Morphological changes in senescing petal cells and the regulatory mechanism of petal senescence.

Abstract

Petal senescence, or programmed cell death (PCD) in petals, is a developmentally regulated and genetically programmed process. During petal senescence, petal cells show morphological changes associated with PCD: tonoplast rupture and rapid destruction of the cytoplasm. This type of PCD is classified as vacuolar cell death or autolytic PCD based on morphological criteria. In PCD of petal cells, characteristic morphological features including an autophagy-like process, chromatin condensation, and nuclear fragmentation are also observed. While the phytohormone ethylene is known to play a crucial role in petal senescence in some plant species, little is known about the early regulation of ethylene-independent petal senescence. Recently, a NAC (NAM/ATAF1,2/CUC2) transcription factor was reported to control the progression of PCD during petal senescence in Japanese morning glory, which shows ethylene-independent petal senescence. In ethylene-dependent petal senescence, functional analyses of transcription factor genes have revealed the involvement of a basic helix-loop-helix protein and a homeodomain-leucine zipper protein in the transcriptional regulation of the ethylene biosynthesis pathway. Here we review the recent advances in our knowledge of petal senescence, mostly focusing on the morphology of senescing petal cells and the regulatory mechanisms of PCD by senescence-associated transcription factors during petal senescence.