The role of actin filaments in the organization of the endoplasmic reticulum in honeybee photoreceptor cells

1994 ◽  
Vol 278 (3) ◽  
pp. 419-432 ◽  
Author(s):  
Otto Baumann ◽  
Birgit Lautenschl�ger
Keyword(s):  
Endoplasmic Reticulum ◽  
Actin Filaments ◽  
Photoreceptor Cells

Actin-dependent light-induced translocation of mitochondria and ER cisternae in the photoreceptor cells of the locust Schistocerca gregaria

1995 ◽  
Vol 108 (6) ◽  
pp. 2273-2283 ◽  
Author(s):  
K. Sturmer ◽  
O. Baumann ◽  
B. Walz
Keyword(s):  
Actin Filaments ◽  
Cytochalasin B ◽  
Schistocerca Gregaria ◽  
Smooth Endoplasmic Reticulum ◽  
Close Association ◽  
Electron Microscopic Examination ◽  
Photoreceptor Cells ◽  
Electron Microscopic ◽  
Filament Bundles

Light-dependent changes in the positioning of organelles in photoreceptor cells of arthropods are a well-known phenomenon. In this study, we examine the role of the cytoskeleton in these light-dependent antagonistic movements. In dark-adapted photoreceptor cells of the locust Schistocerca gregaria, prominent sacs of smooth endoplasmic reticulum (ER) oppose the bases of the photoreceptive microvilli. Light stimulation causes a translocation of the ER elements towards the main cell body, and an aggregation of mitochondria adjacent to the microvilli. Immunofluorescence studies and electron-microscopic examination of chemically fixed or high-pressure-frozen, freeze-substituted specimens demonstrate a lack of microtubules in the submicrovillar region. However, numerous filament bundles are aligned in close association with mitochondria and ER elements, along the track of their movement. Fluorescent phallotoxins and monoclonal anti-actin antibodies label filament bundles in the submicrovillar region, indicating that they are composed of F-actin. Finally, depolymerization of the submicrovillar actin filaments by incubation with cytochalasin B results in a blockade of the movement of mitochondria and ER cisternae towards the rhabdom. These results suggest that the light-dependent translocation of both ER cisternae and mitochondria occurs along actin filaments.

scholarly journals Light-induced structural changes of cytoskeleton in squid photoreceptor microvilli detected by rapid-freeze method.

1988 ◽  
Vol 106 (4) ◽  
pp. 1151-1160 ◽  
Author(s):  
S Tsukita ◽  
S Tsukita ◽  
G Matsumoto
Keyword(s):  
Electron Microscopy ◽  
Actin Filaments ◽  
Plasma Membranes ◽  
Structural Changes ◽  
Physiological Role ◽  
Freeze Substitution ◽  
Photoreceptor Cells ◽  
Rapid Freezing ◽  
Light Stimulation

The cytoskeleton in squid photoreceptor microvilli was studied by freeze-substitution electron microscopy combined with rapid freezing using liquid helium, under dark-adapted and light-illuminated conditions. In the dark-adapted microvilli, actin filaments were regularly associated with granular structures on their surface; these granular structures were cross-linked to the rhodopsin-bearing plasma membranes through slender strands. Upon exposure to light, the granular components detached from the actin filaments, which then appeared to be fragmented and/or depolymerized. These observations have led us to conclude that light stimulation triggers the breakdown of the microvillar actin filament complex in squid photoreceptor cells. The results are discussed with special reference to the physiological role of actin filaments in photoreception.

Localization of Intracisternal a Particle Antigens in Neoplastic Cells and Preimplantation Mouse Embryos

1980 ◽  
Vol 38 ◽  
pp. 696-697
Author(s):  
Thomas T.F. Huang ◽  
Patricia G. Calarco
Keyword(s):  
Endoplasmic Reticulum ◽  
Normal Development ◽  
Mouse Embryos ◽  
Neoplastic Cells ◽  
Large Numbers ◽  
Preimplantation Mouse Embryos ◽  
Preimplantation Mouse ◽  
Intracisternal A Particle ◽  
Normal Feature

The stage specific appearance of a retravirus, termed the Intracisternal A particle (IAP) is a normal feature of early preimplantation development. To date, all feral and laboratory strains of Mus musculus and even Asian species such as Mus cervicolor and Mus pahari express the particles during the 2-8 cell stages. IAP form by budding into the endoplasmic reticulum and appear singly or as groups of donut-shaped particles within the cisternae (fig. 1). IAP are also produced in large numbers in several neoplastic cells such as certain plasmacytomas and rhabdomyosarcomas. The role of IAP, either in normal development or in neoplastic behavior, is unknown.

MODY Signal Pathway in the Endoplasmic Reticulum Stress and the Role of Nkx6.1 in the Glucolipotoxicity of INS-1-3 Cells

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 2110-P
Author(s):  
YANAN DONG ◽  
YUKUN LI ◽  
JIANZHONG XIAO
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Signal Pathway

scholarly journals Platelet Shape Changes during Thrombus Formation: Role of Actin-Based Protrusions

2021 ◽  
Vol 41 (01) ◽  
pp. 014-021
Author(s):  
Markus Bender ◽  
Raghavendra Palankar
Keyword(s):  
Blood Loss ◽  
Actin Filaments ◽  
Thrombus Formation ◽  
Short Review ◽  
Critical Component ◽  
Clot Retraction ◽  
Shape Changes ◽  
Platelet Shape

AbstractPlatelet activation and aggregation are essential to limit blood loss at sites of vascular injury but may also lead to occlusion of diseased vessels. The platelet cytoskeleton is a critical component for proper hemostatic function. Platelets change their shape after activation and their contractile machinery mediates thrombus stabilization and clot retraction. In vitro studies have shown that platelets, which come into contact with proteins such as fibrinogen, spread and first form filopodia and then lamellipodia, the latter being plate-like protrusions with branched actin filaments. However, the role of platelet lamellipodia in hemostasis and thrombus formation has been unclear until recently. This short review will briefly summarize the recent findings on the contribution of the actin cytoskeleton and lamellipodial structures to platelet function.

scholarly journals Molecular Targets of Manganese-Induced Neurotoxicity: A Five-Year Update

2021 ◽  
Vol 22 (9) ◽  
pp. 4646
Author(s):  
Alexey A. Tinkov ◽  
Monica M. B. Paoliello ◽  
Aksana N. Mazilina ◽  
Anatoly V. Skalny ◽  
Airton C. Martins ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Mitochondrial Dysfunction ◽  
Synaptic Dysfunction ◽  
Future Research ◽  
Protective Mechanism ◽  
Autophagic Flux ◽  
Future Research Directions ◽  
The Impact

Understanding of the immediate mechanisms of Mn-induced neurotoxicity is rapidly evolving. We seek to provide a summary of recent findings in the field, with an emphasis to clarify existing gaps and future research directions. We provide, here, a brief review of pertinent discoveries related to Mn-induced neurotoxicity research from the last five years. Significant progress was achieved in understanding the role of Mn transporters, such as SLC39A14, SLC39A8, and SLC30A10, in the regulation of systemic and brain manganese handling. Genetic analysis identified multiple metabolic pathways that could be considered as Mn neurotoxicity targets, including oxidative stress, endoplasmic reticulum stress, apoptosis, neuroinflammation, cell signaling pathways, and interference with neurotransmitter metabolism, to name a few. Recent findings have also demonstrated the impact of Mn exposure on transcriptional regulation of these pathways. There is a significant role of autophagy as a protective mechanism against cytotoxic Mn neurotoxicity, yet also a role for Mn to induce autophagic flux itself and autophagic dysfunction under conditions of decreased Mn bioavailability. This ambivalent role may be at the crossroad of mitochondrial dysfunction, endoplasmic reticulum stress, and apoptosis. Yet very recent evidence suggests Mn can have toxic impacts below the no observed adverse effect of Mn-induced mitochondrial dysfunction. The impact of Mn exposure on supramolecular complexes SNARE and NLRP3 inflammasome greatly contributes to Mn-induced synaptic dysfunction and neuroinflammation, respectively. The aforementioned effects might be at least partially mediated by the impact of Mn on α-synuclein accumulation. In addition to Mn-induced synaptic dysfunction, impaired neurotransmission is shown to be mediated by the effects of Mn on neurotransmitter systems and their complex interplay. Although multiple novel mechanisms have been highlighted, additional studies are required to identify the critical targets of Mn-induced neurotoxicity.

AMPA induced cognitive impairment in rats: Establishing the role of endoplasmic reticulum stress inhibitor, 4‐PBA

2021 ◽  
Author(s):  
Ankita Bhardwaj ◽  
Rishi Bhardwaj ◽  
Shweta Sharma ◽  
Suresh Kumar Sharma ◽  
Devinder Kumar Dhawan ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Cognitive Impairment ◽  
Endoplasmic Reticulum Stress
Sign in / Sign up

Export Citation Format

Share Document