Cadmium induces GAPDH- and- MDH mediated delayed cell aging and dysfunction in Candida tropicalis 3Aer.

Eukaryotes employ various mechanisms to survive environmental stress conditions. Multicellular organisms eliminate permanently damaged cells by apoptosis, while unicellular eukaryotes like yeast react by decelerating cell aging. In the present study, transcriptomic and proteomic approaches were employed to elucidate the underlying mechanism of delayed apoptosis. Our findings suggest that Candida tropicalis 3Aer has a set of tightly controlled genes that are activated under Cd+2 exposition. Acute exposure to Cd+2 halts the cell cycle at the G2/M phase checkpoint and activates multiple cytoplasmic proteins that overcome effects of Cd+2-induced reactive oxygen species. Prolonged Cd+2 stress damages DNA and initiates GAPDH amyloid formation. This is the first report that Cd+2 challenge initiates dynamic redistribution of GAPDH and MDH and alters various metabolic pathways including the pentose phosphate pathway. In conclusion, the intracellular redistribution of GAPDH and MDH induced by prolonged cadmium stress modulates various cellular reactions, which facilitate delayed aging in the yeast cell.