Choose an application

• Reference Manager
• EndNote
• RefWorks (Direct export to RefWorks)

Autophagy (also known as macroautophagy) is an evolutionarily conserved process by which cytoplasmic components are nonselectively enclosed within a double-membrane vesicle known as the autophagosome and delivered to the vacuole for degradation of toxic components and recycling of needed nutrients. This catabolic process is required for the adequate adaptation and response of the cell, and correspondingly the whole organism, to different types of stress including nutrient starvation or oxidative damage. Autophagy has been extensively investigated in yeasts and mammals but the identification of autophagy-related (ATG) genes in plant and algal genomes together with the characterization of autophagy-deficient mutants in plants have revealed that this process is structurally and functionally conserved in photosynthetic eukaryotes. Recent studies have demonstrated that autophagy is active at a basal level under normal growth in plants and is upregulated during senescence and in response to nutrient limitation, oxidative stress, salt and drought conditions and pathogen attack. Autophagy was initially considered as a non-selective pathway, but numerous observations mainly obtained in yeasts revealed that autophagy can also selectively eliminate specific proteins, protein complexes and organelles. Interestingly, several types of selective autophagy appear to be also conserved in plants, and the degradation of protein aggregates through specific adaptors or the delivery of chloroplast material to the vacuole via autophagy has been reported. This research topic aims to gather recent progress on different aspects of autophagy in plants and algae. We welcome all types of articles including original research, methods, opinions and reviews that provide new insights about the autophagy process and its regulation.

Botany --- Autophagy. --- Lipid degradation --- selective autophagy --- pexophagy --- algae --- Plants

Choose an application

• Reference Manager
• EndNote
• RefWorks (Direct export to RefWorks)

Autophagy (also known as macroautophagy) is an evolutionarily conserved process by which cytoplasmic components are nonselectively enclosed within a double-membrane vesicle known as the autophagosome and delivered to the vacuole for degradation of toxic components and recycling of needed nutrients. This catabolic process is required for the adequate adaptation and response of the cell, and correspondingly the whole organism, to different types of stress including nutrient starvation or oxidative damage. Autophagy has been extensively investigated in yeasts and mammals but the identification of autophagy-related (ATG) genes in plant and algal genomes together with the characterization of autophagy-deficient mutants in plants have revealed that this process is structurally and functionally conserved in photosynthetic eukaryotes. Recent studies have demonstrated that autophagy is active at a basal level under normal growth in plants and is upregulated during senescence and in response to nutrient limitation, oxidative stress, salt and drought conditions and pathogen attack. Autophagy was initially considered as a non-selective pathway, but numerous observations mainly obtained in yeasts revealed that autophagy can also selectively eliminate specific proteins, protein complexes and organelles. Interestingly, several types of selective autophagy appear to be also conserved in plants, and the degradation of protein aggregates through specific adaptors or the delivery of chloroplast material to the vacuole via autophagy has been reported. This research topic aims to gather recent progress on different aspects of autophagy in plants and algae. We welcome all types of articles including original research, methods, opinions and reviews that provide new insights about the autophagy process and its regulation.

Botany --- Lipid degradation --- selective autophagy --- pexophagy --- algae --- Plants --- Autophagy.

Choose an application

• Reference Manager
• EndNote
• RefWorks (Direct export to RefWorks)

Plasma cells (PCs) are terminally differentiated B-cells producing large amounts of immunoglobulins (Ig). In humans, most of circulating Ig are produced by bone marrow plasma cells. PCs differentiate from activated naïve or memory B-cells usually activated by specific antigens. It is still controversial whether the regulation of PCs numbers and the “active” in vivo Ig diversity depend or not on non-specific reactivation of B-cells during infections. Depending on the stimulus (T-independent/T-dependent antigen, cytokines, partner cells) and B-cell types (naïve or memory, circulating or germinal center, lymph nodes or spleen, B1 or B2...), both the phenotype and isotype of PCs differ suggesting that PC diversity is either linked to B-cell diversity or to the type of stimulus or to both. Knowledge of the mechanisms supporting PC diversity has important consequences for the management of i) plasma cell neoplasia such as Multiple Myeloma and Waldenström's Macroglobulinemia, ii) vaccine protection against pathogens and iii) auto-immune diseases.

IL21 --- Autoimmunity --- differentiation --- Cell Cycle --- B-cell --- Plasma cell --- Myeloma --- Autophagy --- B1

Choose an application

• Reference Manager
• EndNote
• RefWorks (Direct export to RefWorks)

Plasma cells (PCs) are terminally differentiated B-cells producing large amounts of immunoglobulins (Ig). In humans, most of circulating Ig are produced by bone marrow plasma cells. PCs differentiate from activated naïve or memory B-cells usually activated by specific antigens. It is still controversial whether the regulation of PCs numbers and the “active” in vivo Ig diversity depend or not on non-specific reactivation of B-cells during infections. Depending on the stimulus (T-independent/T-dependent antigen, cytokines, partner cells) and B-cell types (naïve or memory, circulating or germinal center, lymph nodes or spleen, B1 or B2...), both the phenotype and isotype of PCs differ suggesting that PC diversity is either linked to B-cell diversity or to the type of stimulus or to both. Knowledge of the mechanisms supporting PC diversity has important consequences for the management of i) plasma cell neoplasia such as Multiple Myeloma and Waldenström's Macroglobulinemia, ii) vaccine protection against pathogens and iii) auto-immune diseases.

IL21 --- Autoimmunity --- differentiation --- Cell Cycle --- B-cell --- Plasma cell --- Myeloma --- Autophagy --- B1

Choose an application

• Reference Manager
• EndNote
• RefWorks (Direct export to RefWorks)

Unfolded protein response (UPR) is a cellular adaptive response for restoring endoplasmic reticulum (ER) homeostasis in response to ER stress. Perturbation of the UPR and failure to restore ER homeostasis inevitably leads to diseases. It has now become evident that perturbation of the UPR is the cause of many important human diseases such as neurodegenerative diseases, cystic fibrosis, diabetes and cancer. It has recently emerged that virus infections can trigger the UPR but the relationship between virus infections and host UPR is intriguing. On one hand, UPR is harmful to the virus and virus has developed means to subvert the UPR. On the other hand, virus exploits the host UPR to assist in its own infection, gene expression, establishment of persistence, reactivation from latency and to evade the immune response. When this delicate balance of virus-host UPR interaction is broken down, it may cause diseases. This is particularly challenging for viruses that establish a chronic infection to maintain this balance. Each virus interacts with the host UPR in a different way to suit their life style and how the virus interacts with the host UPR can define the characteristic of a particular virus infection. Understanding how a particular virus interacts with the host UPR may pave the way to the design of a new class of anti-viral that targets this particular pathway to skew the response towards anti-virus. This knowledge can also be translated into the clinics to help re-design oncolytic virotherapy and gene therapy. In this research topic we aimed to compile a collection of focused review articles, original research articles, commentary, opinion, hypothesis and methods to highlight the current advances in this burgeoning area of research, in an attempt to provide an in-depth understanding of how viruses interact with the host UPR, which may be beneficial to the future combat of viral and human diseases.

Virus diseases. --- Viruses. --- ERAD --- virus-host interaction --- innate immunity --- Gene Therapy --- Pathogenesis --- Endoplasmic Reticulum Stress --- Unfolded Protein Response --- Autophagy