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

Area of Science:

• Cellular Biology
• Environmental Stress Response
• Biochemistry

Background:

• Eukaryotes utilize distinct strategies to cope with environmental stressors, such as apoptosis in multicellular organisms and decelerated aging in unicellular eukaryotes like yeast.
• Understanding the molecular mechanisms behind stress-induced aging delay in yeast is crucial for comprehending cellular resilience.

Purpose of the Study:

• To investigate the molecular mechanisms underlying delayed apoptosis and aging in the yeast Candida tropicalis under cadmium (Cd⁺²) exposure.
• To identify specific genes, proteins, and metabolic pathways involved in the yeast's response to acute and prolonged cadmium stress.

Main Methods:

• Transcriptomic and proteomic analyses were performed to elucidate gene and protein expression changes.
• Cell cycle progression and cellular responses to cadmium were monitored.

Main Results:

• Acute cadmium exposure arrests the cell cycle at the G₂/M phase checkpoint and triggers cytoplasmic proteins to counteract reactive oxygen species.
• Prolonged cadmium stress leads to DNA damage and the formation of Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) amyloid.
• Cadmium stress induces dynamic redistribution of GAPDH and malate dehydrogenase (MDH) and alters metabolic pathways, including the pentose phosphate pathway.

Conclusions:

• The intracellular redistribution of GAPDH and MDH, triggered by prolonged cadmium stress, plays a key role in modulating cellular reactions.
• These stress-induced cellular modifications facilitate a delayed aging process in yeast cells, enhancing their survival under adverse conditions.