scholarly journals Automated single-cell motility analysis on a chip using lensfree microscopy

2014 ◽  
Vol 4 (1) ◽  
Author(s):  
Ivan Pushkarsky ◽  
Yunbo Liu ◽  
Westbrook Weaver ◽  
Ting-Wei Su ◽  
Onur Mudanyali ◽  
...  
Keyword(s):  
Cell Motility ◽  
Single Cell

scholarly journals Cell Shape and Population Migration Are Distinct Steps ofProteus mirabilisSwarming That Are Decoupled on High-Percentage Agar

2019 ◽  
Vol 201 (11) ◽  
Author(s):  
Kristin Little ◽  
Jacob Austerman ◽  
Jenny Zheng ◽  
Karine A. Gibbs
Keyword(s):  
Cell Motility ◽  
Single Cell ◽  
Cell Elongation ◽  
Cell Shape ◽  
Population Migration ◽  
Content Type ◽  
Agar Concentration ◽  
Collective Interactions ◽  
Cell Phenotypes ◽  
Rigid Surfaces

ABSTRACTSwarming on rigid surfaces requires movement of cells as individuals and as a group of cells. For the bacteriumProteus mirabilis, an individual cell can respond to a rigid surface by elongating and migrating over micrometer-scale distances. Cells can form groups of transiently aligned cells, and the collective population is capable of migrating over centimeter-scale distances. To address howP. mirabilispopulations swarm on rigid surfaces, we asked whether cell elongation and single-cell motility are coupled to population migration. We first measured the relationship between agar concentration (a proxy for surface rigidity), single-cell phenotypes, and swarm colony phenotypes. We find that cell elongation and single-cell motility are coupled with population migration on low-percentage hard agar (1% to 2.5%) and become decoupled on high-percentage hard agar (>2.5%). Next, we evaluate how disruptions in lipopolysaccharide (LPS), specifically the O-antigen components, affect responses to hard agar. We find that LPS is not essential for elongation and motility of individual cells, as predicted, and instead functions to broaden the range of agar concentrations on which cell elongation and motility are coupled with population migration. These findings demonstrate that cell elongation and motility are coupled with population migration under a permissive range of surface conditions; increasing agar concentration is sufficient to decouple these behaviors. Since swarm colonies cover greater distances when these steps are coupled than when they are not, these findings suggest that collective interactions amongP. mirabiliscells might be emerging as a colony expands outwards on rigid surfaces.IMPORTANCEHow surfaces influence cell size, cell-cell interactions, and population migration for robust swarmers likeP. mirabilisis not fully understood. Here, we have elucidated how cells change length along a spectrum of sizes that positively correlates with increases in agar concentration, regardless of population migration. Single-cell phenotypes can be decoupled from collective population migration simply by increasing agar concentration. A cell’s lipopolysaccharides function to broaden the range of agar conditions under which cell elongation and single-cell motility remain coupled with population migration. In eukaryotes, the physical environment, such as a surface matrix, can impact cell development, shape, and migration. These findings support the idea that rigid surfaces similarly act on swarming bacteria to impact cell shape, single-cell motility, and collective population migration.

scholarly journals Probabilistic Voxel-Fe model for single cell motility in 3D

2014 ◽  
Vol 1 (1) ◽  
pp. 2 ◽  
Author(s):  
Carlos Borau ◽  
William J Polacheck ◽  
Roger D Kamm ◽  
José García-Aznar
Keyword(s):  
Cell Motility ◽  
Single Cell ◽  
Fe Model

The developmental regulation of single-cell motility in Dictyostelium discoideum

1986 ◽  
Vol 113 (1) ◽  
pp. 218-227 ◽  
Author(s):  
Barbara Varnum ◽  
Kevin B. Edwards ◽  
David R. Soll
Keyword(s):  
Cell Motility ◽  
Single Cell ◽  
Dictyostelium Discoideum ◽  
Developmental Regulation

Correlating single cell motility with population growth dynamics for flagellated bacteria

2007 ◽  
Vol 97 (6) ◽  
pp. 1644-1649 ◽  
Author(s):  
Sucheta Arora ◽  
Vidya Bhat ◽  
Aditya Mittal
Keyword(s):  
Population Growth ◽  
Cell Motility ◽  
Single Cell ◽  
Growth Dynamics

scholarly journals Single-cell Transcriptomic Analysis of Eutopic Endometrium and Ectopic Lesions of Adenomyosis

2020 ◽  
Author(s):  
Zhiyong Liu ◽  
Zhonghua Sun ◽  
Hongyun Liu ◽  
Weipin Niu ◽  
Xin Wang ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Cell Motility ◽  
Single Cell ◽  
Periodic Acid ◽  
Expression Patterns ◽  
Vasculogenic Mimicry ◽  
Cell Subpopulation ◽  
Periodic Acid Schiff ◽  
Eutopic Endometrium ◽  
Invasion And Migration

Abstract Background: Adenomyosis (AM) is a common benign chronic gynaecological disorder; however, the precise pathogenesis of adenomyosis is still poorly understood. Single-cell RNA sequencing (scRNA-seq) can uncover rare subpopulations, explore genetic and functional heterogeneity, and reveal the uniqueness of each cell. It provides us a new approach to reveal biological issues from a more detailed and microscopic perspective. Here, we utilize this revolutionary technology to identify the changes of gene expression patterns between ectopic lesions and the eutopic endometrium at the single-cell level and explore a potential novel pathogenesis of AM.Methods: A control endometrium (sample with leiomyoma excluding endometrial disorders, n=1), eutopic endometrium and ectopic lesion (from a patient with adenomyosis, n=1) samples were analysed by scRNA-seq, and additional leiomyoma (n=3) and adenomyosis (n=3) samples were used to confirm colocalization and vasculogenic mimicry (VM) formation. Protein colocalization was visualized by immunofluorescence, and CD34-periodic acid-Schiff (PAS) double staining was used to assess the formation of VM.Results: The scRNA-seq results suggest that cancer-, cell motility- and inflammation- (CMI) associated terms, cell proliferation and angiogenesis play important roles in the progression of AM. Moreover, the colocalization of EPCAM and PECAM1 increased significantly in the ectopic endometrium group (P < 0.05), cell subpopulation with high copy number variation (CNV) levels possessing tumour-like features existed in the ectopic lesion sample, and VNN1- and EPCAM-positive cell subcluster displayed active cell motility in endometrial epithelial cells. Furthermore, the epithelial cells transformed to endothelial cells with the obvious accumulation of vasculogenic mimicry formations (positively stained with PAS but not CD34, P < 0.05) in ectopic lesions.Conclusions: In the present study, our results support the theory of adenomyosis derived from the invasion and migration of the endometrium. Moreover, cell subcluster with high CNV level and tumour-associated characteristics is identified. Furthermore, epithelial-endothelial transition (EET) and the formation of VM in tumours, the latter of which facilitates the blood supply and plays an important role in maintaining cell growth, were also confirmed to occur in AM. These results indicated that the inhibition of EET and VM formation may be a potential strategy for AM management.

scholarly journals The tumor suppressor p53 promotes carcinoma invasion and collective cellular migration

2018 ◽  
Author(s):  
Shijie He ◽  
Christopher V. Carman ◽  
Jung Hyun Lee ◽  
Bo Lan ◽  
Stephan Koehler ◽  
...  
Keyword(s):  
Tumor Suppressor ◽  
Colorectal Carcinoma ◽  
Cell Motility ◽  
Single Cell ◽  
Cell Layer ◽  
Carcinoma Cells ◽  
Cellular Migration ◽  
Loss Of Function ◽  
Tumor Suppressor P53 ◽  
Increase Cell Motility

SummaryLoss of function of the tumor suppressor p53 is generally thought to increase cell motility and invasiveness. Using 2-D confluent and 3-D spheroidal cell motility assays with bladder carcinoma cells and colorectal carcinoma cells, we report, to the contrary, that loss of p53 can decrease cell motility and invasion.AbstractFor migration of the single cell studied in isolation, loss of function of the tumor suppressor p53 is thought to increase cell motility. Here by contrast we used the 2-D confluent cell layer and the 3-D multicellular spheroid to investigate how p53 impacts dissemination and invasion of cellular collectives. We used two human carcinoma cell lines, the bladder carcinoma EJ and the colorectal carcinoma HCT116. We began by replicating single cell invasion in the traditional Boyden chamber assay, and found that the number of invading cells increased with loss of p53, as expected. In the confluent 2-D cell layer, however, for both EJ and HCT, speeds and effective diffusion coefficients for the p53 null types compared to their p53 expressing counterparts were significantly smaller. Compared to p53 expressers, p53 null cells exhibited more organized cortical actin rings together with reduced front-rear cell polarity. Furthermore, loss of p53 caused cells to exert smaller traction forces upon their substrates, and reduced formation of cryptic lamellipodia. In a 3-D collagen matrix, p53 consistently promoted invasion of the multicellular spheroids into surrounding matrix. Together, these results show that p53 expression in these carcinoma model systems increases collective cellular migration and invasion. As such, these studies point to paradoxical contributions of p53 in single cell versus collective cellular migration.

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