Senescence-Associated Programmed Cell Death

Abstract

Senescence is key component of plant development. It enables remobilisation of nutrients from organs that are no longer needed or have been compromised and ends with programmed cell death (PCD) of all the cells in the organ. Cytological features of senescence-associated PCD are distinct, though shared in part with other forms of plant PCD triggered by abiotic stress or pathogen attack. These cytological features define a form of PCD termed vacuolar cell death and share some characteristics of autophagy. Key features are enlargement of the vacuole through fusion of vesicles carrying cytoplasmic cargo and vacuolar rupture releasing lytic enzymes into the cytoplasm. Biochemical processes are common to many forms of plant PCD including the activation of proteases, lipases, nucleases and transporters. Vacuolar processing enzymes (VPEs) that have caspase activity have emerged as important players in several forms of PCD. However, less is known about upstream signals and regulatory mechanisms that control the initiation and progression of senescence and trigger the onset of PCD. Here, the signals and mechanisms triggering senescence-associated PCD are reviewed, and their conservation across different tissues is assessed. Key questions that remain to be answered in future research are discussed.