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JXB Advance Access first published online on February 28, 2008
This version published online on March 3, 2008

Journal of Experimental Botany, doi:10.1093/jxb/erm356
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© The Author [2008]. Published by Oxford University Press [on behalf of the Society for Experimental Biology]. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

FOCUS REVIEW

Physiology and molecular biology of petal senescence*

Wouter G. van Doorn{dagger},{ddagger} and Ernst J. Woltering

Wageningen University and Research Centre, PO Box 17, 6700 AA Wageningen, The Netherlands
{dagger}Present address: Mann Laboratory, Plant Science Department, University of California, Davis, One Shields Avenue, Davis, CA 95616, USA

{ddagger} To whom correspondence should be addressed. E-mail: wgvandoorn{at}ucdavis.edu

Petal senescence is reviewed, with the main emphasis on gene expression in relation to physiological functions. Autophagy seems to be the major mechanism for large-scale degradation of macromolecules, but it is still unclear if it contributes to cell death. Depending on the species, petal senescence is controlled by ethylene or is independent of this hormone. EIN3-like (EIL) transcription factors are crucial in ethylene-regulated senescence. The presence of adequate sugar levels in the cell delays senescence and prevents an increase in the levels of EIL mRNA and the subsequent up-regulation of numerous senescence-associated genes. A range of other transcription factors and regulators are differentially expressed in ethylene-sensitive and ethylene-insensitive petal senescence. Ethylene-independent senescence is often delayed by cytokinins, but it is still unknown whether these are natural regulators. A role for caspase-like enzymes or metacaspases has as yet not been established in petal senescence, and a role for proteins released by organelles such as the mitochondrion has not been shown. The synthesis of sugars, amino acids, and fatty acids, and the degradation of nucleic acids, proteins, lipids, fatty acids, and cell wall components are discussed. It is claimed that there is not enough experimental support for the widely held view that a gradual increase in cell leakiness, resulting from gradual plasma membrane degradation, is an important event in petal senescence. Rather, rupture of the vacuolar membrane and subsequent rapid, complete degradation of the plasma membrane seems to occur. This review recommends that more detailed analysis be carried out at the level of cells and organelles rather than at that of whole petals.

Key words: Autophagy, cell death, cell wall, gene expression, hormones, lipids, nucleic acids, pathogens, proteins, reactive oxygen species, regulation, remobilization, senescence, transcriptions factors, ultrastucture


* This paper is dedicated to the memory of our colleague Abraham Halevy, who passed away in 2006. Abe kindly suggested one of us (WvD) that we should produce the present review.

Received 7 September 2007; Revised 16 December 2007 Accepted 17 December 2007


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