Heavy metal tolerance of microorganisms is the basis of heavy metal removal by growing cells. In this study, a cross-protection effect generated by salt stress significantly enhanced the cadmium tolerance of multi-stress-tolerant Pichia kudriavzevii. Comparative transcriptome analysis using RNA-Seq linked with physiological and biochemical observation was used to elucidate the underlying mechanisms of the improved cadmium tolerance. The expression of cadmium transport related genes (GSTY2, GLR1, GLO2, YCF1 and YOR1), GSH content and GST activity were elevated by salt stress, suggesting enhanced cadmium conjugation and detoxification in yeast cells. The inhibited cadmium uptake by ZRT1 and enhanced cadmium efflux by YOR1 contributed to the decrease in the intracellular cadmium concentration. The improved expression of antioxidant enzyme genes (SOD1, SOD2, SOD6, CAT1 and PRXIID), along with the enhanced activities of antioxidant enzymes (SOD, CAT and POD) resulted in a decrease in cadmium-induced ROS production, protein carbonylation, lipid peroxidation and cell death. The abundant expression of heat shock protein genes (HSP12, HSP10 and SSC1) and genes related to trehalose synthesis (TPS1 and TSL1) induced by salt stress protected yeast cells against complex stress conditions, contributing to the improved cadmium tolerance. These findings will be useful to develop cadmium-tolerant yeasts for cadmium removal by growing cells.

微生物对重金属的耐受性是生长细胞去除重金属的基础。在这项研究中，盐胁迫产生的交叉保护作用显着提高了耐多胁迫毕赤酵母（Pichia kudriavzevii）对镉的耐受性。使用与生理和生化观察相联系的RNA-Seq进行比较转录组分析，以阐明改善的镉耐受性的潜在机制。镉转运相关基因（GSTY2，GLR1，GLO2，YCF1和YOR1）的表达。），盐胁迫提高了GSH含量和GST活性，表明酵母细胞中镉的结合和解毒作用增强。ZRT1抑制了镉的吸收，而YOR1增强了镉的外流，导致细胞内镉浓度的降低。抗氧化酶基因（SOD1，SOD2，SOD6，CAT1和PRXIID）的表达改善，以及抗氧化酶（SOD，CAT和POD）的活性增强，导致镉诱导的ROS产生，蛋白质羰基化，脂质过氧化作用降低和细胞死亡。热休克蛋白基因（HSP12，HSP10和SSC1）的大量表达。）以及与盐胁迫诱导的海藻糖合成相关的基因（TPS1和TSL1）可保护酵母细胞免受复杂的胁迫条件的影响，从而有助于提高镉的耐受性。这些发现将有助于开发耐受镉的酵母，以通过生长中的细胞去除镉。