scholarly journals The Ubiquitin Proteasome System as a Double Agent in Plant-Virus Interactions

Plants ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 928
Author(s):  
Ullrich Dubiella ◽  
Irene Serrano

The ubiquitin proteasome is a rapid, adaptive mechanism for selective protein degradation, crucial for proper plant growth and development. The ubiquitin proteasome system (UPS) has also been shown to be an integral part of plant responses to stresses, including plant defence against pathogens. Recently, significant progress has been made in the understanding of the involvement of the UPS in the signalling and regulation of the interaction between plants and viruses. This review aims to discuss the current knowledge about the response of plant viral infection by the UPS and how the viruses counteract this system, or even use it for their own benefit.

Cells ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 283
Author(s):  
Daniel Aghaie Madsen ◽  
Sissel Ida Schmidt ◽  
Morten Blaabjerg ◽  
Morten Meyer

Parkin and α-synuclein are two key proteins involved in the pathophysiology of Parkinson’s disease (PD). Neurotoxic alterations of α-synuclein that lead to the formation of toxic oligomers and fibrils contribute to PD through synaptic dysfunction, mitochondrial impairment, defective endoplasmic reticulum and Golgi function, and nuclear dysfunction. In half of the cases, the recessively inherited early-onset PD is caused by loss of function mutations in the PARK2 gene that encodes the E3-ubiquitin ligase, parkin. Parkin is involved in the clearance of misfolded and aggregated proteins by the ubiquitin-proteasome system and regulates mitophagy and mitochondrial biogenesis. PARK2-related PD is generally thought not to be associated with Lewy body formation although it is a neuropathological hallmark of PD. In this review article, we provide an overview of post-mortem neuropathological examinations of PARK2 patients and present the current knowledge of a functional interaction between parkin and α-synuclein in the regulation of protein aggregates including Lewy bodies. Furthermore, we describe prevailing hypotheses about the formation of intracellular micro-aggregates (synuclein inclusions) that might be more likely than Lewy bodies to occur in PARK2-related PD. This information may inform future studies aiming to unveil primary signaling processes involved in PD and related neurodegenerative disorders.


2018 ◽  
Vol 25 (2) ◽  
pp. 253-267 ◽  
Author(s):  
Sandra Fonseca ◽  
Dhanya Radhakrishnan ◽  
Kalika Prasad ◽  
Andrea Chini

Living organisms are part of a highly interconnected web of interactions, characterised by species nurturing, competing, parasitizing and preying on one another. Plants have evolved cooperative as well as defensive strategies to interact with neighbour organisms. Among these, the plant-fungus associations are very diverse, ranging from pathogenic to mutualistic. Our current knowledge of plant-fungus interactions suggests a sophisticated coevolution to ensure dynamic plant responses to evolving fungal mutualistic/pathogenic strategies. The plant-fungus communication relies on a rich chemical language. To manipulate the plant defence mechanisms, fungi produce and secrete several classes of biomolecules, whose modeof- action is largely unknown. Upon perception of the fungi, plants produce phytohormones and a battery of secondary metabolites that serve as defence mechanism against invaders or to promote mutualistic associations. These mutualistic chemical signals can be co-opted by pathogenic fungi for their own benefit. Among the plant molecules regulating plant-fungus interaction, phytohormones play a critical role since they modulate various aspects of plant development, defences and stress responses. Intriguingly, fungi can also produce phytohormones, although the actual role of fungalproduced phytohormones in plant-fungus interactions is poorly understood. Here, we discuss the recent advances in fungal production of phytohormone, their putative role as endogenous fungal signals and how fungi manipulate plant hormone balance to their benefits.


Cells ◽  
2019 ◽  
Vol 8 (1) ◽  
pp. 40 ◽  
Author(s):  
Katarzyna Zientara-Rytter ◽  
Suresh Subramani

The ubiquitin-proteasome system (UPS) and autophagy are the two major intracellular protein quality control (PQC) pathways that are responsible for cellular proteostasis (homeostasis of the proteome) by ensuring the timely degradation of misfolded, damaged, and unwanted proteins. Ubiquitination serves as the degradation signal in both these systems, but substrates are precisely targeted to one or the other pathway. Determining how and when cells target specific proteins to these two alternative PQC pathways and control the crosstalk between them are topics of considerable interest. The ubiquitin (Ub) recognition code based on the type of Ub-linked chains on substrate proteins was believed to play a pivotal role in this process, but an increasing body of evidence indicates that the PQC pathway choice is also made based on other criteria. These include the oligomeric state of the Ub-binding protein shuttles, their conformation, protein modifications, and the presence of motifs that interact with ATG8/LC3/GABARAP (autophagy-related protein 8/microtubule-associated protein 1A/1B-light chain 3/GABA type A receptor-associated protein) protein family members. In this review, we summarize the current knowledge regarding the Ub recognition code that is bound by Ub-binding proteasomal and autophagic receptors. We also discuss how cells can modify substrate fate by modulating the structure, conformation, and physical properties of these receptors to affect their shuttling between both degradation pathways.


Plants ◽  
2022 ◽  
Vol 11 (2) ◽  
pp. 203
Author(s):  
Lizette Liliana Rodríguez-Verástegui ◽  
Candy Yuriria Ramírez-Zavaleta ◽  
María Fernanda Capilla-Hernández ◽  
Josefat Gregorio-Jorge

Trees and herbs that produce fruits represent the most valuable agricultural food commodities in the world. However, the yield of these crops is not fully achieved due to biotic factors such as bacteria, fungi, and viruses. Viruses are capable of causing alterations in plant growth and development, thereby impacting the yield of their hosts significantly. In this work, we first compiled the world′s most comprehensive list of known edible fruits that fits our definition. Then, plant viruses infecting those trees and herbs that produce fruits with commercial importance in the global market were identified. The identified plant viruses belong to 30 families, most of them containing single-stranded RNA genomes. Importantly, we show the overall picture of the host range for some virus families following an evolutionary approach. Further, the current knowledge about plant-virus interactions, focusing on the main disorders they cause, as well as yield losses, is summarized. Additionally, since accurate diagnosis methods are of pivotal importance for viral diseases control, the current and emerging technologies for the detection of these plant pathogens are described. Finally, the most promising strategies employed to control viral diseases in the field are presented, focusing on solutions that are long-lasting.


2015 ◽  
Vol 43 (5) ◽  
pp. 1089-1094 ◽  
Author(s):  
Mara Salomè ◽  
Joana Campos ◽  
Karen Keeshan

Tribbles family of pseudokinase proteins are known to mediate the degradation of target proteins in Drosophila and mammalian systems. The main protein proteolysis pathway in eukaryotic cells is the ubiquitin proteasome system (UPS). The tribbles homolog 2 (TRIB2) mammalian family member has been well characterized for its role in murine and human leukaemia, lung and liver cancer. One of the most characterized substrates for TRIB2-mediated degradation is the myeloid transcription factor CCAAT enhancer binding protein α (C/EBPα). However, across a number of cancers, the molecular interactions that take place between TRIB2 and factors involved in the UPS are varied and have differential downstream effects. This review summarizes our current knowledge of these interactions and how this information is important for our understanding of TRIB2 in cancer.


F1000Research ◽  
2015 ◽  
Vol 4 ◽  
pp. 367 ◽  
Author(s):  
Maisha Chowdhury ◽  
Cordula Enenkel

The ubiquitin-proteasome system is the major degradation pathway for short-lived proteins in eukaryotic cells. Targets of the ubiquitin-proteasome-system are proteins regulating a broad range of cellular processes including cell cycle progression, gene expression, the quality control of proteostasis and the response to geno- and proteotoxic stress. Prior to degradation, the proteasomal substrate is marked with a poly-ubiquitin chain. The key protease of the ubiquitin system is the proteasome. In dividing cells, proteasomes exist as holo-enzymes composed of regulatory and core particles. The regulatory complex confers ubiquitin-recognition and ATP dependence on proteasomal protein degradation. The catalytic sites are located in the proteasome core particle. Proteasome holo-enzymes are predominantly nuclear suggesting a major requirement for proteasomal proteolysis in the nucleus. In cell cycle arrested mammalian or quiescent yeast cells, proteasomes deplete from the nucleus and accumulate in granules at the nuclear envelope (NE) / endoplasmic reticulum ( ER) membranes. In prolonged quiescence, proteasome granules drop off the nuclear envelopeNE / ER membranes and migrate as droplet-like entitiesstable organelles  throughout the cytoplasm, as thoroughly investigated in yeast. When quiescence yeast cells are allowed to resume growth, proteasome granules clear and proteasomes are rapidly imported into the nucleus.Here, we summarize our knowledge about the enigmatic structure of proteasome storage granules and the trafficking of proteasomes and their substrates between the cyto- and nucleoplasm.Most of our current knowledge is based on studies in yeast. Their translation to mammalian cells promises to provide keen insight into protein degradation in non-dividing cells, which comprise the majority of our body’s cells.


Author(s):  
Alan E. Renton ◽  
Alison M. Goate

The genetic architecture of dementia is polygenic and complex, with risk alleles spanning frequency–effect size space. Despite significant progress, most genes influencing these disorders await discovery. Known risk loci implicate perturbed pathways that coalesce around recurring mechanistic themes, notably the autophagosome-lysosome system, the cytoskeleton, endocytosis, innate immunity, lipid metabolism, mitochondria, and the ubiquitin-proteasome system. Phenotypic and pathophysiological pleiotropy suggests some conditions form continuous clinicopathogenetic disease spectra blurring classical diagnoses. Future large-scale genome sequencing of global populations will significantly elucidate etiopathogenesis and is likely to reframe nosology. Furthermore integrative prospective cohort studies have the potential to revolutionize our understanding of dementia.


Cells ◽  
2018 ◽  
Vol 8 (1) ◽  
pp. 2 ◽  
Author(s):  
Qiuhong Xiong ◽  
Wenjing Li ◽  
Ping Li ◽  
Min Yang ◽  
Changxin Wu ◽  
...  

Autophagy and the ubiquitin proteasome system (UPS) are the two major cellular degradation pathways, which are critical for the maintenance of cell homeostasis. The two pathways differ in their mechanisms and clients. The evolutionary conserved ATG16 plays a key role in autophagy and appears to link autophagy with the UPS. Here, we review the role of ATG16 in different species. We summarize the current knowledge of its functions in autophagosome membrane expansion and autophagosome formation, in Crohn’s disease, and in bacterial sequestration. In addition, we provide information on its autophagy-independent functions and its role in the crosstalk between autophagy and the UPS.


Author(s):  
Julia Jülg ◽  
Laura Strohm ◽  
Christian Behrends

Besides the ubiquitin-proteasome-system, autophagy is a major degradation pathway within cells. It delivers invading pathogens, damaged organelles, aggregated proteins and other macromolecules from the cytosol to the lysosome for bulk degradation. This so-called canonical autophagy activity contributes to the maintenance of organelle, protein and metabolite homeostasis as well as innate immunity. Over the past years, numerous studies rapidly deepened our knowledge on the autophagy machinery and its regulation; driven by the fact that impairment of autophagy is associated with several human pathologies including cancer, immune diseases and neurodegenerative disorders. Unexpectedly, components of the autophagic machinery were also found to participate in various processes that did not involve lysosomal delivery of cytosolic constituents. These functions are hereafter defined as non-canonical autophagy. Regarding neurodegenerative diseases, most research was performed in neurons, while for a long-time microglia received considerably less attention. Concomitant with the notion that microglia greatly contribute to brain health, the understanding of the role of autophagy in microglia expanded. To facilitate an overview of the current knowledge, we present herein the fundamentals as well as the recent advances of canonical and non-canonical autophagy functions in microglia.


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