development since its gene abnormalities cause early infantile epileptic encephalopathy with suppression-burst (Ohtahara syndrome), neonatal epileptic encephalopathy and other neurodevelopmental disorders. We thus analyzed physiological significance of Munc18-1 during cortical development. Munc18-1-knockdown impaired cortical neuron positioning during mouse corticogenesis. Time-lapse imaging revealed that the mispositioning was attributable to defects in radial migration in the intermediate zone and cortical plate. Notably, Syntaxin1A was critical for radial migration downstream of Munc18-1. As for the underlying mechanism, Munc18-1-knockdown in cortical neurons hampered post-Golgi vesicle trafficking and subsequent vesicle fusion at the plasma membrane in vivo and in vitro, respectively. Notably, Syntaxin1A-silencing did not affect the post-Golgi vesicle trafficking. Taken together, Munc18-1 was suggested to regulate radial migration by modulating not only vesicle fusion at the plasma membrane to distribute various proteins on the cell surface for interaction with radial fibers, but also preceding vesicle transport from Golgi to the plasma membrane. Although knockdown experiments suggested that Syntaxin1A does not participate in the vesicle trafficking, it was supposed to regulate subsequent vesicle fusion under the control of Munc18-1. These observations may shed light on the mechanism governing radial migration of cortical neurons. Disruption of Munc18-1 function may result in the abnormal corticogenesis, leading to neurodevelopmental disorders with MUNC18-1 gene abnormalities.

Twitter Demographics

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Mendeley readers

The data shown below were compiled from readership statistics for 50 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 50 100%

Demographic breakdown

Readers by professional status Count As %
Researcher 13 26%
Student > Ph. D. Student 10 20%
Student > Master 7 14%
Student > Bachelor 6 12%
Student > Postgraduate 3 6%
Other 6 12%
Unknown 5 10%
Readers by discipline Count As %
Neuroscience 16 32%
Agricultural and Biological Sciences 11 22%
Biochemistry, Genetics and Molecular Biology 8 16%
Medicine and Dentistry 4 8%
Social Sciences 2 4%
Other 2 4%
Unknown 7 14%

Attention Score in Context

This research output has an Altmetric Attention Score of 2. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 20 March 2018.
All research outputs
#11,164,396
of 17,826,855 outputs
Outputs from Acta Neuropathologica Communications
#865
of 1,095 outputs
Outputs of similar age
#228,638
of 420,647 outputs
Outputs of similar age from Acta Neuropathologica Communications
#70
of 88 outputs
Altmetric has tracked 17,826,855 research outputs across all sources so far. This one is in the 35th percentile – i.e., 35% of other outputs scored the same or lower than it.
So far Altmetric has tracked 1,095 research outputs from this source. They typically receive a lot more attention than average, with a mean Attention Score of 11.5. This one is in the 19th percentile – i.e., 19% of its peers scored the same or lower than it.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 420,647 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 42nd percentile – i.e., 42% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 88 others from the same source and published within six weeks on either side of this one. This one is in the 20th percentile – i.e., 20% of its contemporaries scored the same or lower than it.