Abstract

Abstract Salt-induced oxidative stress accounts for redox imbalance and cell death in the food spoilage yeasts. However, the physiological mechanisms underlying this imbalance and succeeding effective tolerance are still poorly understood. To elucidate this cellular protective mechanism governing in moderately halotolerant yeasts, Zygosaccharomyces bisporus was analyzed under sub-lethal conditions of sodium salt. For most stress intervals; high activity of enzymic antioxidants suggested their broad panorama in rescuing salt prompted apoptosis, attenuating intracellular degenerative reactive species with simultaneous reversal of characteristic apoptotic changes as nuclear fragmentation and chromatin condensation. In addition, the synergistic role of cell membrane cation transporters; plasma membrane ATPase and Na+/H+ like antiporter have been investigated by quantifying the external pH of the medium under stress, with the aid of specific ion transporter inhibitors like N,N'-Dicyclohexylcarbodiimide, sodium azide, and amiloride respectively. Taken together, the major outcomes from this study provide the evidence of salt imposed cell death by triggering unbalanced redox status via several key mitochondrial reactive species, allied with yeast defensive pleiotropic manipulations like antioxidants, expulsion of toxic Na+ by Nha transporters and re-establishing the optimal growth pH in alliance with PM-ATPase as a stress response resulting redox homeostasis restoration and osmoregulation. This study critically claims a proteostatic crosstalk mechanism between mitochondria and the cytosol, thus plays an important role in cell survival and advance halo-tolerance. Thereby, this inter-relationship can be further exploited for biotechnological and industrial applications in spoilage yeasts.

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