Although 30 years have passed since the description of sugar-induced cell death (SICD), the specific molecular mechanism that triggers this process remains unclear. This paper attempts to shed light on the relationship between SICD and glucose catabolism. In yeast cells, glucose is involved not only in energy-producing processes but also in the synthesis of reserve hydrocarbons. It is known that disruption of trehalose synthesis leads to significant changes in the physiology of Saccharomyces cerevisiae. The present study shows that deletion of the TPS1 gene resulted in a 44% suppression of SICD and a 75% reduction in the number of cells with excess ROS (reactive oxygen species). The suppression was comparable to the suppression of SICD (38%) and ROS (71%) with deletion of the HXK2 gene. Since HXK2 is the first enzyme in the glycolytic pathway, the effect of two other key glycolytic enzymes on SICD was tested. Deletion of the TDH3 gene (glyceraldehyde-3-phosphate dehydrogenase) resulted in a 39% suppression of SICD and ROS by 48%. Inhibition of Tdh3p with 1 mM iodoacetamide also suppressed SICD by 67% and ROS by 58%. Deletion of the PFK1 (phosphofructokinase 1) gene resulted in a complete block of SICD (97%) but unexpectedly resulted in a significant increase in the number of cells with excess ROS. The results obtained suggest that such a phenomenon as SICD is the result of an imbalance in the cellular pathways of glucose catabolism.

• PMID: 39953899
• DOI full text
• PubMed
• PubTator

Reference Type

Journal Article

Authors

Valiakhmetov A

Primary Lit For

Additional Lit For

Review For