Analysis of aging yeast cells using the in-vivo roGFP2-based probe reveals redox-dependent heterogeneity, reflected in a bi-modal distribution of the oxidation status, differential growth and replication, as well as distinct proteomic and transcriptomic profiles.

The use of genetically encoded redox sensors in phagocytized bacteria reveals that, among the toxic cocktail of oxidants released into the neutrophil's phagolysosome, HOCl is the main component responsible for the oxidative modification of bacterial protein thiols.

Adapting a cytosolic enzyme that breaks down glutathione to function in the lumen of the endoplasmic reticulum challenges the long-held view that reduced glutathione fuels disulfide rearrangements during protein folding.

African trypanosomes have a trypanothione-based mitochondrial thiol redox metabolism.

The organic insecticide spinosad severely impacts metabolism, the cell biology, and the visual system of the model insect Drosophila, suggesting that it poses a threat to other non-pest insect exposed to it in the field.

Single-cell analysis of the chloroplast redox response to high light and oxidative stress revealed light-dependent heterogeneity, and was linked to cell fate determination within isogenic diatom populations.

An efficient response to DNA damage requires the assembly of actin filaments in the nucleus.

Genome-scale integration of transposon mutagenesis with a redox biosensor identified a hypothetical transcription factor- Rv0158 required to calibrate the growth, cytoplasmic redox potential, and respiration of Mycobacterium tuberculosis in response to metabolic switching from glucose to fatty acids.

In mouse models of Huntington's disease, the subthalamic nucleus, which suppresses movements, also exhibits impaired glutamate homeostasis, NMDA receptor-dependent mitochondrial oxidant stress, firing disruption, and 30% neuronal loss.

In response to neuronal activity in vivo, mitochondria in dendrites of excitatory neurons inhibit recruitment of ionotropic glutamate receptors through a reactive oxygen signaling mechanism.