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• W1567227627 abstract "Senescence is a ubiquitous developmental process that leads to the death of a cell, an organ, or an organism and occurs at the final stage of their development. There is a striking divergence and convergence between plants and animals regarding senescence regulation (Kenyon, 2001). The mechanisms of regulation of ageing in animals including p53, telomerase and telomere dynamics, DNA damage sensing and repair, and transcriptional activation and inactivation by histone acetylation/deacetylation are either not present or do not appear to play an important role in plant ageing. On the contrary, plants have evolved their own unique senescence-regulating mechanisms. These include the modulation of senescence by phytohormones, photosynthetic machinery, and protein degradation. In plants, the chloroplast is reported to be the first origin and target for initiating senescence (Misra and Biswal, 1980, 1981; 1982a, b, c, Biswal et al., 2001; Dilnawaz et al. 2001; Misra et al. 2011a), whereas in animals the mitochondrion serves as the initiator (Thomas, 2002). Thus, we may infer that plants and animals have evolved conserved strategies for the regulation of senescence, while employing diverse molecular mechanisms that have been shaped during the long history of evolution. Senescence is a genetically-controlled developmental programme, but it has no adaptive advantages in animals, except that in plants leaf senescence is a recruited nutrient recycle programme and hence is considered to have a strong adaptive advantage (Bleecker, 1998). This is the final developmental phase of a leaf which starts with nutrient salvage and ends with cell death. However, until late in senescence the process requires cell viability and is often reversible (Thomas et al., 2003). There has been some debate about the degree of overlap of senescence and PCD (Thomas et al., 2003; van Doorn & Woltering, 2004, 2008). van Doorn & Woltering (2004, 2008) identified three positions regarding the overlap in senescence and PCD. Some authors assumed total overlap (Nooden, 2004), but van Doorn & Woltering (2004, 2008) postulated that overlap is complete and senescence and PCD are synchronous. However a minority, argued that there was no overlap (Delorme et al., 2000; Thomas et al., 2003). van Doorn & Woltering (2008)" @default.
• W1567227627 created "2016-06-24" @default.
• W1567227627 creator A5015156253 @default.
• W1567227627 creator A5062454871 @default.
• W1567227627 creator A5077894727 @default.
• W1567227627 date "2012-02-17" @default.
• W1567227627 modified "2023-09-27" @default.
• W1567227627 title "Nitric Oxide Signaling During Senescence and Programmed Cell Death in Leaves" @default.
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