Senescence in plants is usually viewed as an intemally programmed degeneration 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 major groupings, nutrient deficiencies (e.g., starvation) and genetic programming (i.e., senescence-promoting and senescence-inhibiting genes). Considerable evidence indicates that nutrient deficiencies are not central senescence program components, while increasing evidence supports genetic programming. Because chlorophyll (Chi) and chloroplast (CP) breakdown are so prominent, leaf senescence is generally measured in terms of Chi loss. Although CP breakdown may not be the proximate cause of leaf cell death, it certainly is important as a source of nutrients for use elsewhere, e.g., for developing reproductive structures in monocarpic plants, and this loss limits assimilatory capacity. The CP is dismantled in an orderly sequence. Individual protein complexes seem to be taken out all at once, not one subunit at a time. Removal of any component, e.g., Chi, seems to destabilize the whole complex. It is of special interest that senescing CPs secrete Chl-containing globules indicating that some CP components are broken down outside the CP. Senescence appears to be imposed on the CP by the nucleus, and all the known senescencealtering genes except one, cytG in soybean, are nuclear. Only the djd2 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 death, and this suggests that proteases play a key role.

SummaryTo determine the role of ethylene during tomato (Lycopersicon esculentum Mill. cv. Ailsa Craig} leaf senescence, transgenic ACC oxidase antisense plants were analysed. Northern analysis of wild-type plants indicated that ACC oxidase mRNA accumulation normally begins in pre-senescent green leaves but was severely reduced in the antisense plants. Although the levels of ethylene evolved by wild-type and transgenic leaves increased during the progression of senescence, levels were extremely low in transgenic leaves. Leaf senescence, as assessed by colour change from green to yellow, was clearly delayed by 10-14 days in the antisense plants when compared with wild-type plants. Northern analysis of the photosynthesis-associated genes, cab and rbcS, indicated that levels of the corresponding mRNAs were higher in transgenic leaves which were not yet senescing compared with senescing wild-type leaves of exactly the same age. Northern analysis using probes for tomato fruit ripening-related genes expressed during leaf senescence indicated that once senescence was initiated the expression pattern of these mRNAs was similar in transgenic and wildtype leaves. In the anticense plants chlorophyll levels, photosynthetic capacity and chlorophyll fluorescence were higher when compared with senescing wild-type plants of the same age. Photosynthetic capacity and the quantum efficiency of photosystem II were maintained for longer in the transformed plants at values close to those observed in wild-type leaves prior to the visible onset of senescence. These results indicate that inhibiting ACC oxidase expression and ethylene synthesis results in delayed leaf senes- cence, rather then inducing a stay-green phenotype. Once senescence begins, it progresses normally. Onset of senescence is not, therefore, related to a critical level of ethylene. The correlation between higher levels prior to senescence and early onset, however, suggests that ethylene experienced by the plant may be a significant contributing factor in the timing of senescence.

Senescence in plants is usually viewed as an internally programmed degeneration 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 major groupings, nutrient deficiencies (e.g., starvation) and genetic programming (i.e., senescence‐promoting and senescence‐inhibiting genes). Considerable evidence indicates that nutrient deficiencies are not central senescence program components, while increasing evidence supports genetic programming. Because chlorophyll (Chl) and chloroplast (CP) breakdown are so prominent, leaf senescence is generally measured in terms of Chl loss. Although CP breakdown may not be the proximate cause of leaf cell death, it certainly is important as a source of nutrients for use elsewhere, e.g., for developing reproductive structures in monocarpic plants, and this loss limits assimilatory capacity. The CP is dismantled in an orderly sequence. Individual protein complexes seem to be taken out all at once, not one subunit at a time. Removal of any component, e.g., Chl, seems to destabilize the whole complex. It is of special interest that senescing CPs secrete Chl‐containing globules indicating that some CP components are broken down outside the CP. Senescence appears to be imposed on the CP by the nucleus, and all the known senescence‐altering genes except one, cytG in soybean, are nuclear. Only the d1d2 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 death, and this suggests that proteases play a key role.

Several cDNAs for mRNAs that change in abundance during tomato leaf senescence were isolated. In this paper we report molecular cloning and expression analysis of two cysteine proteases. SENU2 is identical to the cDNA C14 which encodes a cysteine protease previously shown to be expressed in response to extremes of temperature in tomato fruit [43]. SENU3 cDNA clone was 1.2 kb in length and hybridized to a transcript of 1.4 kb which suggested that the clone was not full-length. The missing 5' end was isolated using rapid amplification of cDNA ends (RACE). Southern blot analysis of tomato genomic DNA indicates that SENU3 is encoded by a single or low copy gene. SENU3 was also shown to have significant homology with known cysteine proteases. These two senescence-associated cysteine proteases are also expressed during other developmental processes, including seed germination, consistent with a role in protein turnover. SENU2 and SENU3 mRNAs were detectable in young fully expanded leaves and increased in abundance with leaf age, reaching a maximum during the later stages of visible leaf senescence. Such a pattern of expression suggests that the onset of leaf senescence is a gradual event. Analysis of senescence in transgenic plants deficient in ethylene biosynthesis, in which leaf senescence is delayed, indicated that enhanced accumulation of SENU2 and SENU3 mRNA was similarly delayed but not prevented.

A near full-length cDNA clone (pZRP3) corresponding to an mRNA that accumulates specifically in roots of maize was isolated. The ZRP3 mRNA is ca. 600 nucleotides in length. The amino acid sequence of the predicted polypeptide is rich in leucine (16%), proline (11%), and cysteine (8.5%). The zrp3 gene appears to be expressed exclusively in roots, whereas other ZRP3-related genes are expressed in additional organs of the maize plant. In situ hybridization shows that ZRP3 mRNA accumulation is largely confined to the cells of the cortical ground meristem. Furthermore, accumulation of this mRNA occurs within a distinct subset of cortical cells, the inner three to four cell layers.