Genetic programming of senescence

This article is under construction

One of the landmarks in the application of genetic approaches to the analysis of plant senescence was the SEB Symposium entitled Aspects of the biology of ageing, held at Sheffield University, UK in 1966 (Woolhouse 1967). The idea of senescence as a programmed process was in the air in both the animal and plant research communities, although the molecular tools to establish the nature of the program had yet to be established. The first use of mutants and genetic variants for functionally dissecting the senescence syndrome was reported in the 1970s (Thomas and Stoddart 1975, Abu-Shakra et al. 1978, Thomas and Smart 1993) and studies with inhibitors of translation and transcription at around the same time (Thomas and Stoddart 1981) allowed the concept of a senescence program to be defined and differentiated from deteriorative processes such as ageing, necrosis and morbidity. Before libraries of senescence-associated genes and omic-type profiling of gene expression became available from the 1990s, the program needed physiological and biochemical characterisation to identify the genes likely to contribute to the execution phase of the program. Since photosynthesis was the best-understood metabolic process in green tissues, and its decline diagnostic of senescence both in compositional and functional terms (Makino et al. 1984, Hensel et al. 1993) the down-regulation of genes such as those for the CO₂-fixing enzyme rubisco was the subject of some of the earliest molecular studies of the senescence program (Imai et al. 2008). Differential cDNA screening revealed a comparatively large number of up- and down-regulated genes, many of which had no known function or could not be fitted in to the known biochemistry of senescence (Smart 1993, Buchanan-Wollaston 1997).

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