scholarly journals Entangled architecture of rough endoplasmic reticulum (RER) and vacuoles enables topological damping in cytoplasm of an ultra-fast giant cell

2021 ◽  
Author(s):  
Ray Chang ◽  
Manu Prakash
Keyword(s):  
Endoplasmic Reticulum ◽  
Giant Cell ◽  
Rough Endoplasmic Reticulum ◽  
Volume Fraction ◽  
Single Cells ◽  
Cellular Systems ◽  
Confocal Imaging ◽  
Dynamics Simulation ◽  
Cellular Damage ◽  
Novel Association

Cellular systems are known to exhibit some of the fastest movements in the biological world - but little is known as to how single cells can dissipate this energy rapidly and adapt to such large accelerations without sub-cellular damage. To study intracellular adaptations under extreme forces - we investigate Spirostomum ambiguum - a giant cell (1-4mm in length) well known to exhibit ultrafast contractions (50% of body length) within 5 msec with a peak acceleration of 15g. Utilizing transmitted electron microscopy (TEM) and confocal imaging, we discover a novel association of rough endoplasmic reticulum (RER) and vacuoles throughout the cell - forming a contiguous fenestrated cubic membrane architecture that topologically entangles these two organelles. A nearly uniform inter-organelle spacing of 60nm is observed between RER and vacuoles, closely packing the entire cell. Using an overdamped molecular dynamics simulation, we demonstrate how this unique entangled metamaterial responds to external loads by rapidly dissipating energy and helps preserve spatial relationships between organelles. Because this dynamics arises primarily from entanglement of two networks incurring jamming transition at a subcritical volume fraction - we term this phenomena "topological damping". Our findings suggest a new mechanical role of RER-vacuolar meshwork as a metamaterial capable of dissipating energy in an ultra-fast contraction event.

Cotyledon cell development in Arabidopsis thaliana during reserve deposition

1992 ◽  
Vol 70 (1) ◽  
pp. 151-164 ◽  
Author(s):  
S. G. Mansfield ◽  
L. G. Briarty
Keyword(s):  
Arabidopsis Thaliana ◽  
Endoplasmic Reticulum ◽  
Rough Endoplasmic Reticulum ◽  
Volume Fraction ◽  
Biological Membrane ◽  
Lipid Body ◽  
Cell Development ◽  
Volume Fractions ◽  
Short Period ◽  
Cotyledon Cell

Cotyledon cell development in Arabidopsis thaliana L. during reserve deposition has been analyzed qualitatively and quantitatively. Development has been related to the previously defined time scale for Arabidopsis, hours after flowering. Between 144 and 216 h after flowering the major cell changes in the cotyledon are an increase in the cell volume, a decrease in the volume fraction of cytoplasm and plastids, and an increase in lipid and vacuole volume fractions. The endoplasmic reticulum and dictyosome volume fractions are high during early reserve formation (144 – 168 h after flowering) but decrease significantly thereafter. Evidence as to the origin of the storage lipid is inconclusive, although a dual involvement of plastids and rough endoplasmic reticulum is a likely theory. The 3-nm lipid body membrane, which allows the bodies to retain their individuality during accumulation, is probably a half-unit biological membrane, derived from closely associated rough endoplasmic reticulum cisternae. Much of the evidence obtained in this study indicates that both the endoplasmic reticulum and dictyosomes are involved in protein synthesis and transport to the vacuole. The accumulation of reserves occurs in a well-defined and relatively short period during late embryogenesis (144–216 h after flowering). Key words: Arabidopsis, cotyledons, embryogenesis, reserve deposition, stereology.

scholarly journals Ultrastructure of a Feline Extraskeletal Giant Cell Tumor (Malignant Fibrous Histiocytoma)

1981 ◽  
Vol 18 (6) ◽  
pp. 738-744 ◽  
Author(s):  
A. W. Confer ◽  
F. M. Enright ◽  
G. B. Beard
Keyword(s):  
Endoplasmic Reticulum ◽  
Giant Cell Tumor ◽  
Giant Cell ◽  
Rough Endoplasmic Reticulum ◽  
Malignant Fibrous Histiocytoma ◽  
Mononuclear Cells ◽  
Fibrous Histiocytoma ◽  
Giant Cells ◽  
Cell Tumor ◽  
Multinucleated Giant Cells

A subcutaneous extraskeletal giant cell tumor (malignant fibrous histiocytoma) was excised repeatedly from a 9-year-old Domestic Shorthair cat. Ultrastructurally, the mass was composed of fibroblast-like, histiocyte-like, and multinucleated giant cells, and some undifferentiated cells and mononuclear cells intermediate between the fibroblast-like and histiocyte-like cells. Fibroblast-like cells were characterized by abundant well-developed rough endoplasmic reticulum, relatively smooth cytoplasmic membranes, few lysosomal structures, and finely granular chromatin. Histiocyte-like cells resembled immature macrophages. The cell membranes had many villous projections. Rough endoplasmic reticulum varied in quantity. Lysosomes were numerous. Multinucleated giant cells had characteristics of both the fibroblast-like and histiocyte-like cells. No viral particles were seen.

Modification of Pineal Ultrastructure by Exogenous Hormones

1967 ◽  
Vol 25 ◽  
pp. 170-171
Author(s):  
R. A. Turner ◽  
A. E. Rodin ◽  
D. K. Roberts
Keyword(s):  
Electron Microscopy ◽  
Endoplasmic Reticulum ◽  
Rough Endoplasmic Reticulum ◽  
Estradiol Benzoate ◽  
Female Rats ◽  
List Type ◽  
Type Number ◽  
Pregnant Rats ◽  
Gonadal Atrophy ◽  
Pineal Ultrastructure

There have been many reports which establish a relationship between the pineal and sexual structures, including gonadal hypertrophy after pinealectomy, and gonadal atrophy after injection of pineal homogenates or of melatonin. In order to further delineate this relationship the pineals from 5 groups of female rats were studied by electron microscopy:ControlsPregnant ratsAfter 4 weekly injections of 0.1 mg. estradiol benzoate.After 8 daily injections of 150 mcgm. melatonin (pineal hormone).After 8 daily injections of 3 mg. serotonin (melatonin precursor).No ultrastructural differences were evident between the control, and the pregnancy and melatonin groups. However, the estradiol injected animals exhibited a marked increase in the amount and size of rough endoplasmic reticulum within the pineal cells.

Membrane-associated microtubular areays induced in proximal myelinated processes of dorsal root ganglia by large doses of vitamin B6

1986 ◽  
Vol 44 ◽  
pp. 368-369
Author(s):  
V.J. Montpetit ◽  
S. Dancea ◽  
L. Tryphonas ◽  
D.F. Clapin
Keyword(s):  
Animal Model ◽  
Endoplasmic Reticulum ◽  
Dorsal Root Ganglia ◽  
Rough Endoplasmic Reticulum ◽  
Dorsal Root ◽  
Vitamin B6 ◽  
Morphological Changes ◽  
Model System ◽  
Sensory Nerves ◽  
Peripheral Sensory

Very large doses of pyridoxine (vitamin B6) are neurotoxic in humans, selectively affecting the peripheral sensory nerves. We have undertaken a study of the morphological and biochemical aspects of pyridoxine neurotoxicity in an animal model system. Early morphological changes in dorsal root ganglia (DRG) associated with pyridoxine megadoses include proliferation of neurofilaments, ribosomes, rough endoplasmic reticulum, and Golgi complexes. We present in this report evidence of the formation of unique aggregates of microtubules and membranes in the proximal processes of DRG which are induced by high levels of pyridoxine.

scholarly journals EGFRvIII Promotes Cell Survival during Endoplasmic Reticulum Stress through a Reticulocalbin 1-Dependent Mechanism

Cancers ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 1198
Author(s):  
Juliana Gomez ◽  
Zammam Areeb ◽  
Sarah F. Stuart ◽  
Hong P. T. Nguyen ◽  
Lucia Paradiso ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Cell Viability ◽  
Er Stress ◽  
Cell Survival ◽  
Glioblastoma Cells ◽  
Over Expression ◽  
Stress Markers ◽  
Apoptotic Protein ◽  
Novel Association ◽  
Reduced Activity

Reticulocalbin 1 (RCN1) is an endoplasmic reticulum (ER)-residing protein, involved in promoting cell survival during pathophysiological conditions that lead to ER stress. However, the key upstream receptor tyrosine kinase that regulates RCN1 expression and its potential role in cell survival in the glioblastoma setting have not been determined. Here, we demonstrate that RCN1 expression significantly correlates with poor glioblastoma patient survival. We also demonstrate that glioblastoma cells with expression of EGFRvIII receptor also have high RCN1 expression. Over-expression of wildtype EGFR also correlated with high RCN1 expression, suggesting that EGFR and EGFRvIII regulate RCN1 expression. Importantly, cells that expressed EGFRvIII and subsequently showed high RCN1 expression displayed greater cell viability under ER stress compared to EGFRvIII negative glioblastoma cells. Consistently, we also demonstrated that RCN1 knockdown reduced cell viability and exogenous introduction of RCN1 enhanced cell viability following induction of ER stress. Mechanistically, we demonstrate that the EGFRvIII-RCN1-driven increase in cell survival is due to the inactivation of the ER stress markers ATF4 and ATF6, maintained expression of the anti-apoptotic protein Bcl-2 and reduced activity of caspase 3/7. Our current findings identify that EGFRvIII regulates RCN1 expression and that this novel association promotes cell survival in glioblastoma cells during ER stress.

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