Sites at which mitochondria contact the endoplasmic reticulum co-localize the replication of mitochondria and their DNA to help ensure that DNA is distributed appropriately between the newly formed organelles in cells.

A cell-free biochemical assay for protein lipidation identifies the ER–Golgi intermediate compartment as a key early station in the formation of an autophagosome.

A cell-free system combined with cell-based assays elucidate the biochemical mechanism of signal transduction mediated by the mitochondrial protein MAVS and delineates the role of ubiquitin E3 ligases in antiviral innate immune responses.

The proteins Bax and Bak, which increase the permeability of the mitochondrial membrane during apoptosis, are also crucial for generating a mitochondrial membrane pore that is specifically involved in necrosis.

Cavin-3 is a tumor suppressor protein that inhibits Akt signaling, suppresses Warburg metabolism, promotes apoptosis, and protects against cachexia.

Reoxygenation of anoxic cardiac tissue promotes massive endocytosis that is triggered by release of coenzymeA from mitochondria, followed by palmitoylation of membrane proteins, sarcolemma vesiculation, and transfer of sarolemma vesicles to large endosomes and vacuoles.

Mitochondrial anti-viral signaling proteins form three-stranded helical filaments in launching innate immune responses against RNA viruses.

Close examination of lanceolate mechanosensory complexes has revealed clues about the ways that sensory nerves detect the movement of hairs and shown than terminal Schwann cells are needed to maintain and regenerate these intricate structures.

Two GAP proteins bound to mitochondria regulate the enyzme Rab7, and thereby the expansion of the isolation membrane during mitophagy, downstream of PINK1 and Parkin, two proteins that are mutated in familial Parkinson's disease.