Effect of Ca deficiency on growth and leaf acid soluble proteins of tomato.

摘要

The effects of temporary Ca (Ca) deficiency lasting 2, 3, 4, or 5 days were investigated on tomato plants at the 6-leaf stage, grown hydroponically under controlled conditions. With 2, 3, or 4 days of Ca deficiency, the dry weight of the tomato leaves, shoots, or roots was not different from control. A significant decrease in tomato growth, of up to 70%, appeared on the fifth day. Some visual symptoms were observed on the tomato leaves. The phenomenon of concern was an irreversible mechanism that led to plant death after 12 days, even when Ca was added to the root medium after 2, 3, 4, or 5 days. This is the first report of such a rapid and drastic effect of an essential macronutrient. Moreover, Ca content in leaves during root deprivation showed a decrease in all plants, related to a remobilization toward the apex. Ca could also be considered as a partly mobile element: the observation of the youngest leaf limbs by transmission electronic microscopy after 4 d of treatment showed disorganized tissues in a necrotic zone, due to wall impairment related to Ca deficiency. During temporary Ca deficiency, acid soluble proteins were analyzed in leaves (SDS PAGE electrophoresis/Maldi-TOF). After 4 d of Ca deficiency, protein induction in young leaves was revealed. Three proteins were identified as pathogenesis related proteins (PR-1, PR-3, and PR-7) and a threonine deaminase precursor was also found. It was also the first time that pathogenesis related (PR) protein appearance has been shown to be related to Ca deficiency. The PR proteins are generally elicited by pathogen attack. This phenomenon seems to be Ca dependent because other mineral stresses, such as potassium (K) deficiency or sodium (Na) excess, did not reveal acid soluble protein changes. The retranslocation of Ca to young tissue could entail eliciting effects via wall fragments leading to a plant response similar to the response to pathogen attack. Consequently, activation by Ca deficiency of gene transcription coding for defense proteins could be hypothesized..