Leaf senescence induced by mild water deficit follows the same sequence of macroscopic, biochemical, and molecular events as monocarpic senescence in pea

被引:85
作者
Pic, E
de la Serve, BT
Tardieu, F
Turc, O
机构
[1] Univ Montpellier 2, Ecole Natl Super Agron Montpellier, CNRS,INRA, Lab Biochim & Physiol Mol Plantes,UMR 5004, F-34060 Montpellier 1, France
[2] Univ Montpellier 2, Ecole Natl Super Agron Montpellier, Lab Ecophysiol Plantes Stress Environm, INRA,UMR, F-34060 Montpellier, France
关键词
D O I
10.1104/pp.010634
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
We have compared the time course of leaf senescence in pea (Pisum sativum L. cv Messire) plants subjected to a mild water deficit to that of monocarpic senescence in leaves of three different ages in well-watered plants and to that of plants in which leaf senescence was delayed by flower excision. The mild water deficit (with photosynthesis rate maintained at appreciable levels) sped up senescence by 15 d (200degreesCd), whereas flower excision delayed it by 17 d (270degreesCd) compared with leaves of the same age in well-watered plants. The range of life spans in leaves of different ages in control plants was 25 d (340degreesCd). In all cases, the first detected event was an increase in the mRNA encoding a cysteine-proteinase homologous to Arabidopsis SAG2. This happened while the photosynthesis rate and the chlorophyll and protein contents were still high. The 2-fold variability in life span of the studied leaves was closely linked to the duration from leaf unfolding to the beginning of accumulation of this mRNA. In contrast, the duration of the subsequent phases was essentially conserved in all studied cases, except in plants with excised flowers, where the degradation processes were slower. These results suggest that senescence in water-deficient plants was triggered by an early signal occurring while leaf photosynthesis was still active, followed by a program similar to that of monocarpic senescence. They also suggest that reproductive development plays a crucial role in the triggering of senescence.
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页码:236 / 246
页数:11
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