Myelin subfractions isolated from mouse brain: Analysis of the lipid composition at three developmental stages

Lipids ◽  
1981 ◽  
Vol 16 (7) ◽  
pp. 502-507 ◽  
Author(s):  
Linda D. Rhein ◽  
Joseph Sampugna

PROTEOMICS ◽  
2007 ◽  
Vol 7 (21) ◽  
pp. 4008-4015 ◽  
Author(s):  
Jing Wang ◽  
Yong Gu ◽  
Lihong Wang ◽  
Xingyi Hang ◽  
Yan Gao ◽  
...  


eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
David M Young ◽  
Siavash Fazel Darbandi ◽  
Grace Schwartz ◽  
Zachary Bonzell ◽  
Deniz Yuruk ◽  
...  

3D imaging data necessitate 3D reference atlases for accurate quantitative interpretation. Existing computational methods to generate 3D atlases from 2D-derived atlases result in extensive artifacts, while manual curation approaches are labor-intensive. We present a computational approach for 3D atlas construction that substantially reduces artifacts by identifying anatomical boundaries in the underlying imaging data and using these to guide 3D transformation. Anatomical boundaries also allow extension of atlases to complete edge regions. Applying these methods to the eight developmental stages in the Allen Developing Mouse Brain Atlas (ADMBA) led to more comprehensive and accurate atlases. We generated imaging data from 15 whole mouse brains to validate atlas performance and observed qualitative and quantitative improvement (37% greater alignment between atlas and anatomical boundaries). We provide the pipeline as the MagellanMapper software and the eight 3D reconstructed ADMBA atlases. These resources facilitate whole-organ quantitative analysis between samples and across development.





2002 ◽  
Vol 66 (1) ◽  
pp. 277-285 ◽  
Author(s):  
Zhizhong Guan ◽  
Magnus Söderberg ◽  
Pavel Sindelar ◽  
Stanley B. Prusiner ◽  
Krister Kristensson ◽  
...  


2019 ◽  
Vol 116 (41) ◽  
pp. 20689-20699 ◽  
Author(s):  
Akio Mori ◽  
Taku Hatano ◽  
Tsuyoshi Inoshita ◽  
Kahori Shiba-Fukushima ◽  
Takahiro Koinuma ◽  
...  

Mutations in the iPLA2-VIA/PLA2G6 gene are responsible for PARK14-linked Parkinson’s disease (PD) with α-synucleinopathy. However, it is unclear how iPLA2-VIA mutations lead to α-synuclein (α-Syn) aggregation and dopaminergic (DA) neurodegeneration. Here, we report that iPLA2-VIA–deficient Drosophila exhibits defects in neurotransmission during early developmental stages and progressive cell loss throughout the brain, including degeneration of the DA neurons. Lipid analysis of brain tissues reveals that the acyl-chain length of phospholipids is shortened by iPLA2-VIA loss, which causes endoplasmic reticulum (ER) stress through membrane lipid disequilibrium. The introduction of wild-type human iPLA2-VIA or the mitochondria–ER contact site-resident protein C19orf12 in iPLA2-VIA–deficient flies rescues the phenotypes associated with altered lipid composition, ER stress, and DA neurodegeneration, whereas the introduction of a disease-associated missense mutant, iPLA2-VIA A80T, fails to suppress these phenotypes. The acceleration of α-Syn aggregation by iPLA2-VIA loss is suppressed by the administration of linoleic acid, correcting the brain lipid composition. Our findings suggest that membrane remodeling by iPLA2-VIA is required for the survival of DA neurons and α-Syn stability.



2020 ◽  
Author(s):  
David M Young ◽  
Siavash Fazel Darbandi ◽  
Grace Schwartz ◽  
Zachary Bonzell ◽  
Deniz Yuruk ◽  
...  

Abstract3D imaging data necessitate 3D reference atlases for accurate quantitative interpretation. Existing computational methods to generate 3D atlases from 2D-derived atlases result in extensive artifacts, while manual curation approaches are labor-intensive. We present a computational approach for 3D atlas construction that substantially reduces artifacts by identifying anatomical boundaries in the underlying imaging data and using these to guide 3D transformation. Anatomical boundaries also allow extension of atlases to complete edge regions. Applying these methods to the eight developmental stages in the Allen Developing Mouse Brain Atlas (ADMBA) led to more comprehensive and accurate atlases. We generated imaging data from fifteen whole mouse brains to validate atlas performance and observed qualitative and quantitative improvement (37% greater alignment between atlas and anatomical boundaries). We provide the methods as the MagellanMapper software and the eight 3D reconstructed ADMBA atlases. These resources facilitate whole-organ quantitative analysis between samples and across development.



1980 ◽  
Vol 20 (2) ◽  
pp. 211-215 ◽  
Author(s):  
C. Linington ◽  
T.V. Waehneldt ◽  
V. Neuhoff


BMC Biology ◽  
2020 ◽  
Vol 18 (1) ◽  
Author(s):  
Elin Lundin ◽  
Chenglin Wu ◽  
Albin Widmark ◽  
Mikaela Behm ◽  
Jens Hjerling-Leffler ◽  
...  

Abstract Background Adenosine-to-inosine (A-to-I) RNA editing is a process that contributes to the diversification of proteins that has been shown to be essential for neurotransmission and other neuronal functions. However, the spatiotemporal and diversification properties of RNA editing in the brain are largely unknown. Here, we applied in situ sequencing to distinguish between edited and unedited transcripts in distinct regions of the mouse brain at four developmental stages, and investigate the diversity of the RNA landscape. Results We analyzed RNA editing at codon-altering sites using in situ sequencing at single-cell resolution, in combination with the detection of individual ADAR enzymes and specific cell type marker transcripts. This approach revealed cell-type-specific regulation of RNA editing of a set of transcripts, and developmental and regional variation in editing levels for many of the targeted sites. We found increasing editing diversity throughout development, which arises through regional- and cell type-specific regulation of ADAR enzymes and target transcripts. Conclusions Our single-cell in situ sequencing method has proved useful to study the complex landscape of RNA editing and our results indicate that this complexity arises due to distinct mechanisms of regulating individual RNA editing sites, acting both regionally and in specific cell types.



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