Factors affecting expression of Les1 in leaves

Last year it was reported that light is a required factor for leaf lesion induction in Les1/Les1 plants (C. Echt, MNL 60:49). Through a series of light and temperature shift experiments the time-course, and the physiologically separable stages, of light-induced necrosis of Les1/Les1 leaf tissue now have been determined. The term 'light-induction' is defined as the process of exposing dark-adapted leaf tissue to light for a length of time sufficient to induce necrosis of that tissue in Les1/Les1 plants.

The time course of light-induced necrosis proceeds as follows (at 25 C): the first 2 hours of exposure to light represent a lag phase during which time induction can be reversed by returning the leaf section to the dark; the time from 2 to 6 hours after exposure is when an increasing proportion of the cells become irreversibly set to die; necrosis occurs over a period of time from 8 to 20 hours after exposure. The observed family-to-family variability in the timing of the various stages is presumably due to segregation of unidentified loci that modify Les1 expression.

The three stages of light-induced necrosis that have been determined so far are (1) development of lesion-forming potential in the maturing leaf, (2) induction, and (3) necrosis. Each of these stages has a different light and temperature requirement. Lesion-forming potential is independent of light and temperature and appears to be determined solely by the age of the leaf. Induction generally requires light and has a temperature optimum of around 25 C. Temperatures between 30 C and 35 C during the induction period decrease the necrosis response by 90-95%. Necrosis is independent of light and is inhibited by temperatures over 30 C.

An "action spectrum" of light-induction was determined with the use of monochromatic light filters obtained from Carolina Biological Supply Co. White light is most efficient for induction. Induction did not occur with blue light (350-550 nm, peak at 450) and was reduced by about 90% with red light (550-750 nm, peak at 650). Far-red light (650-750+ nm, max. at >750 nm) does not inhibit the induction response elicited by white or red light. It thus appears that light induces lesion formation by a general stimulation of photosynthetic activity. The active photosynthetic product(s) must be translocatable, however, because lesions can form within sectors of white leaf tissue bordered by green tissue (Hoisington, MNL 60:57) and, on occasion, within dark-adapted leaf sections prior to exposure to light (C. Echt, MNL 60:49).

Several experiments suggest that translational and transcriptional events may be involved in lesion formation. It was found that cycloheximide (50-200 µM) is effective at inhibiting light-induced necrosis when administered through cut leaf tips for 2 hours prior to, and during, a 7 hour light-induction period. Light-induced necrosis is also prevented when a 6 hour light exposure at 25 C is preceded by a 4 hour light exposure under heat shock conditions (42 C, 100% R.H.). In contrast, necrosis proceeds normally when a 6 hour exposure at 25 C is preceded by a 4 hour exposure at 30 C.

These observations are consistent with the hypothesis that a translocatable photosynthetic metabolite is involved in the induction of the Les1 phenotype and that the expression of Les1 may require the activation of a specific gene or genes.

Craig Echt
 
 


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