Autophagy and modular restructuring of metabolism control germline tumor differentiation and proliferation in C. elegans.

Autophagy can act either as a tumor suppressor or as a survival mechanism for established tumors. To understand how autophagy plays this dual role in cancer, in vivo models are required. By using a highly heterogeneous C.

Autophagy in antimicrobial immunity.

Autophagy plays a key role in cellular homeostasis, responding to various environmental stresses. In particular, pathogen invasion leads to rapid induction of autophagy, which is critical for both innate and adaptive immune responses. In this review, we focus on the emerging molecular mechanisms of pathogen elimination by autophagy (a process known as xenophagy) and on the strategies developed by pathogens to subvert autophagy.

Binding of OTULIN to the PUB domain of HOIP controls NF-κB signaling.

Linear ubiquitin chains are implicated in the regulation of the NF-κB pathway, immunity, and inflammation. They are synthesized by the LUBAC complex containing the catalytic subunit HOIL-1-interacting protein (HOIP) and are disassembled by the linear ubiquitin-specific deubiquitinase OTULIN. Little is known about the regulation of these opposing activities.

Mitochondrial cristae shape determines respiratory chain supercomplexes assembly and respiratory efficiency.

Respiratory chain complexes assemble into functional quaternary structures called supercomplexes (RCS) within the folds of the inner mitochondrial membrane, or cristae. Here, we investigate the relationship between respiratory function and mitochondrial ultrastructure and provide evidence that cristae shape determines the assembly and stability of RCS and hence mitochondrial respiratory efficiency. Genetic and apoptotic manipulations of cristae structure affect assembly and activity of RCS in vitro and in vivo, independently of changes to mitochondrial protein synthesis or apoptotic outer mitochondrial membrane permeabilization.

Mitochondrial morphology in mitophagy and macroautophagy.

Mitochondria are critical organelles in energy conversion, metabolism and amplification of signalling. They are however also major sources of reactive oxygen species and when dysfunctional they consume cytosolic ATP. Maintenance of a cohort of healthy mitochondria is therefore crucial for the overall cell fitness.

Essential amino acids and glutamine regulate induction of mitochondrial elongation during autophagy.

Regulated changes in mitochondrial morphology and ultrastructure regulate several cellular processes, including apoptosis and, as we recently described, autophagy. Elongated mitochondria are spared from autophagic degradation and possess more cristae, where activity of the ATP synthase is increased, maintaining ATP levels in periods of nutrient depletion. Ultimately, mitochondrial elongation is crucial for cell survival during macroautophagy.

Mitochondrial elongation during autophagy: a stereotypical response to survive in difficult times.

Mitochondrial morphological and structural changes play a role in several cellular processes, including apoptosis. We recently reported that mitochondrial elongation is also critical to sustain cell viability during macroautophagy. During macroautophagy unopposed mitochondrial fusion leads to organelle elongation both in vitro and in vivo.

During autophagy mitochondria elongate, are spared from degradation and sustain cell viability.

A plethora of cellular processes, including apoptosis, depend on regulated changes in mitochondrial shape and ultrastructure. The role of mitochondria and of their morphology during autophagy, a bulk degradation and recycling process of eukaryotic cells' constituents, is not well understood. Here we show that mitochondrial morphology determines the cellular response to macroautophagy.

High levels of Fis1, a pro-fission mitochondrial protein, trigger autophagy.

Damaged mitochondria can be eliminated in a process of organelle autophagy, termed mitophagy. In most cells, the organization of mitochondria in a network could interfere with the selective elimination of damaged ones. In principle, fission of this network should precede mitophagy; but it is unclear whether it is per se a trigger of autophagy.