No abstract

Although the results of some studies indicate that salt stress affects the organization of microtubules, it remains an open question whether microtubules play an active role in the plant's ability to withstand salt stress. In the present study, we showed that salt stress-induced wild-type Arabidopsis seedling roots display right-handed skewed growth and depolymerization of the cortical microtubules. The results of a long-term observational study showed that cortical microtubules depolymerized then reorganized themselves under salt stress. Stabilization of microtubules with paclitaxel resulted in more seedling death under salt stress, while disruption of microtubules with oryzalin or propyzamide rescued seedlings from death. Seedlings in which the cortical microtubules were reorganized did not succumb to salt stress. These results suggest that both depolymerization and reorganization of the cortical microtubules are important for the plant's ability to withstand salt stress. Depolymerizing microtubules by drugs rescues seedlings from death under salt stress. This rescue effect was abolished by removing calcium from the medium or treatment with a calcium channel inhibitor. Depolymerization of the microtubules is followed by an increase in the free cytoplasmic calcium concentration. The addition of calcium to the growth medium increased the number of seedlings in which recovery of the cortical microtubules occurred, whereas the removal of calcium decreased the number of seedlings in which recovery occurred. Therefore, depolymerization of the cortical microtubules raises intracellular calcium concentrations, while reorganization of the cortical microtubules and seedling survival may be mediated by calcium influx in salt stress.

Microtubule-associated proteins (MAPs) play important roles in the regulation of microtubule function in cells. We describe Arabidopsis thaliana MAP18, which binds to microtubules and inhibits tubulin polymerization in vitro and colocalizes along cortical microtubules as patches of dot-like structures. MAP18 is expressed mostly in the expanding cells. Cells overexpressing MAP18 in Arabidopsis exhibit various growth phenotypes with loss of polarity. Cortical microtubule arrays were significantly altered in cells either overexpressing MAP18 or where it had been downregulated by RNA interference (RNAi). The cortical microtubules were more sensitive to treatment with microtubule-disrupting drugs when MAP18 was overexpressed, but more resistant when MAP18 was eliminated in cells expressing MAP18 RNAi. Our study demonstrated that MAP18 may play a role in regulating directional cell growth and cortical microtubule organization by destabilizing microtubules.

No abstract

Sucrose transporters (SUCs or SUTs) play a central role, as they orchestrate sucrose allocation both intracellularly and at the whole plant level. Previously, we found AtSUC4 mutants changing sucrose distribution under drought and salt stresses. Here, we systematically examined the role of Arabidopsis AtSUC2 and AtSUC4 in response to abiotic stress. The results showed significant induction of AtSUC2 and AtSUC4 in salt, osmotic, low temperature and exogenous abscisic acid (ABA) treatments by public microarray data and real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR) analyses. The loss-of-function mutation of AtSUC2 and AtSUC4 led to hypersensitive responses to abiotic stress and ABA treatment in seed germination and seedling growth. These mutants also showed higher sucrose content in shoots and lower sucrose content in roots, as compared with that in wild-type plants, and inhibited the ABA-induced expression of many stress- and ABA-responsive genes, especially ABFs and ABF-downstream and upstream genes. The loss-of-function mutant of AtSUC3, a unique putative sucrose sensor, reduced the expression of AtSUC2 and AtSUC4 in response to abiotic stresses and ABA. These findings confirmed that AtSUC2 and AtSUC4 are important regulators in plant abiotic stress tolerance that use an ABA signaling pathway, which may be crossed with sucrose signaling.