A review of fossilization processes in different sedimentary environments (With special reference to the time factor of deposition of ore minerals associated with fossil material, in particular the coprolitic phosphate deposits)

This thesis offers a cross/section through some principal fossilization processes involving organic matter (animals and plants) during and after sedimentation. The influence of different environments during fossilization is considered. The chemical composition of some classes of living invertebrates and plants is compared with the chemical composition of same organisms as found in consolidated sediments as fossils. Some literature on carbonates, oxides, silicates, phosphates, and sulphides in fossils is reviewed with particular attention to those instances where the fossils are associated with ore minerals. Special consideration is given to the occurrence and composition of fecal matter in recent and consolidated sediments. Emphasis was placed throughout on the time value of depositional criteria such as fillings and replacements. It was found that workers in the field of fossilization and sedimentation consider filling and replacement processes to be pre- or syndiagenetic and thus syngenetic. The samples studied for this thesis appear to corroborate the conclusions offered in this literature --Abstract, page v

A Dimer to Bridge Early Autophagosomal Membranes

The Atg1/ULK complex plays a key role in the early stages of autophagosome assembly. In this issue, Ragusa et al. reveal the molecular basis for some interactions within this complex, finding that the crescent-shaped Atg17 dimer is critical for autophagy, whereas Atg1 may have the ability to cluster membranes

Molecular regulation of autophagosome formation

Macroautophagy, hereafter autophagy, is a degradative process conserved among eukaryotes, which is essential to maintain cellular homeostasis. Defects in autophagy lead to numerous human diseases, including various types of cancer and neurodegenerative disorders. The hallmark of autophagy is the de novo formation of autophagosomes, which are double-membrane vesicles that sequester and deliver cytoplasmic materials to lysosomes/vacuoles for degradation. The mechanism of autophagosome biogenesis entered a molecular era with the identification of autophagy-related (ATG) proteins. Although there are many unanswered questions and aspects that have raised some controversies, enormous advances have been done in our understanding of the process of autophagy in recent years. In this review, we describe the current knowledge about the molecular regulation of autophagosome formation, with a particular focus on budding yeast and mammalian cells

At the Center of Macroautophagy:Autophagosomes

Autophagosomes are double-membrane vesicles that are the hallmark of the intracellular catabolic process called macroautophagy. They are formed by the orchestrated interplay of the AuTophaGy-related (ATG) proteins. The cargo molecules sequestered by autophagosomes include long-lived proteins, protein complexes or aggregates, superfluous or excess organelles, and invading pathogens. Complete autophagosomes fuse with lysosomes delivering the sequestered material in the interior of these organelles where it is degraded by resident hydrolases. Autophagy represents a key survival mechanism because it clears the cytoplasm from unwanted and potentially toxic structures, but it can also represent an intracellular source of metabolites that is induced by cells to generate new macromolecules or energy in times of need.</p

Wait, can you remind me just why we need another journal focused on autophagy?

Well, because you ask that question, we are going to attempt to explain exactly why we do indeed need another journal focused on autophagy. If you are reading this far, you presumably know what “autophagy” means, so we do not have to impress upon you the importance of this topic, and how autophagic dysfunction is associated with numerous diseases in humans (okay, we felt compelled to slip that in anyway). Nor do we think that you need to be introduced to the journal Autophagy, which is just starting its eighteenth year and publishes papers on pretty much any topic; at least any topic that is connected to autophagy, which, after all, means pretty much any topic, if you get our drift. So, if Autophagy has done so well and serves such an important purpose, why do we need another journal? To find the answer, read on

Reticulophagy and Ribophagy: Regulated Degradation of Protein Production Factories

During autophagy, cytosol, protein aggregates, and organelles are sequestered into double-membrane vesicles called autophagosomes and delivered to the lysosome/vacuole for breakdown and recycling of their basic components. In all eukaryotes this pathway is important for adaptation to stress conditions such as nutrient deprivation, as well as to regulate intracellular homeostasis by adjusting organelle number and clearing damaged structures. For a long time, starvation-induced autophagy has been viewed as a nonselective transport pathway; however, recent studies have revealed that autophagy is able to selectively engulf specific structures, ranging from proteins to entire organelles. In this paper, we discuss recent findings on the mechanisms and physiological implications of two selective types of autophagy: ribophagy, the specific degradation of ribosomes, and reticulophagy, the selective elimination of portions of the ER

A novel in vitro assay reveals SNARE topology and the role of Ykt6 in autophagosome fusion with vacuoles

Autophagy is a catabolic pathway that delivers intracellular material to the mammalian lysosomes or the yeast and plant vacuoles. The final step in this process is the fusion of autophagosomes with vacuoles, which requires SNARE proteins, the homotypic vacuole fusion and protein sorting tethering complex, the RAB7-like Ypt7 GTPase, and its guanine nucleotide exchange factor, Mon1-Ccz1. Where these different components are located and function during fusion, however, remains to be fully understood. Here, we present a novel in vitro assay to monitor fusion of intact and functional autophagosomes with vacuoles. This process requires ATP, physiological temperature, and the entire fusion machinery to tether and fuse autophagosomes with vacuoles. Importantly, we uncover Ykt6 as the autophagosomal SNARE. Our assay and findings thus provide the tools to dissect autophagosome completion and fusion in a test tube

Autophagy: More Than a Nonselective Pathway

Autophagy is a catabolic pathway conserved among eukaryotes that allows cells to rapidly eliminate large unwanted structures such as aberrant protein aggregates, superfluous or damaged organelles, and invading pathogens. The hallmark of this transport pathway is the sequestration of the cargoes that have to be degraded in the lysosomes by double-membrane vesicles called autophagosomes. The key actors mediating the biogenesis of these carriers are the autophagy-related genes (ATGs). For a long time, it was assumed that autophagy is a bulk process. Recent studies, however, have highlighted the capacity of this pathway to exclusively eliminate specific structures and thus better fulfil the catabolic necessities of the cell. We are just starting to unveil the regulation and mechanism of these selective types of autophagy, but what it is already clearly emerging is that structures targeted to destruction are accurately enwrapped by autophagosomes through the action of specific receptors and adaptors. In this paper, we will briefly discuss the impact that the selective types of autophagy have had on our understanding of autophagy

Genetic aberrations in macroautophagy genes leading to diseases

The catabolic process of macroautophagy, through the rapid degradation of unwanted cellular components, is involved in a multitude of cellular and organismal functions that are essential to maintain homeostasis. Those functions include adaptation to starvation, cell development and differentiation, innate and adaptive immunity, tumor suppression, autophagic cell death, and maintenance of stem cell stemness. Not surprisingly, an impairment or block of macroautophagy can lead to severe pathologies. A still increasing number of reports, in particular, have revealed that mutations in the autophagy-related (ATG) genes, encoding the key players of macroautophagy, are either the cause or represent a risk factor for the development of several illnesses. The aim of this review is to provide a comprehensive overview of the diseases and disorders currently known that are or could be caused by mutations in core ATG proteins but also in the so-called autophagy receptors, which provide specificity to the process of macroautophagy. Our compendium underlines the medical relevance of this pathway and underscores the importance of the eventual development of therapeutic approaches aimed at modulating macroautophagy

Unconventional Use of LC3 by Coronaviruses through the Alleged Subversion of the ERAD Tuning Pathway

Pathogens of bacterial and viral origin hijack pathways operating in eukaryotic cells in many ways in order to gain access into the host, to establish themselves and to eventually produce their progeny. The detailed molecular characterization of the subversion mechanisms devised by pathogens to infect host cells is crucial to generate targets for therapeutic intervention. Here we review recent data indicating that coronaviruses probably co-opt membranous carriers derived from the endoplasmic reticulum, which contain proteins that regulate disposal of misfolded polypeptides, for their replication. In addition, we also present models describing potential mechanisms that coronaviruses could employ for this hijacking