The role of vimentin in directional migration of rat fibroblasts

Cytoskeleton ◽  
2019 ◽  
Vol 76 (9-10) ◽  
pp. 467-476 ◽  
Author(s):  
Anna Vakhrusheva ◽  
Sofia Endzhievskaya ◽  
Vsevolod Zhuikov ◽  
Tatyana Nekrasova ◽  
Evgenia Parshina ◽  
...  
2011 ◽  
Vol 9 (67) ◽  
pp. 222-233 ◽  
Author(s):  
Yoshimi Tanaka ◽  
Kentaro Ito ◽  
Toshiyuki Nakagaki ◽  
Ryo Kobayashi

Limbless crawling is a fundamental form of biological locomotion adopted by a wide variety of species, including the amoeba, earthworm and snake. An interesting question from a biomechanics perspective is how limbless crawlers control their flexible bodies in order to realize directional migration. In this paper, we discuss the simple but instructive problem of peristalsis-like locomotion driven by elongation–contraction waves that propagate along the body axis, a process frequently observed in slender species such as the earthworm. We show that the basic equation describing this type of locomotion is a linear, one-dimensional diffusion equation with a time–space-dependent diffusion coefficient and a source term, both of which express the biological action that drives the locomotion. A perturbation analysis of the equation reveals that adequate control of friction with the substrate on which locomotion occurs is indispensable in order to translate the internal motion (propagation of the elongation–contraction wave) into directional migration. Both the locomotion speed and its direction (relative to the wave propagation) can be changed by the control of friction. The biological relevance of this mechanism is discussed.


2018 ◽  
Vol 32 (S1) ◽  
Author(s):  
Suzannah Miller ◽  
Bryan Murillo ◽  
Mary Katherine Connacher ◽  
Natalie Ahn

2020 ◽  
Vol 12 (9) ◽  
pp. 0-0
Author(s):  
Nazmul Haque ◽  
Ismail M Fareez ◽  
Liew Fong Fong ◽  
Chanchal Mandal ◽  
Noor Hayaty Abu Kasim ◽  
...  

Mathematics ◽  
2018 ◽  
Vol 6 (3) ◽  
pp. 36 ◽  
Author(s):  
Nikhil Pal ◽  
Sudip Samanta ◽  
Maia Martcheva ◽  
Joydev Chattopadhyay

1987 ◽  
Vol 7 (5) ◽  
pp. 1638-1645 ◽  
Author(s):  
M B Small ◽  
N Hay ◽  
M Schwab ◽  
J M Bishop

Amplification and abundant expression of a gene known as N-myc are found frequently in advanced stages of human neuroblastoma and may play a role in the genesis of several malignant human tumors. Previous studies have shown that N-myc can cooperate with a mutant allele of the proto-oncogene c-Ha-ras to transform embryonic rat cells in culture. Here we show that N-myc can also act alone to elicit neoplastic growth of an established line of rat fibroblasts (Rat-1). We used recombinant DNA vectors to express either N-myc or its kindred gene c-myc in transfected cells. Both genes caused morphological transformation, anchorage-independent growth, and tumorigenicity. We noticed two variables that appeared to influence the ability to isolate cells transformed by N-myc and c-myc: the abundance in which the genes were expressed and biological selection to eliminate untransformed cells from the cultures. Our findings sustain the belief that N-myc is an authentic proto-oncogene, lend further credibility to the role of N-myc in the genesis of human tumors, and establish a convenient assay that can be used to explore further the properties of both N-myc and c-myc.


2005 ◽  
Vol 25 (14) ◽  
pp. 6225-6234 ◽  
Author(s):  
Feng Li ◽  
Yunyue Wang ◽  
Karen I. Zeller ◽  
James J. Potter ◽  
Diane R. Wonsey ◽  
...  

ABSTRACT Although several genes involved in mitochondrial function are direct Myc targets, the role of Myc in mitochondrial biogenesis has not been directly established. We determined the effects of ectopic Myc expression or the loss of Myc on mitochondrial biogenesis. Induction of Myc in P493-6 cells resulted in increased oxygen consumption and mitochondrial mass and function. Conversely, compared to wild-type Myc fibroblasts, Myc null rat fibroblasts have diminished mitochondrial mass and decreased number of normal mitochondria. Reconstitution of Myc expression in Myc null fibroblasts partially restored mitochondrial mass and function and normal-appearing mitochondria. Concordantly, we also observed in primary hepatocytes that acute deletion of floxed murine Myc by Cre recombinase resulted in diminished mitochondrial mass in primary hepatocytes. Our microarray analysis of genes responsive to Myc in human P493-6 B lymphocytes supports a role for Myc in mitochondrial biogenesis, since genes involved in mitochondrial structure and function are overrepresented among the Myc-induced genes. In addition to the known direct binding of Myc to many genes involved in mitochondrial structure and function, we found that Myc binds the TFAM gene, which encodes a key transcriptional regulator and mitochondrial DNA replication factor, both in P493-6 lymphocytes with high ectopic MYC expression and in serum-stimulated primary human 2091 fibroblasts with induced endogenous MYC. These observations support a pivotal role for Myc in regulating mitochondrial biogenesis.


2009 ◽  
Vol 122 (7) ◽  
pp. 1025-1034 ◽  
Author(s):  
R. Bhattacharya ◽  
J. Kwon ◽  
X. Li ◽  
E. Wang ◽  
S. Patra ◽  
...  

2017 ◽  
Vol 28 (23) ◽  
pp. 3457-3470 ◽  
Author(s):  
Alex C. Szatmary ◽  
Ralph Nossal ◽  
Carole A. Parent ◽  
Ritankar Majumdar

Migrating cells often exhibit signal relay, a process in which cells migrating in response to a chemotactic gradient release a secondary chemoattractant to enhance directional migration. In neutrophils, signal relay toward the primary chemoattractant N-­formylmethionyl-leucyl-phenylalanine (fMLP) is mediated by leukotriene B4 (LTB4). Recent evidence suggests that the release of LTB4 from cells occurs through packaging in exosomes. Here we present a mathematical model of neutrophil signal relay that focuses on LTB4 and its exosome-mediated secretion. We describe neutrophil chemotaxis in response to a combination of a defined gradient of fMLP and an evolving gradient of LTB4, generated by cells in response to fMLP. Our model enables us to determine the gradient of LTB4 arising either through directed secretion from cells or through time-varying release from exosomes. We predict that the secondary release of LTB4 increases recruitment range and show that the exosomes provide a time delay mechanism that regulates the development of LTB4 gradients. Additionally, we show that under decaying primary gradients, secondary gradients are more stable when secreted through exosomes as compared with direct secretion. Our chemotactic model, calibrated from observed responses of cells to gradients, thereby provides insight into chemotactic signal relay in neutrophils during inflammation.


1996 ◽  
Vol 109 (8) ◽  
pp. 2005-2012 ◽  
Author(s):  
A. Veithen ◽  
P. Cupers ◽  
P. Baudhuin ◽  
P.J. Courtoy

The role of v-Src as regulator of fluid-phase pinocytosis was investigated in Rat-1 cells expressing a stable (Rat-1/BB16) or a thermosensitive (Rat-1/tsLA29) v-Src protein. In the second cell line, this protein is inactive when cells are cultured at 40 degrees C but recovers its tyrosine kinase activity upon transfer to 34 degrees C, resulting into a transformed phenotype. The rate of fluid-phase pinocytosis of the tracer horseradish peroxidase was 2-fold higher in v-Src-transformed fibroblasts (Rat-1/BB16, Rat-1/tsLA29 cultured at 34 degrees C) as compared to non-transformed cells (Rat-1, Rat-1/tsLA29 kept at 40 degrees C). In contrast, receptor-mediated endocytosis of transferrin was poorly affected, suggesting that structures distinct from clathrin-coated pits are involved in pinocytosis stimulation. By light and electron microscopy, transformed cells frequently contained large peroxidase-labeled pinocytic vesicles located near to membrane ruffles, demonstrating that stimulation of pinocytosis corresponds to induction of constitutive macropinocytosis. Stimulation of pinocytosis occurred more than 8 hours after transfer to the permissive temperature, whereas transfer to the non-permissive temperature partially reversed the stimulation within 2 hours. Protein synthesis inhibition for 6 hours abrogated pinocytosis stimulation in transformed cells, indicating that constitutive macropinocytosis induced by v-Src depends on continuous synthesis of a short-lived regulatory machinery.


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