Towards Understanding the Involvement of H<sup>+</sup>-ATPase in Programmed Cell Death of <i>Psammosilene tunicoides</i> after Oxalic Acid Application

<i>Psammosilene tunicoides</i> is a unique perennial medicinal plant species native to the Southwestern regions of China. Its wild population is rare and endangered due to over-excessive collection and extended growth (4–5 years). This research shows that H<sup>+</sup>-ATPase...

Descripción completa

Guardado en:
Detalles Bibliográficos
Autores principales: Xinyu Jiang, Mohammad Aqa Mohammadi, Yuan Qin, Zongshen Zhang
Formato: article
Lenguaje:EN
Publicado: MDPI AG 2021
Materias:
Acceso en línea:https://doaj.org/article/491f43bee8684eaaad2606f35a334ce1
Etiquetas: Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
Descripción
Sumario:<i>Psammosilene tunicoides</i> is a unique perennial medicinal plant species native to the Southwestern regions of China. Its wild population is rare and endangered due to over-excessive collection and extended growth (4–5 years). This research shows that H<sup>+</sup>-ATPase activity was a key factor for oxalate-inducing programmed cell death (PCD) of <i>P. tunicoides</i> suspension cells. Oxalic acid (OA) is an effective abiotic elicitor that enhances a plant cell’s resistance to environmental stress. However, the role of OA in this process remains to be mechanistically unveiled. The present study evaluated the role of OA-induced cell death using an inverted fluorescence microscope after staining with Evans blue, FDA, PI, and Rd123. OA-stimulated changes in K<sup>+</sup> and Ca<sup>2+</sup> trans-membrane flows using a patch-clamp method, together with OA modulation of H<sup>+</sup>-ATPase activity, were further examined. OA treatment increased cell death rate in a dosage-and duration-dependent manner. OA significantly decreased the mitochondria activity and damaged its electron transport chain. The OA treatment also decreased intracellular pH, while the FC increased the pH value. Simultaneously, NH<sub>4</sub>Cl caused intracellular acidification. The OA treatment independently resulted in 90% and the FC led to 25% cell death rates. Consistently, the combined treatments caused a 31% cell death rate. Furthermore, treatment with EGTA caused a similar change in intracellular pH value to the La<sup>3+</sup> and OA application. Combined results suggest that OA-caused cell death could be attributed to intracellular acidification and the involvement of OA in the influx of extracellular Ca<sup>2+</sup>, thereby leading to membrane depolarization. Here we explore the resistance mechanism of <i>P</i>. <i>tunicoides</i> cells against various stresses endowed by OA treatment.