double membrane
Recently Published Documents


TOTAL DOCUMENTS

331
(FIVE YEARS 64)

H-INDEX

56
(FIVE YEARS 7)

Pharmaceutics ◽  
2022 ◽  
Vol 14 (1) ◽  
pp. 178
Author(s):  
Joanna Kopecka

Mitochondria, organelles surrounded by a double membrane and with their own small genome, are the cells’ energy centres [...]


Author(s):  
Satoshi Minami ◽  
Shuhei Nakamura ◽  
Tamotsu Yoshimori

Autophagy is a conserved cellular degradation system that maintains intracellular homeostasis. Cytoplasmic components are engulfed into double-membrane vesicles called autophagosomes, which fuse with lysosomes, and resulting in the degradation of sequestered materials. Recently, a close association between autophagy and the pathogenesis of metabolic diseases and ageing has become apparent: autophagy is dysregulated during metabolic diseases and ageing; dysregulation of autophagy is intimately associated with the pathophysiology. Rubicon (Run domain Beclin-1 interacting and cysteine-rich containing protein) has been identified as a Beclin-1 associated protein. Notably, Rubicon is one of few negative regulators of autophagy whereas many autophagy-related genes are positive regulators of autophagy. Rubicon also has autophagy-independent functions including phagocytosis and endocytosis. In this mini-review, we focus on the various roles of Rubicon in different organs in the settings of metabolic diseases and ageing, and discuss its potential role as a promising therapeutic target.


eLife ◽  
2022 ◽  
Vol 11 ◽  
Author(s):  
Omar Peña-Ramos ◽  
Lucia Chiao ◽  
Xianghua Liu ◽  
Xiaomeng Yu ◽  
Tianyou Yao ◽  
...  

Autophagosomes are double-membrane intracellular vesicles that degrade protein aggregates, intracellular organelles, and other cellular components. During the development of the nematode Caenorhabditis elegans, many somatic and germ cells undergo apoptosis. These cells are engulfed and degraded by their neighboring cells. We discovered a novel role of autophagosomes in facilitating the degradation of apoptotic cells using a real-time imaging technique. Specifically, the double-membrane autophagosomes in engulfing cells are recruited to the surfaces of phagosomes containing apoptotic cells and subsequently fuse to phagosomes, allowing the inner vesicle to enter the phagosomal lumen. Mutants defective in the production of autophagosomes display significant defects in the degradation of apoptotic cells, demonstrating the importance of autophagosomes to this process. The signaling pathway led by the phagocytic receptor CED-1, the adaptor protein CED-6, and the large GTPase dynamin (DYN-1) promotes the recruitment of autophagosomes to phagosomes. Moreover, the subsequent fusion of autophagosomes with phagosomes requires the functions of the small GTPase RAB-7 and the HOPS complex components. Further observations suggest that autophagosomes provide apoptotic cell-degradation activities in addition to and in parallel of lysosomes. Our findings reveal that, unlike the single-membrane, LC3-associated phagocytosis (LAP) vesicles reported for mammalian phagocytes, the canonical double-membrane autophagosomes facilitate the clearance of C. elegans apoptotic cells. These findings add autophagosomes to the collection of intracellular organelles that contribute to phagosome maturation, identify novel crosstalk between the autophagy and phagosome maturation pathways, and discover the upstream signaling molecules that initiate this crosstalk.


2021 ◽  
Vol 24 (6) ◽  
pp. 54-65
Author(s):  
V. V. Ovchinnikov ◽  
Yu. V. Petrov ◽  
Sh. F. Ganiev

Double-membrane gliding parachutes (DGP) obtain their wide variety of application, including the solution of cargo transportation problems. This parachute is a flexible canopy, which shape is maintained by ram air. In terms of the aerodynamic performance calculation and analysis when operating, DGP is the most complex aero elastic system. The computation of DPG aerodynamic performance is only possible, utilizing the methods of nonlinear aerodynamics and the nonlinear theory of elasticity methods.This paper investigates the aerodynamic characteristics of stable geometric shapes for various gliding parachutes, taking into account their dome shape both chord-wise and span-wise. Notably, the volumetric parachute profile is modeled by its median surface. The research, conducted by the authors, showed that such an aero elastic model of DGP allows you to obtain results that reflect correctly the qualitative effects of detached and free streamline flow. To solve the problem about the airflow over a gliding parachute, considering its canopy curvature, the method of discrete vortices with closed frames is employed, which allows you to calculate the paragliding wing aerodynamic performance within a wide range of angles of attack. There is also a possibility of flow separation simulation. The ideal incompressible liquid flow over the median surface of a stable shape for a double-membrane gliding parachute is regarded. The parachute fabric porosity is not analyzed, since the upper and lower DGP panels are made of either the low permeable or non-porous fabric. In the separated flow past, the aerodynamic coefficients are identified by time averaging to its large values after computing. The DGP aerodynamic performance computation results are given at a different value of its dome shape, as in the free streamline flow as in the flow separation. The computed coefficients, that allow us to consider the influence of canopy dome shape on its aerodynamic characteristics, are obtained. The proposed technique can be used for operational estimates of aerodynamic forces while designing and planning a pipe experiment.


2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Keisuke Tabata ◽  
Vibhu Prasad ◽  
David Paul ◽  
Ji-Young Lee ◽  
Minh-Tu Pham ◽  
...  

AbstractDouble membrane vesicles (DMVs) serve as replication organelles of plus-strand RNA viruses such as hepatitis C virus (HCV) and SARS-CoV-2. Viral DMVs are morphologically analogous to DMVs formed during autophagy, but lipids driving their biogenesis are largely unknown. Here we show that production of the lipid phosphatidic acid (PA) by acylglycerolphosphate acyltransferase (AGPAT) 1 and 2 in the ER is important for DMV biogenesis in viral replication and autophagy. Using DMVs in HCV-replicating cells as model, we found that AGPATs are recruited to and critically contribute to HCV and SARS-CoV-2 replication and proper DMV formation. An intracellular PA sensor accumulated at viral DMV formation sites, consistent with elevated levels of PA in fractions of purified DMVs analyzed by lipidomics. Apart from AGPATs, PA is generated by alternative pathways and their pharmacological inhibition also impaired HCV and SARS-CoV-2 replication as well as formation of autophagosome-like DMVs. These data identify PA as host cell lipid involved in proper replication organelle formation by HCV and SARS-CoV-2, two phylogenetically disparate viruses causing very different diseases, i.e. chronic liver disease and COVID-19, respectively. Host-targeting therapy aiming at PA synthesis pathways might be suitable to attenuate replication of these viruses.


Viruses ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 2034
Author(s):  
Shan-Ying Wu ◽  
Yu-Lun Chen ◽  
Ying-Ray Lee ◽  
Chiou-Feng Lin ◽  
Sheng-Hui Lan ◽  
...  

Autophagic machinery is involved in selective and non-selective recruitment as well as degradation or exocytosis of cargoes, including pathogens. Dengue virus (DENV) infectioninduces autophagy that enhances virus replication and vesicle release to evade immune systemsurveillance. This study reveals that DENV2 induces autophagy in lung and liver cancer cells andshowed that DENV2 capsid, envelope, NS1, NS3, NS4B and host cell proinflammatory high mobilitygroup box 1 (HMGB1) proteins associated with autophagosomes which were purified by gradientcentrifugation. Capsid, NS1 and NS3 proteins showing high colocalization with LC3 protein in thecytoplasm of the infected cells were detected in the purified double-membrane autophagosome byimmunogold labeling under transmission electron microscopy. In DENV infected cells, the levels ofcapsid, envelope, NS1 and HMGB1 proteins are not significantly changed compared to the dramaticaccumulation of LC3-II and p62/SQSTM1 proteins when autophagic degradation was blocked bychloroquine, indicating that these proteins are not regulated by autophagic degradation machinery.We further demonstrated that purified autophagosomes were infectious when co-cultured withuninfected cells. Notably, these infectious autophagosomes contain DENV2 proteins, negativestrandand full-length genomic RNAs, but no viral particles. It is possible that the infectivity ofthe autophagosome originates from the full-length DENV RNA. Moreover, we reveal that DENV2promotes HMGB1 exocytosis partially through secretory autophagy. In conclusion, we are the firstto report that DENV2-induced double-membrane autophagosomes containing viral proteins andfull-length RNAs are infectious and not undergoing autophagic degradation. Our novel findingwarrants further validation of whether these intracellular vesicles undergo exocytosis to becomeinfectious autophagic vesicles.


F1000Research ◽  
2021 ◽  
Vol 10 ◽  
pp. 1009
Author(s):  
Pavel Montes de Oca-B

Coronavirus Disease-19 (COVID-19) pandemic is caused by the coronavirus SARS-CoV-2 that has infected in a year more than 200 million people and has killed almost 4.5 million people worldwide. This infection affects mainly certain groups of people that have high susceptibility to present severe COVID-19 due to comorbidities. Moreover, the long-COVID-19 comprises a series of symptoms that may remain in some patients for months after infection that further compromises health of individuals. Therefore, this pandemic poses a serious emergency worldwide. Thus, since this pandemic is profoundly affecting economic and social life of societies, a deeper understanding of SARS-CoV-2 infection cycle could help to envisage novel therapeutic alternatives that limit or stop COVID-19. Several recent findings have unexpectedly found that mitochondria play a critical role in SARS-CoV-2 cell infection. Indeed, it has been suggested that this organelle could be the origin of its replication niches, the double membrane vesicles (DMV), as its been observed with another virus. In this regard, mitochondria derived vesicles (MDV), involved in mitochondria quality control, were discovered more than 10 years ago and interestingly there is a population characterized by a double membrane. MDV shedding is induced by mitochondrial stress and it has a fast assembly dynamic, reason that perhaps has precluded their identification in electron microscopy or tomography studies. These and other features of MDV together with recent SARS-CoV-2 protein interactome with the host and other findings linking SARS-CoV-2 to mitochondria, support that these vesicles are the precursors of SARS-CoV-2 induced DMV. In this work, the celular, molecular, phenotypical and biochemical evidence that supports this hypothesis is reviewed and integrated into the current model of SARS-CoV-2 cell infection. In this scheme, some relevant questions are raised as pending topics for research that would help in the near future to test this hypothesis. The intention (abstract truncated).


Viruses ◽  
2021 ◽  
Vol 13 (9) ◽  
pp. 1880
Author(s):  
Huyen Tran Ho ◽  
Stefan Peischard ◽  
Nathalie Strutz-Seebohm ◽  
Karin Klingel ◽  
Guiscard Seebohm

Evidence is emerging that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can infect various organs of the body, including cardiomyocytes and cardiac endothelial cells in the heart. This review focuses on the effects of SARS-CoV-2 in the heart after direct infection that can lead to myocarditis and an outline of potential treatment options. The main points are: (1) Viral entry: SARS-CoV-2 uses specific receptors and proteases for docking and priming in cardiac cells. Thus, different receptors or protease inhibitors might be effective in SARS-CoV-2-infected cardiac cells. (2) Viral replication: SARS-CoV-2 uses RNA-dependent RNA polymerase for replication. Drugs acting against ssRNA(+) viral replication for cardiac cells can be effective. (3) Autophagy and double-membrane vesicles: SARS-CoV-2 manipulates autophagy to inhibit viral clearance and promote SARS-CoV-2 replication by creating double-membrane vesicles as replication sites. (4) Immune response: Host immune response is manipulated to evade host cell attacks against SARS-CoV-2 and increased inflammation by dysregulating immune cells. Efficiency of immunosuppressive therapy must be elucidated. (5) Programmed cell death: SARS-CoV-2 inhibits programmed cell death in early stages and induces apoptosis, necroptosis, and pyroptosis in later stages. (6) Energy metabolism: SARS-CoV-2 infection leads to disturbed energy metabolism that in turn leads to a decrease in ATP production and ROS production. (7) Viroporins: SARS-CoV-2 creates viroporins that lead to an imbalance of ion homeostasis. This causes apoptosis, altered action potential, and arrhythmia.


Medicina ◽  
2021 ◽  
Vol 57 (9) ◽  
pp. 928
Author(s):  
José J. Valdés-Aguayo ◽  
Idalia Garza-Veloz ◽  
José I. Badillo-Almaráz ◽  
Sofia Bernal-Silva ◽  
Maria C. Martínez-Vázquez ◽  
...  

Background and Objectives. The importance of mitochondria in inflammatory pathologies, besides providing energy, is associated with the release of mitochondrial damage products, such as mitochondrial DNA (mt-DNA), which may perpetuate inflammation. In this review, we aimed to show the importance of mitochondria, as organelles that produce energy and intervene in multiple pathologies, focusing mainly in COVID-19 and using multiple molecular mechanisms that allow for the replication and maintenance of the viral genome, leading to the exacerbation and spread of the inflammatory response. The evidence suggests that mitochondria are implicated in the replication of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which forms double-membrane vesicles and evades detection by the cell defense system. These mitochondrion-hijacking vesicles damage the integrity of the mitochondrion’s membrane, releasing mt-DNA into circulation and triggering the activation of innate immunity, which may contribute to an exacerbation of the pro-inflammatory state. Conclusions. While mitochondrial dysfunction in COVID-19 continues to be studied, the use of mt-DNA as an indicator of prognosis and severity is a potential area yet to be explored.


2021 ◽  
Author(s):  
Noorah Abdulaziz Othman Alkubaisi ◽  
Nagwa Mohammed Amin Aref

Photosynthesis is a crucial process for plants on earth that changes light energy to chemical energy. Virus infection can cause dramatic photosynthesis changes: respiration and the translocation of carbohydrates and other substances around the host plant. Chlorosis in virus-infected leaves like Barley Yellow Dwarf Virus (BYDV- PAV).infection can result from damage to chloroplasts resulting from inhibition of photosynthetic activity. Our present study combines TEM and chlorophyll-level content in the presence of Gold nanoparticles (AuNPS) to explore the repair mechanism for the yellowing leaf symptom development caused by infection with BYDV- PAV by illustrating TEM micrographs; showing fragmentized grana, deformation of the myelin like bodies (MLB), many vesicles; osmiophilic lipid granules/plastoglobulus, starch body, and plasmolysis in the chloroplast, distribution of AuNPs & VLPs near and inside the chloroplast. Mitochondria, Double-membrane-bound organelle, Distorted mitochondrion, Amorphous inclusion bodies.


Sign in / Sign up

Export Citation Format

Share Document