Winter wheat cells subjected to freezing temperature undergo death process with features of programmed cell death

Abstract

Programmed cell death is a process defined as genetically regulated self-destruction or cell suicide. It can be activated by different internal and external factors, but few studies have investigated whether this process occurs under cold and freezing temperatures. In this study, a freezing treatment (-8 °C for 6 h) induced cell death with features of programmed cell death in suspension cultures of winter wheat (Triticum aestivum L.). This process occurred for 10 days after cold exposure. The death of cells in culture was slow and prolonged, and was accompanied by protoplast shrinkage, DNA fragmentation, and an increase in the level of reactive oxygen species. Other changes observed after the freezing treatment included an increase in the respiration rate, changes in mitochondrial transmembrane potential (∆Ψ m ), and the release of cytochrome c from mitochondria into the cytosol. These findings indicated that mitochondria are involved in the cell death process that occurs after a freezing treatment in cells of winter wheat.

ROS-mediated abiotic stress-induced programmed cell death in plants

“…Low temperature (both chilling and freezing) on its own can also induce PCD in plants ( Koukalova et al, 1997 ; Lyubushkina et al, 2014 ). Tobacco BY-2 suspension cells progressively develop characteristic features of PCD, including DNA condensation and fragmentation (laddering), after exposure to 5–6 ∘ C for two to 5 weeks ( Koukalova et al, 1997 ).…”

“…Interestingly, 11% of the cells did not die even after prolonged incubation at low temperature. Winter wheat ( Triticum aestivum L.) cell cultures exposed to freezing treatment (-8 ∘ C) undergo PCD accompanied by ROS accumulation, DNA fragmentation, and the release of cytochrome c from mitochondria into the cytosol ( Lyubushkina et al, 2014 ). LESION SIMULATING DISEASE RESISTANCE 1 (LSD1) is a plant-specific negative regulator of PCD and its mutation causes ROS accumulation and runaway cell death ( Jabs et al, 1996 ; Dietrich et al, 1997 ).…”

The Permeability Transition in Plant Mitochondria: The Missing Link

“…The role of mitochondria in PCD is confirmed in heat-stressed rice protoplasts, where mHSP70 overexpression maintains mitochondrial ΔΨ, partially inhibits cytochrome c release and suppresses PCD by lowering ROS formation ( Qi et al, 2011 ). In wheat cells subjected to freezing, ROS-dependent PCD is associated to ΔΨ collapse and cytochrome c release ( Lyubushkina et al, 2014 ). In salt-stressed tobacco protoplasts, PCD is triggered by ROS produced by mitochondria, through a process controlled by a CsA-sensitive PT ( Lin et al, 2006 ).…”

Mitochondrial Membrane Potential and Reactive Oxygen Species, as Indicators of Stress Status of Plants

“…Есть данные, свидетельствующие, что генерация АФК митохондриями усиливается при понижении митохондриального мембранного потенциала (ММП) [Vianello et al, 2007]. Однако в ряде случаях может наблюдаться и обратная зависимость: повышение уровня АФК в клетках растений происходит параллельно увеличению ММП [Федяева и др., 2014;Lyubushkina et al, 2014;Sun et al, 2012]. Известно, что обработка некоторыми гербицидами приводит к усилению генерации АФК [Chen et al, 2015;Pazmino et al, 2011].…”

“…Однако это правило не всегда выполняется. Известны случаи, когда в клетках растений наблюдается одновременное усиление продукции АФК и повышение ММП [Sun et al, 2012;Федяева и др., 2014;Lyubushkina et al, 2014]. Действительно, при повышении продукции АФК в клетках растений при действии теплового и холодового шока, а также при обработке диуроном наблюдалось одновременное повышение ММП и уровня АФК (рисунок).…”