Senescence is a ubiquitous characteristic in the biological world. From an ontogenetic perspective, senescence is now established as a developmental and genetic program acquired during evolution (Wojciechowska et al., 2018). Like in other organisms, senescence in plants is genetically programmed (Nam, 1997; van Doorn and Woltering, 2004; Wojciechowska et al., 2018). In plants, senescence is a prelude to cell (organ) death, and during this process metabolites and macromolecules released are salvaged for utilization by the plant for growth. Generally, senescence occurs prior to programmed cell death (PCD), since symptomatic leaf yellowing can be reversed based on the timing of senescence while PCD is a terminal, irreversible program. It has been suggested that the term "PCD" in plants should be restricted to the specific stage of intrinsic senescence program when it has reached a "point of no return" and leaf yellowing is no longer reversible (Mattoo and Handa, 2003). Programmed cell death in plants was described as a sequential process that included apoptosis-like necrosis and autophagy (van Doorn et al., 2011). Autophagy under normal growth conditions favors turnover of cellular components for maintaining homeostasis,
Senescence is the final stage of plant ontogeny before death. Senescence may occur naturally because of age or may be induced by various endogenous and exogenous factors. Despite its destructive character, senescence is a precisely controlled process that follows a well-defined order. It is often inseparable from programmed cell death (PCD), and a correlation between these processes has been confirmed during the senescence of leaves and petals. Despite suggestions that senescence and PCD are two separate processes, with PCD occurring after senescence, cell death responsible for senescence is accompanied by numerous changes at the cytological, physiological and molecular levels, similar to other types of PCD. Independent of the plant organ analysed, these changes are focused on initiating the processes of cellular structural degradation via fluctuations in phytohormone levels and the activation of specific genes. Cellular structural degradation is genetically programmed and dependent on autophagy. Phytohormones/plant regulators are heavily involved in regulating the senescence of plant organs and can either promote [ethylene, abscisic acid (ABA), jasmonic acid (JA), and polyamines (PAs)] or inhibit [cytokinins (CKs)] this process. Auxins and carbohydrates have been assigned a dual role in the regulation of senescence, and can both inhibit and stimulate the senescence process. In this review, we introduce the basic pathways that regulate senescence in plants and identify mechanisms involved in controlling senescence in ephemeral plant organs. Moreover, we demonstrate a universal nature of this process in different plant organs; despite this process occurring in organs that have completely different functions, it is very similar. Progress in this area is providing opportunities to revisit how, when and which way senescence is coordinated or decoupled by plant regulators in different organs and will provide a powerful tool for plant physiology research.
The aim of this study was to analyze whether polyamine (PA) metabolism is involved in dark-induced Hordeum vulgare L. ‘Nagrad’ leaf senescence. In the cell, the titer of PAs is relatively constant and is carefully controlled. Senescence-dependent increases in the titer of the free PAs putrescine, spermidine, and spermine occurred when the process was induced, accompanied by the formation of putrescine conjugates. The addition of the anti-senescing agent cytokinin, which delays senescence, to dark-incubated leaves slowed the senescence-dependent PA accumulation. A feature of the senescence process was initial accumulation of PAs at the beginning of the process and their subsequent decrease during the later stages. Indeed, the process was accompanied by both enhanced expression of PA biosynthesis and catabolism genes and an increase in the activity of enzymes involved in the two metabolic pathways. To confirm whether the capacity of the plant to control senescence might be linked to PA, chlorophyll fluorescence parameters, and leaf nitrogen status in senescing barley leaves were measured after PA catabolism inhibition and exogenously applied γ-aminobutyric acid (GABA). The results obtained by blocking putrescine oxidation showed that the senescence process was accelerated. However, when the inhibitor was applied together with GABA, senescence continued without disruption. On the other hand, inhibition of spermidine and spermine oxidation delayed the process. It could be concluded that in dark-induced leaf senescence, the initial accumulation of PAs leads to facilitating their catabolism. Putrescine supports senescence through GABA production and spermidine/spermine supports senescence-dependent degradation processes, is verified by H2O2 generation.
Leaf senescence is a tightly regulated developmental or stress-induced process. It is accompanied by dramatic changes in cell metabolism and structure, eventually leading to the disintegration of chloroplasts, the breakdown of leaf proteins, internucleosomal fragmentation of nuclear DNA and ultimately cell death. In light of the global and intense reorganization of the senescing leaf transcriptome, measuring time-course gene expression patterns in this model is challenging due to the evident problems associated with selecting stable reference genes. We have used oligonucleotide microarray data to identify 181 genes with stable expression in the course of dark-induced senescence of barley leaf. From those genes, we selected 5 candidates and confirmed their invariant expression by both reverse transcription quantitative PCR and droplet digital PCR (ddPCR). We used the selected reference genes to normalize the level of the expression of the following senescence-responsive genes in ddPCR assays: SAG12, ICL, AGXT, CS and RbcS. We were thereby able to achieve a substantial reduction in the data variability. Although the use of reference genes is not considered mandatory in ddPCR assays, our results show that it is advisable in special cases, specifically those that involve the following conditions: i) a low number of repeats, ii) the detection of low-fold changes in gene expression or iii) series data comparisons (such as time-course experiments) in which large sample variation greatly affects the overall gene expression profile and biological interpretation of the data.
Programmed cell death (PCD) is a process that occurs throughout the life span of every plant life, from initial germination of the seed to the senescence of the plant. It is a normal physiological milestone during the plant's developmental process, but it can also be induced by external factors, including a variety of environmental stresses and as a response to pathogen infections. Changes in the morphology of the nucleus is one of the most noticeable during PCD but all the components of the plant cell (cytoplasm, cytoskeleton and organelles) are involved in this fascinating process. To date, relatively little is known about PCD in plants, but several factors, among which polyamines (PAs) and plant growth regulators, have been shown to play an important role in the initiation and regulation of the process. The role of PAs in plant PCD appears to be multifaceted acting in some instances as pro-survival molecules, whereas in others seem to be implicated in accelerating PCD. The molecular mechanism is still under study. Here we present some PCD plant models, focusing on the role of the enzyme responsible for PA conjugation to proteins: transglutaminase (TGase), an enzyme linked with the process of PCD also in some animal models. The role of PAs and plant TGase in the senescence and PCD in flowers, leaf and the self-incompatibility of pollen will be discussed and examined in depth.
We analysed the level of polyamines (PAs) bound to thylakoids and the level and activity of thylakoid transglutaminases throughout barley leaf senescence, retarded by kinetin. The level of PAs bound to thylakoids changed in senescing barley leaves: bound putrescine (PU) and spermidine (SD) increased throughout senescence, whereas bound spermine (SM) decreased. Kinetin diminished the increase in thylakoid-bound PU and SD and almost completely abolished the decrease of the bound SM. These data suggest different roles of PU/SD and SM in thylakoid degradation. Immunodetection of transglutaminases (TGase) in thylakoid fraction revealed three bands of 33, 58 and 78 kDa. During senescence the intensity of all bands increased and it was correlated with an increase in TGase activity. Kinetin down-regulated the accumulation of the 58- and 78-kDa TGases and the TGase activity. We postulate that formation of covalent bonds between PAs and proteins by TGase is involved in chloroplast senescence. The kinetin-mediated preservation of low TGase levels and activity throughout leaf senescence may represent an important component of the mechanism of kinetin action in the retardation of leaf senescence.
Leaf senescence is a terminal step in plant growth and development. Considerable information on processes and signals involved in this process has been obtained, although comparatively little is known about leaf senescence in monocotyledonous plants. In particular, little is known about players involved in leaf senescence imposed by a prolonged dark treatment. New information has now been unveiled on dark-induced leaf senescence in a monocot, barley. A close association has been found between ubiquitous polyamines, reactive oxygen species (ROS), and senescence of barley leaves during prolonged darkness. Although polyamines (putrescine, spermidine, and spermine) are absolutely essential for critical cellular functions, including regulation of nucleic acids and protein synthesis, macromolecular structural integrity, and signalling, a strong link between polyamines and dark-induced leaf senescence has been found using barley plant as a model of monocots. Interestingly, Arabidopsis polyamine back-conversion oxidase mutants deficient in the conversion of spermine to spermidine and/or spermidine to putrescine do not occur and have delayed entry into dark-induced leaf senescence. This review summarizes the recent molecular, physiological, and biochemical evidence implicating concurrently polyamines and ethylene in dark-induced leaf senescence and broadening our knowledge on the mechanistic events involved in this important plant death process.
The amounts of polyamines (PAs) bound to etioplast membranes varied during chloroplast development in cucumber cotyledons (Cucumis sativus L. cv. Racibór). Putrescine (PU) and spermidine (SD) levels increased in the early greening stage (6 h of light exposure) but decreased in the late greening stage (24 h) in the thylakoid‐enriched fraction. In the highly enriched PSIIα fraction, the trend of changes in the amount of bound PAs was different: levels of SD and spermine (SM) increased in the late stage. In both fractions, their levels were additionally increased by kinetin treatment. In the presence of exogenous protein transglutaminase (TGase) substrate (N′,N′‐dimethylcasein) and 5 mM Ca2+, kinetin initially caused a marked increase in thylakoid transglutaminase (ThylTGase) activity (6 h), followed by a decrease at the end of greening. The radiometric assay showed that PU and SM binding to thylakoid proteins was very low, while SD binding was seven to eight times higher. Kinetin increased SD conjugation in the early greening stage by about 36%. When chloroplast membranes were fully organized, ThylTGase activity decreased. In etioplast membranes and during the early greening stage, the 77‐kDa and 30‐kDa bands were mainly immunodetected with antibodies raised against the animal TGase, which were in general slightly stronger for kinetin‐treated than the control samples. At the end of greening, the level of 77‐kDa ThylTGase dramatically decreased. ThylTGase activity was found to be Ca2+ dependent. PAs conjugated via ThylTGase, in addition to the PAs bound by all possible types of linkage, could represent an important component of the mechanism of stimulation of etioplast‐to‐chloroplast transformation by kinetin.
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