Leaf senescence: signals, execution, and regulation

Abstract

Leaf senescence is a type of postmitotic senescence. The onset and progression of leaf senescence are controlled by an array of external and internal factors including age, levels of plant hormones/growth regulators, and reproductive growth. Many environmental stresses and biological insults such as extreme temperature, drought, nutrient deficiency, insufficient light/shadow/darkness, and pathogen infection can induce senescence. Perception of signals often leads to changes in gene expression, and the upregulation of thousands of senescence-associated genes (SAGs) causes the senescence syndrome: decline in photosynthesis, degradation of macromolecules, mobilization of nutrients, and ultimate cell death. Identification and analysis of SAGs, especially genome-scale investigations on gene expression during leaf senescence, make it possible to decipher the molecular mechanisms of signal perception, execution, and regulation of the leaf senescence process. Biochemical and metabolic changes during senescence have been elucidated, and potential components in signal transduction such as receptor-like kinases and MAP kinase cascade have been identified. Studies on some master regulators such as WRKY transcription factors and the senescence-responsive cis element of the senescence-specific SAG12 have shed some light on transcriptional regulation of leaf senescence.