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Ann Bot. 2010 Sep;106(3):395-403. doi: 10.1093/aob/mcq132. Epub 2010 Jul 8.

Sucrose feeding reverses shade-induced kernel losses in maize.

Author information

1
College of Marine Studies and College of Agriculture and Natural Resources, University of Delaware, 700 Pilottown Road, Lewes, DE 19958, USA.

Abstract

BACKGROUND AND AIMS:

Water limitations can inhibit photosynthesis and change gene expression in ways that diminish or prevent reproductive development in plants. Sucrose fed to the plants can reverse the effects. To test whether the reversal acts generally by replacing the losses from photosynthesis, sucrose was fed to the stems of shaded maize plants (Zea mays) during reproductive development.

METHODS:

Shading was adjusted to mimic the inhibition of photosynthesis around the time of pollination in water-limited plants. Glucose and starch were imaged and quantified in the female florets. Sucrose was infused into the stems to vary the sugar flux to the ovaries.

KEY RESULTS:

Ovaries normally grew rapidly and contained large amounts of glucose and starch, with a glucose gradient favouring glucose movement into the developing ovary. Shade inhibited photosynthesis and diminished ovary and kernel size, weight, and glucose and starch contents compared with controls. The glucose gradient became small. Sucrose fed to the stem reversed these losses, and kernels were as large as the controls.

CONCLUSIONS:

Despite similar inhibition of photosynthesis, the depletion of ovary glucose and starch was not as severe in shade as during a comparable water deficit. Ovary abortion prevalent during water deficits did not occur in the shade. It is suggested that this difference may have been caused by more translocation in shade than during the water deficit, which prevented low sugar contents necessary to trigger an up-regulation of senescence genes known to be involved in abortion. Nevertheless, sucrose feeding reversed kernel size losses and it is concluded that feeding acted generally to replace diminished photosynthetic activity.

PMID:
20616114
PMCID:
PMC2924829
DOI:
10.1093/aob/mcq132
[Indexed for MEDLINE]
Free PMC Article

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