scholarly journals Superresolution Microscopy as a Percolation Problem: Maximum Achievable Imaging Density and Resolution Cost

2016 ◽  
Vol 110 (3) ◽  
pp. 161a
Author(s):  
Alexander Small
Keyword(s):  
Superresolution Microscopy ◽  
Percolation Problem

scholarly journals On the Markov Transition Kernels for First Passage Percolation on the Ladder

2011 ◽  
Vol 48 (02) ◽  
pp. 366-388 ◽  
Author(s):  
Eckhard Schlemm
Keyword(s):  
Central Limit Theorem ◽  
Limit Theorem ◽  
Central Limit ◽  
Asymptotic Variance ◽  
Almost Sure Convergence ◽  
First Passage Percolation ◽  
First Passage ◽  
Percolation Problem ◽  
Vertex Set ◽  
Step Transition

We consider the first passage percolation problem on the random graph with vertex set N x {0, 1}, edges joining vertices at a Euclidean distance equal to unity, and independent exponential edge weights. We provide a central limit theorem for the first passage times l n between the vertices (0, 0) and (n, 0), thus extending earlier results about the almost-sure convergence of l n / n as n → ∞. We use generating function techniques to compute the n-step transition kernels of a closely related Markov chain which can be used to explicitly calculate the asymptotic variance in the central limit theorem.

scholarly journals Visualising α-Synuclein Oligomers using Superresolution Microscopy

2020 ◽  
Vol 118 (3) ◽  
pp. 149a
Author(s):  
Craig Leighton ◽  
Mathew Horrocks ◽  
Tilo Kunath
Keyword(s):  
Superresolution Microscopy

scholarly journals Autophagy-Related Protein ATG8 Has a Noncanonical Function for Apicoplast Inheritance in Toxoplasma gondii

mBio ◽  
2015 ◽  
Vol 6 (6) ◽  
Author(s):  
Maude F. Lévêque ◽  
Laurence Berry ◽  
Michael J. Cipriano ◽  
Hoa-Mai Nguyen ◽  
Boris Striepen ◽  
...  
Keyword(s):  
Toxoplasma Gondii ◽  
Growth Conditions ◽  
Model Organisms ◽  
Secondary Endosymbiosis ◽  
Related Protein ◽  
Content Type ◽  
Superresolution Microscopy ◽  
Animal Pathogens ◽  
Cellular Components ◽  
Catabolic Process

ABSTRACT Autophagy is a catabolic process widely conserved among eukaryotes that permits the rapid degradation of unwanted proteins and organelles through the lysosomal pathway. This mechanism involves the formation of a double-membrane structure called the autophagosome that sequesters cellular components to be degraded. To orchestrate this process, yeasts and animals rely on a conserved set of autophagy-related proteins (ATGs). Key among these factors is ATG8, a cytoplasmic protein that is recruited to nascent autophagosomal membranes upon the induction of autophagy. Toxoplasma gondii is a potentially harmful human pathogen in which only a subset of ATGs appears to be present. Although this eukaryotic parasite seems able to generate autophagosomes upon stresses such as nutrient starvation, the full functionality and biological relevance of a canonical autophagy pathway are as yet unclear. Intriguingly, in T. gondii, ATG8 localizes to the apicoplast under normal intracellular growth conditions. The apicoplast is a nonphotosynthetic plastid enclosed by four membranes resulting from a secondary endosymbiosis. Using superresolution microscopy and biochemical techniques, we show that TgATG8 localizes to the outermost membrane of this organelle. We investigated the unusual function of TgATG8 at the apicoplast by generating a conditional knockdown mutant. Depletion of TgATG8 led to rapid loss of the organelle and subsequent intracellular replication defects, indicating that the protein is essential for maintaining apicoplast homeostasis and thus for survival of the tachyzoite stage. More precisely, loss of TgATG8 led to abnormal segregation of the apicoplast into the progeny because of a loss of physical interactions of the organelle with the centrosomes. IMPORTANCE By definition, autophagy is a catabolic process that leads to the digestion and recycling of eukaryotic cellular components. The molecular machinery of autophagy was identified mainly in model organisms such as yeasts but remains poorly characterized in phylogenetically distant apicomplexan parasites. We have uncovered an unusual function for autophagy-related protein ATG8 in Toxoplasma gondii: TgATG8 is crucial for normal replication of the parasite inside its host cell. Seemingly unrelated to the catabolic autophagy process, TgATG8 associates with the outer membrane of the nonphotosynthetic plastid harbored by the parasite called the apicoplast, and there it plays an important role in the centrosome-driven inheritance of the organelle during cell division. This not only reveals an unexpected function for an autophagy-related protein but also sheds new light on the division process of an organelle that is vital to a group of important human and animal pathogens.

scholarly journals Dual-Color 3D Superresolution Microscopy by Combined Spectral-Demixing and Biplane Imaging

2015 ◽  
Vol 109 (1) ◽  
pp. 3-6 ◽  
Author(s):  
Christian M. Winterflood ◽  
Evgenia Platonova ◽  
David Albrecht ◽  
Helge Ewers
Keyword(s):  
Superresolution Microscopy ◽  
Dual Color

Spin glass as a percolation problem

1981 ◽  
Vol 14 (23) ◽  
pp. L707-L711 ◽  
Author(s):  
R E Nettleton ◽  
M J Stephen
Keyword(s):  
Spin Glass ◽  
Percolation Problem

scholarly journals Synaptic abnormalities and cytoplasmic glutamate receptor aggregates in contactin associated protein-like 2/Caspr2 knockout neurons

2015 ◽  
Vol 112 (19) ◽  
pp. 6176-6181 ◽  
Author(s):  
Olga Varea ◽  
Maria Dolores Martin-de-Saavedra ◽  
Katherine J. Kopeikina ◽  
Britta Schürmann ◽  
Hunter J. Fleming ◽  
...  
Keyword(s):  
Ampa Receptors ◽  
Knockout Mice ◽  
Copy Number Variations ◽  
Spine Density ◽  
Structured Illumination ◽  
Single Nucleotide Variants ◽  
Glutamatergic Synapses ◽  
Superresolution Microscopy ◽  
Synaptic Markers ◽  
Cellular Phenotypes

Central glutamatergic synapses and the molecular pathways that control them are emerging as common substrates in the pathogenesis of mental disorders. Genetic variation in the contactin associated protein-like 2 (CNTNAP2) gene, including copy number variations, exon deletions, truncations, single nucleotide variants, and polymorphisms have been associated with intellectual disability, epilepsy, schizophrenia, language disorders, and autism. CNTNAP2, encoded by Cntnap2, is required for dendritic spine development and its absence causes disease-related phenotypes in mice. However, the mechanisms whereby CNTNAP2 regulates glutamatergic synapses are not known, and cellular phenotypes have not been investigated in Cntnap2 knockout neurons. Here we show that CNTNAP2 is present in dendritic spines, as well as axons and soma. Structured illumination superresolution microscopy reveals closer proximity to excitatory, rather than inhibitory synaptic markers. CNTNAP2 does not promote the formation of synapses and cultured neurons from Cntnap2 knockout mice do not show early defects in axon and dendrite outgrowth, suggesting that CNTNAP2 is not required at this stage. However, mature neurons from knockout mice show reduced spine density and levels of GluA1 subunits of AMPA receptors in spines. Unexpectedly, knockout neurons show large cytoplasmic aggregates of GluA1. Here we characterize, for the first time to our knowledge, synaptic phenotypes in Cntnap2 knockout neurons and reveal a novel role for CNTNAP2 in GluA1 trafficking. Taken together, our findings provide insight into the biological roles of CNTNAP2 and into the pathogenesis of CNTNAP2-associated neuropsychiatric disorders.

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