Genetic Alterations of Light Control of Senescence

The information available on genetic controls of the regulation of senescence by light is very incomplete. Nonetheless, it provides a useful glimpse at what can be achieved through genetic probes of these light controls.

Due to the technical ease of screening for mutations to inhibit dark-induced leaf yellowing, several of these have been reported (Chapter 5). All of the stay-green mutations tested delay dark-induced leaf yellowing and sometimes other senescence processes (Thomas, 1987; Canfield et al, 1995). These observations do indicate that natural senescence and dark-induced senescence share some biochemistry even if they are not identical.

Given the usage of chloroplast parameters to measure leaf senescence, it is difficult to separate the effects of light on the amounts of the photosynthetic machinery from its effects on senescence per se. It is well known that light promotes chloroplast development including chlorophyll formation (Scheer, 1991), and therefore, all of these light effects would counter what we normally call senescence, but are they specifically antisenescence effects?

Some evidence (see Section VI above) shows that light may act through effects on the cytokinin, gibberellin and ethylene hormones. Genetic studies indicate that brassinosteroids may mediate some light effects (Chory and Li, 1997). Thus, it is significant that det-2, which blocks brassinosteroid synthesis, also inhibits leaf senescence. Exogenous applications indicate they do, in fact, promote senescence (Clouse and Sasse, 1998).

Engineering tobacco plants to overexpress PHYA inhibits leaf senescence (Cherry et al, 1991; Jordan et al, 1995), but overexpression of PHYB in potato (Thiele et al, 1999) has similar effects. The excess PHYA also counteracts the senescence-promoting effects of continuous FR (Rousseaux et al, 1997). Although these observations do not themselves produce a general explanation of how light controls senescence, it is clear that the use of mutants and genetically-engineered plants will enable the dissection of the roles of the different photoreceptors in the light control of senescence.

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