SENESCENCE MECHANISMS

Senescence in plants is usually viewed as an internally programmed deg eneration leading to death. It is a developmental process that occurs in many different tissues :; and serves different purposes. Generally, apoptosis refers to programmed death of small numbers of animal cells , and it shows some special features at the cell level. Some senescing plant cells show some symptoms typical of apoptosis, while others do not. This review will focus primarily on leaf senescence with ultimate aim of explaining whole plant senescence (i.e., monocarpic senescence ). Traditionally, the ideas on senescence mechanisms fall into two maj or groupings, nutrient deficiencies (e.g., starvation) and genetic pro gramming (i.e., senescence-promoting and senescence-inhibiting genes). Considerable evidence indicates that nutrient deficiencies are not ce ntral senescence program components, while increasing evidence support s genetic programming. Because chlorophyll (Chi) and chloroplast (CP) breakdown are so prominent, leaf senescence is generally measured in t erms of Chi loss. Although CP breakdown may not be the proximate cause of leaf cell death, it certainly is important as a source of nutrient s for use elsewhere, e.g., for developing reproductive structures in m onocarpic plants, and this loss limits assimilatory capacity. The CP i s dismantled in an orderly sequence. Individual protein complexes seem to be taken out all at once, not one subunit at a time. Removal of an y component, e.g., Chi, seems to destabilize the whole complex. It is of special interest that senescing CPs secrete Chi-containing globules indicating that some CP components are broken down outside the CP. Se nescence appears to be imposed on the CP by the nucleus, and all the k nown senescence-altering genes except one, cytG in soybean, are nuclea r. Only the d(1)d(2) mutation(s) in soybean prevents a broad range of leaf senescence processes. Exactly, what causes cell death is unclear; however, the selective thiol protease inhibitor, E-64, does delay dea th, and this suggests that proteases play a key role.