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Kinetin induces microtubular breakdown, cell cycle arrest and programmed cell death in tobacco BY-2 cells.

Andrzej KaźmierczakEwa SiatkowskaRuoxi LiSophie BothePeter Nick
Published in: Protoplasma (2022)
Plant cells can undergo regulated cell death in response to exogenous factors (often in a stress context), but also as regular element of development (often regulated by phytohormones). The cellular aspects of these death responses differ, which implies that the early signalling must be different. We use cytokinin-induced programmed cell death as paradigm to get insight into the role of the cytoskeleton for the regulation of developmentally induced cell death, using tobacco BY-2 cells as experimental model. We show that this PCD in response to kinetin correlates with an arrest of the cell cycle, a deregulation of DNA replication, a loss of plasma membrane integrity, a subsequent permeabilisation of the nuclear envelope, an increase of cytosolic calcium correlated with calcium depletion in the culture medium, an increase of callose deposition and the loss of microtubule and actin integrity. We discuss these findings in the context of a working model, where kinetin, mediated by calcium, causes the breakdown of the cytoskeleton, which, either by release of executing proteins or by mitotic catastrophe, will result in PCD.
Keyphrases
  • cell cycle arrest
  • cell death
  • cell cycle
  • pi k akt
  • induced apoptosis
  • cell proliferation
  • high glucose
  • transcription factor
  • endoplasmic reticulum stress
  • oxidative stress
  • endothelial cells
  • stress induced