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Yahoo Web Search Yahoo Settings. Sign In. Search query. All Images Videos News. Download pdf Download pdf. Case Study. Learn more Learn more. Learn More Learn More. Submit Again. Company Company. Position Position. We generated frequency histograms to determine the distributions of cell velocities Fig.
For velocity, the medians of wild-type and Plp1- null cells were 0. We ran a Mann—Whitney's U test to evaluate the difference in the migration velocities and accumulated distances between wild-type and Plp1 cells.
Studies to understand the mechanisms underlying these differences are ongoing. Despite the absence of the major myelin protein, Plp1- null mice are still able to myelinate axons and produce compact myelin around axons Klugmann et al. EGFP filled the entire cell body and many of the larger processes of oligodendrocytes, while PLP was in processes, but mostly excluded from oligodendrocyte cell bodies.
The total numbers of oligodendrocytes and OPCs throughout the cord were unchanged in Plp1 -null mice at P7 compared with wild type data not shown. Given the expression of PLP-EGFP outside of the oligodendroglial lineage, we counted total numbers of astrocytes and neurons in wild-type and Plp1 -null cords at P7, and found no change in Plp1 -null animals data not shown. These studies demonstrated that Plp1 promoter activity in the spinal cord was biphasic, first occurring very early in the embryonic neuroepithelium and then again postnatally in myelinating oligodendrocytes.
PLP-EGFP was expressed in undifferentiated precursors of the spinal cord as well as by neuronal, astroglial, and oligodendroglial progenitors. However we have shown that at both E In the absence of PLP expression, there was mild disruption of process extension in ventral PLP-EGFP-expressing cells; processes were shorter and often disorganized, with fewer processes aligned radially.
Despite abnormal process development, no differences in OPC numbers, distribution, or onset of myelination were seen in Plp1 -null spinal cords. Within the spinal cord, OPCs arise from either the ventral or dorsal regions. The generation of ventrally derived OPCs is dependent on Sonic hedgehog Shh , while dorsal OPCs arise independently of Shh signaling, possibly dependent on fibroblast growth factor or bone morphogenic factor instead for review, see Richardson et al.
Ventrally and dorsally derived oligodendrocytes preferentially myelinate different tracts in both the brain and spinal cord Tripathi et al. As in other studies Delaunay et al. In vitro studies have reported that reduced levels of PLP can reduce apoptosis and increase oligodendrocyte cell survival, and cultures from Plp1- null mice produce twice as many oligodendrocytes as cultures from wild-type mice Skoff et al.
We saw no changes in OPC numbers in our studies, nor have other studies of Plp1- null mice reported such increases, but it may be that in vivo there is not enough trophic support for excess oligodendrocytes, keeping numbers constant. The dynamic expression of the Plp1 promoter, high in early progenitors, low at intermediate stages, and then high again postnatally, suggests two roles for PLP: an early role in migratory progenitors, followed by a later role in mature oligodendrocytes during myelination.
However, the question of PLP's role in nonmyelinating cell types persists. Although in the current study we did not stimulate cells in our live imaging migration assays, there may be, in the absence of PLP, reduced clustering of integrins in OPCs on fibronectin, causing decreased binding and increased migration speed.
After focal demyelination in the adult mouse corpus callosum, OPCs migrating from the SVZ have been shown to form functional glutamatergic synapses with demyelinated axons Etxeberria et al.
Whether Plp1- null OPCs would be able to make such connections and effectively remyelinate demyelinated axons remains unknown. Despite the process abnormalities of Plp1- null OPCs, we did not see any dramatic differences in the distribution of OPCs throughout the developing spinal cords of Plp1- null mice. Although its role in OPC migration and myelination appears dispensable, PLP clearly has an important role in supporting normal axonal function.
Plp1 -null animals generate normal numbers of oligodendrocytes and produce compact myelin that contacts and wraps axons, but over time develop axonal swellings, problems with retrograde axonal transport, and eventual axonal degeneration Boison and Stoffel, ; Rosenbluth et al. The axonal degeneration seen in Plp1- null mice likely results from a loss of trophic or metabolic support, either from altered myelin structural integrity, perturbed exosome trafficking, or an as yet undefined form of oligodendrocyte-axonal communication.
Future studies on interactions between oligodendrocytes and neurons in Plp1- null animals may reveal additional undiscovered roles for PLP.
The authors declare no competing financial interests. National Center for Biotechnology Information , U. Journal List J Neurosci v. J Neurosci. Danielle E. Harlow , 1 Katherine E. Saul , 1 Cecilia M. Culp , 1 Elisa M. Vesely , 2 and Wendy B. Macklin 1. Katherine E. Cecilia M. Elisa M. Wendy B.
Author information Article notes Copyright and License information Disclaimer. Corresponding author. Correspondence should be addressed to Wendy B. Contributed by Author contributions: D. This article has been cited by other articles in PMC. Abstract Plp1 gene expression occurs very early in development, well before the onset of myelination, creating a conundrum with regard to the function of myelin proteolipid protein PLP , one of the major proteins in compact myelin.
Materials and Methods Animals. In situ hybridization. Cell counts and measurements of process lengths and orientations. Western blotting. Live imaging of OPC migration. Statistical analysis. Dive into thousands of fonts included for free with your Creative Cloud subscription. Match fonts in images with the power of Adobe Sensei. Accepted file types: jpg, png, gif. Dig deep into the world of type and find inspiration in new places.
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