Leaf senescence constitutes the final stage of leaf development and is critical for plants' fitness as nutrient relocation from leaves to reproducing seeds is achieved through this process. Leaf senescence involves a coordinated action at the cellular, tissue, organ, and organism levels under the control of a highly regulated genetic program. Major breakthroughs in the molecular understanding of leaf senescence were achieved through characterization of various senescence mutants and senescence-associated genes, which revealed the nature of regulatory factors and a highly complex molecular regulatory network underlying leaf senescence. The genetically identified regulatory factors include transcription regulators, receptors and signaling components for hormones and stress responses, and regulators of metabolism. Key issues still need to be elucidated, including cellular-level analysis of senescence-associated cell death, the mechanism of coordination among cellular-, organ-, and organism-level senescence, the integration mechanism of various senescence-affecting signals, and the nature and control of leaf age.

Photoperiodic responses in plants include flowering that is day-length-dependent. Mutations in the Arabidopsis thaliana GIGANTEA (GI) gene cause photoperiod-insensitive flowering and alteration of circadian rhythms. The GI gene encodes a protein containing six putative transmembrane domains. Circadian expression patterns of the GI gene and the clock-associated genes, LHY and CCA1, are altered in gi mutants, showing that GI is required for maintaining circadian amplitude and appropriate period length of these genes. The gi-1 mutation also affects light signaling to the clock, which suggests that GI participates in a feedback loop of the plant circadian system.

Cytokinins are plant hormones with profound roles in growth and development, including control of leaf longevity. Although the cytokinin signal is known to be perceived by histidine kinase receptors, the underlying molecular mechanism and specificity of the receptors leading to delayed leaf senescence have not yet been elucidated. Here, we found that AHK3, one of the three cytokinin receptors in Arabidopsis, plays a major role in controlling cytokinin-mediated leaf longevity through a specific phosphorylation of a response regulator, ARR2. This result was obtained through identification of a gain-of-function Arabidopsis mutant that shows delayed leaf senescence because of a missense mutation in the extracellular domain of AHK3. A loss-of-function mutation in AHK3, but not of the other cytokinin receptors, conferred a reduced sensitivity to cytokinin in cytokinin-dependent delay of leaf senescence and abolished cytokinin-dependent phosphorylation of ARR2. Consistently, transgenic overexpression of wild-type, but not an unphosphorylatable mutant ARR2, led to delayed senescence of leaves.histidine kinase 3 ͉ cytokinin ͉ leaf senescence L eaf senescence is typically observed in autumn leaves and during the death process of monocarpic plants (1). During senescence, leaf cells experience striking changes in cellular metabolism and structure (2). The first visible change is yellowing of the leaves caused by chlorophyll breakdown during chloroplast disassembly (3), accompanied by hydrolysis of macromolecules such as lipids, proteins, and nucleic acids. The products of this catabolic process are reallocated to developing organs, such as younger leaves and germinating seeds (4). Therefore, senescence is not a simple degenerative process but is considered as a genetically programmed, active process that contributes to the fitness of plants. Although occurring in an age-dependent manner, leaf senescence is greatly affected by various endogenous and environmental signals to attune the life span of leaves to optimized fitness of plants (5, 6). Among the endogenous developmental signals, the plant hormones cytokinins have a particularly profound effect on longevity of plant organs (7-9). For example, it has been shown that the transgenic modification of cytokinin biosynthesis during the senescence phase can significantly delay the senescence of plant organs, including leaves, and improve plant productivity by up to 50% (8, 10).Besides control of longevity, cytokinins have many critical functions in plants, such as the control of cell proliferation, shoot formation, nutrient relocation, and shoot branching (11,12). In Arabidopsis, cytokinins are known to be perceived by three cytokinin receptors, AHK2, AHK3, and AHK4͞CRE1͞WOL, which possess the structural features of hybrid histidine kinases (13,14). In the model proposed for the cytokinin signaltransduction pathway (15-17), a histidine protein kinase initiates the cytokinin signal-transduction pathway through phosphorelay to histidine phosphotransfer (AHP) proteins. AHP protei...

Leaf senescence is an important developmental process involving orderly disassembly of macromolecules for relocating nutrients from leaves to other organs and is critical for plants’ fitness. Leaf senescence is the response of an intricate integration of various environmental signals and leaf age information and involves a complex and highly regulated process with the coordinated actions of multiple pathways. Impressive progress has been made in understanding how senescence signals are perceived and processed, how the orderly degeneration process is regulated, how the senescence program interacts with environmental signals, and how senescence regulatory genes contribute to plant productivity and fitness. Employment of systems approaches using omics-based technologies and characterization of key regulators have been fruitful in providing newly emerging regulatory mechanisms. This review mainly discusses recent advances in systems understanding of leaf senescence from a molecular network dynamics perspective. Genetic strategies for improving the productivity and quality of crops are also described.

SummaryThe EIN2-mediated senescence signalling pathway coordinates the expression of genes during leaf senescence via the gene regulatory network involving EIN3 and senescence-associated NAC TFs.

SummaryHow do organisms, organs, tissues and cells change their fate when they age towards senescence and death? Plant leaves provide a unique window to explore this question because they show reproducible life history and are readily accessible for experimental assays. Throughout their lifespan, leaves undergo a series of developmental, physiological and metabolic transitions that culminate in senescence and death. Leaf senescence is an 'altruistic death' that allows for the degradation of the nutrients that are produced during the growth phase of the leaf and their redistribution to developing seeds or other parts of the plant, and thus is a strategy that has evolved to maximize the fitness of the plant. During the past decade, there has been significant progress towards understanding the key molecular principles of leaf senescence using genetic and molecular studies, as well as 'omics' analyses. It is now apparent that leaf senescence is a highly complex genetic program that is tightly controlled by multiple layers of regulation, including at the level of chromatin and transcription, as well as by post-transcriptional, translational and post-translational regulation. This Commentary discusses the latest understandings and insights into the underlying molecular mechanisms, and presents the perspectives necessary to enable our systemlevel understanding of leaf senescence, together with their possible implications for aging in general.

Flowering plants possess a unique reproductive strategy, involving double fertilization by twin sperm cells. Unlike animal germ lines, the male germ cell lineage in plants only forms after meiosis and involves asymmetric division of haploid microspores, to produce a large, non-germline vegetative cell and a germ cell that undergoes one further division to produce the twin sperm cells. Although this switch in cell cycle control is critical for sperm cell production and delivery, the underlying molecular mechanisms are unknown. Here we identify a novel F-box protein of Arabidopsis thaliana, designated FBL17 (F-box-like 17), that enables this switch by targeting the degradation of cyclin-dependent kinase A;1 inhibitors specifically in male germ cells. We show that FBL17 is transiently expressed in the male germ line after asymmetric division and forms an SKP1-Cullin1-F-box protein (SCF) E3 ubiquitin ligase complex (SCF(FBL17)) that targets the cyclin-dependent kinase inhibitors KRP6 and KRP7 for proteasome-dependent degradation. Accordingly, the loss of FBL17 function leads to the stabilization of KRP6 and inhibition of germ cell cycle progression. Our results identify SCF(FBL17) as an essential male germ cell proliferation complex that promotes twin sperm cell production and double fertilization in flowering plants.

Two-component signaling elements play important roles in plants, including a central role in cytokinin signaling. We characterized two-component elements from the monocot rice (Oryza sativa) using several complementary approaches. Phylogenetic analysis reveals relatively simple orthologous relationships among the histidine kinases in rice and Arabidopsis (Arabidopsis thaliana). In contrast, the histidine-containing phosphotransfer proteins (OsHPs) and response regulators (OsRRs) display a higher degree of lineage-specific expansion. The intracellular localizations of several OsHPs and OsRRs were examined in rice and generally found to correspond to the localizations of their dicot counterparts. The functionality of rice type-B OsRRs was tested in Arabidopsis; one from a clade composed of both monocot and dicot type-B OsRRs complemented an Arabidopsis type-B response regulator mutant, but a type-B OsRR from a monocot-specific subfamily generally did not. The expression of genes encoding two-component elements and proteins involved in cytokinin biosynthesis and degradation was analyzed in rice roots and shoots and in response to phytohormones. Nearly all type-A OsRRs and OsHK4 were up-regulated in response to cytokinin, but other cytokinin signaling elements were not appreciably affected. Furthermore, multiple cytokinin oxidase (OsCKX) genes were up-regulated by cytokinin. Abscisic acid treatment decreased the expression of several genes involved in cytokinin biosynthesis and degradation. Auxin affected the expression of a few genes; brassinosteroid and gibberellin had only modest effects. Our results support a shared role for two-component elements in mediating cytokinin signaling in monocots and dicots and reveal how phytohormones can impact cytokinin function through modulating gene expression.