Newest Articles
- FRET-based analysis of ER–TGN contact sites
Venditti et al. develop a novel FRET- and FLIM-based approach to monitor ER–trans Golgi network (TGN) contacts and identify VAP proteins, OSBP1, ORP9, and ORP10 as required to maintain contacts. OSBP1 and ORP9 play redundant structural roles, whereas ORP10’s requirement depends on its ability to transfer phosphatidylserine to the TGN.
- FAPP1 controls SAC1 activity at ER–TGN contacts
Venditti et al. identify FAPP1 as a new determinant of ER–trans-Golgi network contacts that interacts with the phosphoinositide phosphatase Sac1 and promotes its phosphatase activity. The results suggest that, by controlling PI4P levels, FAPP1 acts as a gatekeeper of cargo Golgi exit.
- Xiaochen Wang: Building up our understanding of breaking down
Wang studies lysosomal degradation pathways using C. Elegans as a model system.
- Myosin IIB assembly defines mechanoresponsiveness
Schiffhauer et al. use mathematical modeling of Dictyostelium myosin II and experimental approaches in mammalian cells to demonstrate that multiple inputs modulate the ability of myosin II to assemble into filaments. These inputs integrate to govern the myosin II mechanoresponsiveness.
- Saccharopine is a mitochondrial toxin
Leandro and Houten highlight new work from Zhou et al. exploring the disease relevance and toxicity of lysine metabolites in mitochondria.
- Autophagy degrades lamin for herpesvirus egress
Florence Niedergang introduces work by Turan et al. demonstrating that herpes virus egress from dendritic cells is differentially regulated by kinesin-dependent positioning of lysosomes and autophagic degradation of nuclear lamins.
- Remodeling mitochondrial localization during meiosis
Soni Lacefield discusses new findings from Sawyer et al. revealing the developmental regulation of mitochondrial detachment from the cell cortex during meiosis.
- A mosaic of old and young Nups
Shimi and Kimura preview work from the Hetzer laboratory visualizing nuclear long-lived proteins, histones and nucleoporins, and the pattern of nucleoporin renewal, providing insight into protein longevity in nuclear maintenance and its function.
- ATM regulates ATP levels through NRF1
Oxidative stress, resulting from neuronal activity and depleted ATP levels, activates ATM, which phosphorylates NRF1, causing nuclear translocation and up regulation of mitochondrial gene expression. In ATM deficiency, ATP levels recover more slowly, particularly in active neurons with high energy demands.