Senescence Programmed Death

It is easy to understand why plants die when they are eaten, trampled or run out of water. It is not as easy to understand why plants die naturally, unthreatened by external forces at the end of their life cycle. 'Senescence' is the programmed process of deterioration that leads to the natural death of a plant (or plant part). It is an internally controlled process that determines the life span of a whole organism or its parts. Knowledge of when and why a weed senesces has implications for weed management. Here, we discuss whole plant senescence. For reviews of the mechanisms of leaf senescence, see Nooden et al. (1997) and Chandlee (2001).

We do not always know the cause of senescence (Crawley, 1997). It may be due to the accumulation of deleterious mutations, or it may be that the soil becomes unsuitable when trace nutrients are depleted or when allelopathic chemicals accumulate. Alternatively, senescence may be caused by the negative affects of earlier life stages. For example, a high allocation of resources to early reproduction may inevitably lead to senescence because not enough has been allocated to the maintenance of structures. The mechanisms of senescence may differ between monocarpic and polycarpic species.

Senescence in monocarpic species

Wilson (1997) reviewed several hypothesized mechanisms for senescence of monocarpic species. The 'death hormone' hypothesis suggests that the rapid death (plant suicide) of monocarpic plants is pre-programmed and likely hormonally controlled. Most biological evidence supports this hypothesis, although the actual mechanisms are not clear. The alternative hypothesis to the 'death hormone' is that senescence in monocarps is caused by nutrient starvation following flowering. Here it is suggested that the act of reproduction diverts stored photosynthate away from vegetative tissue, causing it to die. For example, senescence is delayed in the annual weed and crop (used in traditional medicine to treat malaria) beggar's tick (Bidens pilosa) when flowers are removed (Zobolo and van Staden, 1999). Wilson (1997) points out that, while this may occur in some species, the biological evidence does not generally support this alternative hypothesis. Among other reasons, he cites:

• leaves do not generally exhibit nutrient deficiency before death nor are reduced minerals evident in leaf tissue;

• the addition of nutrients does not delay senescence;

• senescence is rapid rather than prolonged which is typical of nutrient deficiency;

• other triggers such as long days have been identified as necessary for senescence to occur.

Senescence in polycarpic species

The death of polycarpic perennials is somewhat harder to explain, partly because it is difficult to separate the effects of age and size. As a plant (say a tree) gets larger, it begins to decline physiologically because it has more respiratory tissue to support, it must transport water and nutrients further, and it is more susceptible to herbivores and pathogens (Watkinson, 1992). Thus the effects of size are similar to those of age; however, they do not fully explain senescence of old plants. Senescence of woody plants could be caused by the collapse of structural tissue, but this does not explain why some woody plants that regenerate from dormant meristems (e.g. when a tree resprouts from its base after being cut) often senesce after temporary regrowth (Watkinson, 1992). Alternatively, toxins accumulating in cells may lead to senes cence. The two evolutionary mechanisms explaining senescence in long-lived plants are (Orive, 1995; Pedersen, 1995):

• deleterious mutations accumulate over time and eventually become lethal to the individual;

• genes that increase fitness early in the life cycle may decrease fitness later on (antagonistic pleiotropy).

The senescence of clonal organisms (i.e. the entire clone) is even harder to explain. Some clonal plants appear to have escaped senescence altogether, by evidence of their extremely old age. In other cases, an entire clone can senesce at the same time (Watkinson, 1992).

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