Human VDAC isoforms differ in their capability to interact with minocycline and to contribute to its cytoprotective activity.

It has been previously demonstrated that cytoprotective activity displayed by minocycline in the case of the yeast Saccharomyces cerevisiae cells pretreated with H2O2 requires the presence of functional VDAC (YVDAC1). Thus, we decided to transform YVDAC1-depleted yeast cells (Δpor1 cells) with plasmids expressing human VDAC isoforms (HVDAC1, HVDAC2, HVDAC3) to estimate their involvement in the minocycline cytoprotective effect. We observed that only expression of HVDAC3 in Δpor1 cells provided minocycline-mediated cytoprotection against H2O2 although all human isoforms are functional in Δpor1 cells.

Protein import complexes in the mitochondrial outer membrane of Amoebozoa representatives.

Background: An ancestral trait of eukaryotic cells is the presence of mitochondria as an essential element for function and survival. Proper functioning of mitochondria depends on the import of nearly all proteins that is performed by complexes located in both mitochondrial membranes. The complexes have been proposed to contain subunits formed by proteins common to all eukaryotes and additional subunits regarded as lineage specific.

The TOM Complex of Amoebozoans: the Cases of the Amoeba Acanthamoeba castellanii and the Slime Mold Dictyostelium discoideum.

Protein import into mitochondria requires a wide variety of proteins, forming complexes in both mitochondrial membranes. The TOM complex (translocase of the outer membrane) is responsible for decoding of targeting signals, translocation of imported proteins across or into the outer membrane, and their subsequent sorting. Thus the TOM complex is regarded as the main gate into mitochondria for imported proteins.

VDAC contributes to mRNA levels in Saccharomyces cerevisiae cells by the intracellular reduction/oxidation state dependent and independent mechanisms.

Available data suggest that voltage-dependent anion selective channel (VDAC) constitutes an important component of a cellular regulatory mechanism based on the intracellular reduction/oxidation (redox) state. Here, using quantitative RT-PCR, we demonstrated that depletion of VDAC1 (termed here VDAC) in Saccharomyces cerevisiae cells distinctly affected levels of mRNAs encoding nuclear proteins sensitive to changes of the intracellular redox state including the nuclear transcription factors important for adaptation to the redox state and proteins involved in communication between mitochondria and the nucleus. We also revealed that the changes of the studied protein transcript levels generally correlated with changes of the intracellular redox state although VDAC appears also to affect mRNA levels by a mechanism not based on changes of the intracellular redox states.