Monocarpic senescence is the degeneration leading to death of the whole plant at the end of the reproductive phase in monocarpic plants. As a prerequisite to or as a part of monocarpic senescence, vegetative growth ceases, so the plant can no longer regenerate its assimila-tory structures. Eventually, the existing leaves and other parts senesce, and the plant dies (Nooden, 1988b). The mutations that make plants live longer do so mainly by extending their regenerative ability (Nooden and Penney, 2001). The shift to clonal growth is also an example of life-extending growth.
Whereas genes in the above categories are expressed mainly at the cell and organ level, this group is expressed more at the organ and whole plant levels. Given the important role of correlative controls in whole plant senescence, it is expected that factors that alter those controls likewise influence monocarpic senescence. In many monocarpic plants, the reproductive structures, especially the fruits, control monocarpic senescence and the longevity of the plants (Nooden, 1988b; Nooden and Penney, 2001). This enables the plant to maximize its reproductive output. The older genetics literature contains numerous examples of changes in environmental control of reproductive development with consequences for monocarpic senescence. For example, alteration of a single gene can remove the vernalization requirement in sugar beet and allow reproductive development to proceed without passing through a winter thereby changing the plant from a biennial to an annual (Whaley, 1965). Changing the photoperiod requirement for flowering and fruit development can cause similar alterations of senescence and longevity.
Other mutations seem to affect growth apical meristem activity more directly. One interesting case is the dominant gene combination Sn Hr which makes pea shoot apex senescence dependent on long days (Zhu and Davies, 1997). The result is cessation of vegetative growth and leaf production, locking the plant into monocarpic senescence (Nooden, 1988b; Chapter 15).
Sterility mutations may also delay leaf and whole plant senescence by preventing fruit development, especially in soybean (Nooden, 1988b). Interestingly, sterility mutants in Arabidopsis also prolong the life of a plant but not individual leaves (Hensel etal., 1993; Nooden and Penney, 2001). In Arabidopsis, they act by prolonging growth and the production of new leaves which keeps the plant alive.
Other mutations such as the clavata types act more directly on the apical meristem to prolong leaf production and the life of the plant (Nooden and Penney, 2001). Thus, maintaining regenerative capacity is crucial to maintaining the life of the whole plant.
KN1 is an Arabidopsis gene encoding a homeobox-containing transcriptional factor and is preferentially expressed in the shoot meristem. Loss of function mutation in the KN1 gene shows that the KN1 is essential for meristem maintenance and/or initiation. In addition, phenotypes of plants overexpressing KN1 suggested that the gene is required for maintaining cellular indeterminacy and preventing cellular differentiation (Hake et al., 1995). The transgenic lines overexpressing KN1 under the control of the SAG12 promoter showed delayed leaf senescence. The authors suggested that KN1 is a natural negative regulator of senescence. Since the result was based on overexpression of KN1, it is important to check it with a loss of function mutation or with transgenic plants that specifically lower expression of KN1 on senescence. The authors presented an interesting hypothesis that KN1 may act on senescence and meristems by similar mechanisms, blocking cellular differentiation or blocking developmental progression. This explanation may be in accordance with the general perception that senescence starts after maturation of an organ and KN1 may delay the maturation and thus delay senescence, whether through overproduction of cytokinin and/or through direct regulation of down stream genes involved in senescence.
In many animal tissues, the telomeres shorten as mitosis proceeds and eventually cause cell division to cease or even trigger cell death; however, this does not seem to occur in plant cells (Shippen and McKnight, 1998), which seem to be endowed with more open ended growth potential. Nonetheless, an additional protein was associated via protein-protein interaction with the telomere-protein complex during the onset of senescence (Zentgraf et al., 2000).
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