Cells must adjust their redox state to an ever-changing environment that
could otherwise result in compromised homeostasis. An obvious way to
adapt to changing redox conditions depends on cysteine
post-translational modifications (PTMs) to adapt conformation,
localization, interactions and catalytic activation of proteins. Such
PTMs should occur preferentially in the proximity of oxidative stress
sources. A particular concentration of these sources is found near
membranes where the endoplasmic reticulum (ER) and the mitochondria
interact on domains called MERCs (Mitochondria-Endoplasmic Reticulum
Contacts). Here, fine inter-organelle communication controls metabolic
homeostasis. MERCs achieve this goal through fluxes of Ca2+ions and inter-organellar lipid exchange. Reactive oxygen species
(ROS) that cause PTMs of mitochondria-associated membrane (MAM)
proteins determine these intertwined MERC functions. Chronic changes
of the pattern of these PTMs not only control physiological processes
such as the circadian clock but could also lead to or worsen many
human disorders such as cancer and neurodegenerative diseases.