植物盐胁迫感知与信号转导

One of the strategies that plants adopt to cope with an unfavorable environment is to sacrifice their growth for tolerance. Although moderate salt stress can induce root growth inhibition, the molecular mechanisms regulating this process have yet to be elucidated. Here, we found that overexpression of a zinc finger-homeodomain family transcription factor, HOMEOBOX PROTEIN 24 (HB24), led to longer primary roots than in the wild-type in the presence of 125 mM NaCl, whereas this phenotype was reversed for the hb24 loss-of-function mutant, indicating a negative impact of HB24 on salt-induced root growth inhibition. We then found that salt stress triggered the degradation of HB24 via the ubiquitin–proteasome pathway, as mediated by a plant U-box type E3 ubiquitin ligase 30 (PUB30) that directly targets HB24. We verified that HB24 is able to directly bind to the promoters of Sugars Will Eventually be Exported Transporter 11/12 (SWEET11/12) to regulate their expression in roots. Through genetic and biochemical assays, we further demonstrated that the HB24-SWEET11 module plays a negative role in salt-induced root growth inhibition. Therefore, we propose that under salt stress, PUB30 mediates HB24′s degradation, thereby downregulating the expression of SWEET11, resulting in reduced sucrose supply and root growth inhibition.

Salt acclimation, which is induced by previous salt exposure, increases the resistance of plants to future exposure to salt stress. However, little is known about the underlying mechanism, particularly how plants store the “memory” of salt exposure. In this study, we established a system to study salt acclimation in Arabidopsis thaliana. Following treatment with a low concentration of salt, seedlings were allowed to recover to allow transitory salt responses to subside while maintaining the sustainable effects of salt acclimation. We performed transcriptome profiling analysis of these seedlings to identify genes related to salt acclimation memory. Notably, the expression of Basic-leucine zipper 17 (bZIP17) and Hmg-CoA reductase degradation 3A (HRD3A), which are important in the unfolded protein response (UPR) and endoplasmic reticulum-associated degradation (ERAD), respectively, increased following treatment with a low concentration of salt and remained at stably high levels after the stimulus was removed, a treatment which improved plant tolerance to future high-salinity challenge. Our findings suggest that the upregulated expression of important genes involved in the UPR and ERAD represents a “memory” of the history of salt exposure and enables more potent responses to future exposure to salt stress, providing new insights into the mechanisms underlying salt acclimation in plants.