The ability to follow single objects in 3D in a living organism with high spatiotemporal resolution opens new possibilities for quantitative biophysical studies of complex systems in their physiological context.

A quantitative analysis of glucose-dependent transport regulation indicates that mitochondrial accumulation in regions of high nutrient availability can enhance metabolism in neuronal axons under physiologically relevant conditions.

Channel characteristics of the presequence translocation pore have a direct impact on protein import into the mitochondrial matrix.

A novel and metazoan-specific protein, Tim29, is identified as a subunit of the human TIM22 complex and shown to function in the assembly of hTim22 and facilitate contacts with the TOM complex.

A novel microscopy-based assay shows that dendritic cells encountering pathogenic stimuli form increased complexes of specific SNARE proteins, driving release of large amounts of inflammatory cytokines.

Sec17 (αSNAP) and Sec18 (NSF) are shown to act twice, to promote fusion per se and to recycle SNAREs after fusion.

The ATP7A interactome is the first comprehensive view of putative Menkes disease neurodegeneration mechanisms.

Molecular signals from chloroplasts can synergistically interact with the plant hormone, abscisic acid (ABA), to regulate non-canonical signaling pathways mediating fundamental cellular processes including stomatal closure, seed dormancy and germination.

Analyses of a developmentally regulated Drosophila myofiber remodeling program provide insight into induced autophagy required for T-tubule membrane reorganization, and uncover a conserved Rab2 role in autophagosome-lysosome fusion.

In Drosophila, the loss of Frataxin causes iron accumulation in the nervous system, which in turn enhances sphingolipid synthesis and activation of PDK1 and Mef2, which leads to neurodegeneration.