Format

Send to

Choose Destination
Plant Physiol. 2003 Feb;131(2):568-82.

Comparative transcriptional profiling of placenta and endosperm in developing maize kernels in response to water deficit.

Author information

1
Department of Crop and Soil Sciences, Cornell University, Ithaca, New York 14853, USA.

Erratum in

  • Plant Physiol. 2003 Apr;131(4):1921-2.

Abstract

The early post-pollination phase of maize (Zea mays) development is particularly sensitive to water deficit stress. Using cDNA microarray, we studied transcriptional profiles of endosperm and placenta/pedicel tissues in developing maize kernels under water stress. At 9 d after pollination (DAP), placenta/pedicel and endosperm differed considerably in their transcriptional responses. In placenta/pedicel, 79 genes were significantly affected by stress and of these 89% were up-regulated, whereas in endosperm, 56 genes were significantly affected and 82% of these were down-regulated. Only nine of the stress-regulated genes were in common between these tissues. Hierarchical cluster analysis indicated that different sets of genes were regulated in the two tissues. After rewatering at 9 DAP, profiles at 12 DAP suggested that two regulons exist, one for genes responding specifically to concurrent imposition of stress, and another for genes remaining affected after transient stress. In placenta, genes encoding recognized stress tolerance proteins, including heat shock proteins, chaperonins, and major intrinsic proteins, were the largest class of genes regulated, all of which were up-regulated. In contrast, in endosperm, genes in the cell division and growth category represented a large class of down-regulated genes. Several cell wall-degrading enzymes were expressed at lower levels than in controls, suggesting that stress delayed normal advance to programmed cell death in the central endosperm. We suggest that the responsiveness of placenta to whole-plant stress factors (water potential, abscisic acid, and sugar flux) and of endosperm to indirect factors may play key roles in determining the threshold for kernel abortion.

PMID:
12586881
PMCID:
PMC166833
DOI:
10.1104/pp.014365
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for HighWire Icon for PubMed Central
Loading ...
Support Center