Transgenic Arabidopsis thaliana plants expressing a ß-1,3-glucanase from sweet sorghum (Sorghum bicolor†L.) show reduced callose deposition and increased tolerance to aluminium toxicity.

Seventy-one cultivars of sweet sorghum (Sorghum bicolor L.) were screened for aluminium (Al) tolerance by measuring relative root growth (RRG). Two contrasting cultivars, ROMA (Al tolerant) and POTCHETSTRM (Al sensitive), were selected to study shorter term responses to Al stress. POTCHETSTRM had higher callose synthase activity, lower ß-1,3-glucanase activity and more callose deposition in the root apices during Al treatment compared with ROMA. We monitored the expression of 12 genes involved in callose synthesis and degradation and found that one of these, SbGlu1 (Sb03g045630.1), which encodes a ß-1,3-glucanase enzyme, best explained the contrasting deposition of callose in ROMA and POTCHETSTRM during Al treatment. Full-length cDNAs of SbGlu1 was prepared from ROMA and POTCHETSTRM and expressed in Arabidopsis thaliana using the constitutive cauliflower mosaic virus (CaMV) 35S promoter. Independent transgenic lines displayed significantly greater Al tolerance than wild-type plants and vector-only controls. This phenotype was associated with greater total ß-1,3-glucanase activity, less Al accumulation and reduced callose deposition in the roots. These results suggest that callose production is not just an early indicator of Al stress in plants but likely to be part of the toxicity pathway that leads to the inhibition of root growth.

[Calcium involved in the signaling pathway of jasmonic acid induced stomatal closure of Vicia faba L].

Ca2+, an ubiquitous second messenger in the signal transudation pathway, is required for various physiological and developmental processes in plant. Jasmonic acid (JA) has been known to induce the stomatal closure. By monitoring the changes of [Ca2+]cyt with fluorescent probe Fluo-3 AM under the confocal microscopy, we observed that exogenous JA increased [Ca2+]cyt in guard cells of Vicia faba L. while the control and linolenic acid (LA), which is a precursor of JA, could hardly affect the change of [Ca2+]cyt. EGTA, a chelator of Ca2+ completely blocked JA-induced stomatal closure. After epidermis pretreated with EGTA, JA failed to result in [Ca2+]cyt increasing. Ruthenium red that blocked Ca2+ released from intracellular Ca2+ store could not significantly change JA-induced stomatal closure, while JA still increased [Ca2+]cyt. Furthermore, Ca2+ channel inhibitor of nifedipine (NIF) reduced the effectiveness of JA-induced stomatal closure and JA-induced increasing fluorescent intensity in guard cells. The results demonstrated that Ca2+ is involved in the signal transduction of JA induced stomatal closure, and the source of [Ca2+]cyt increasing in guard cells induced by JA might derive mainly from the external stores.