Awwad Fatima, Bertrand Guillaume, Grandbois Michel, Beaudoin Nathalie
Centre SÈVE, Département de Biologie, Université de Sherbrooke, Sherbrooke, QC J1K 2R1, Canada.
Groupe de Recherche en Biologie Végétale, Département de Chimie, Biochimie et Physique, Université du Québec à Trois-Rivières, Trois-Rivières, QC G9A 5H7, Canada.
Plants (Basel). 2019 Sep 6;8(9):332. doi: 10.3390/plants8090332.
Thaxtomin A (TA) is a cellulose biosynthesis inhibitor synthesized by the soil actinobacterium , which is the main causal agent of potato common scab. TA is essential for the induction of scab lesions on potato tubers. When added to cell cultures, TA induces an atypical programmed cell death (PCD). Although production of reactive oxygen species (ROS) often correlates with the induction of PCD, we observed a decrease in ROS levels following TA treatment. We show that this decrease in ROS accumulation in TA-treated cells is not due to the activation of antioxidant enzymes. Moreover, cell cultures treated with hydrogen peroxide (HO) prior to TA treatment had significantly fewer dead cells than cultures treated with TA alone. This suggests that HO induces biochemical or molecular changes in cell cultures that alleviate the activation of PCD by TA. Investigation of the cell wall mechanics using atomic force microscopy showed that HO treatment can prevent the decrease in cell wall rigidity observed after TA exposure. While we cannot exclude the possibility that HO may promote cell survival by altering the cellular redox environment or signaling pathways, our results suggest that HO may inhibit cell death, at least partially, by reinforcing the cell wall to prevent or compensate for damages induced by TA.
毒莠定A（TA）是一种由土壤放线菌合成的纤维素生物合成抑制剂，该放线菌是马铃薯普通疮痂病的主要致病菌。TA对于马铃薯块茎上疮痂病斑的形成至关重要。当添加到细胞培养物中时，TA会诱导一种非典型的程序性细胞死亡（PCD）。尽管活性氧（ROS）的产生通常与PCD的诱导相关，但我们观察到TA处理后ROS水平下降。我们发现，TA处理细胞中ROS积累的这种下降并非由于抗氧化酶的激活。此外，在TA处理之前用过氧化氢（HO）处理的细胞培养物中的死细胞明显少于仅用TA处理的培养物。这表明HO在细胞培养物中诱导了生化或分子变化，从而减轻了TA对PCD的激活。使用原子力显微镜对细胞壁力学进行研究表明，HO处理可以防止TA暴露后观察到的细胞壁刚性下降。虽然我们不能排除HO可能通过改变细胞氧化还原环境或信号通路来促进细胞存活的可能性，但我们的结果表明，HO可能至少部分地通过增强细胞壁来防止或补偿TA诱导的损伤从而抑制细胞死亡。
