Abstract
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.
Highlights
In plants and animals, developmental and growth processes require selective elimination of either single cells or groups of cells
We have studied the process of senescence of barley leaves using a dark-induction model that we routinely use in our research (Legocka and Zajchert, 1999; Sobieszczuk-Nowicka et al, 2009, 2015)
Our recent observations regarding symptoms of chlorophyll loss in senescing leaves, decomposition of chloroplasts, internucleosomal fragmentation of chromatin, condensation of nuclear DNA and the disruption of the nucleus indicate that dark-induced leaf senescence engages programmed cell death (PCD) mechanisms (Zmienko et al, 2015a)
Summary
Developmental and growth processes require selective elimination of either single cells or groups of cells. This process, termed PCD, is actively controlled by the organism. PCD may involve the elimination of an entire organ; e.g., a leaf that for many reasons no longer has a useful role When senescence occurs, it is not a steady state but a gradual evolution of the entire cell, even though it can sometimes be delayed or reversed, preceding cell death (Cai et al, 2015). The addition of SD or SM inhibited protein degradation and chlorophyll loss, and stabilized thylakoid proteins such as D1, D2, cyt f and the large subunit of RuBisCO (Besford et al, 1993; Legocka and Zajchert, 1999; Serafini-Fracassini et al, 2010)
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