Transcription factor MYB8 regulates iron deficiency stress response in Arabidopsis.

Iron (Fe) is a crucial microelement for humans, animals, and plants. Insufficient Fe levels in plants impede growth and diminish photosynthesis, thus decreasing crop production. Notably, approximately one-third of the soil worldwide is alkaline and prone to Fe deficiency. Therefore, understanding the mechanisms underlying Fe absorption and transportation in plants can enhance Fe bioavailability in crops. In this study, the role of the transcription factor MYB8 in plant response to Fe deficiency in Arabidopsis was investigated via reverse genetics. Phenotype analysis revealed that the functional deletion mutant of MYB8 gene exhibited sensitivity to Fe deficiency stress, as indicated by shorter root length, lower chlorophyll content, and Fe concentration. Conversely, MYB8 overexpression strain showed a tolerant phenotype. Furthermore, qRT-PCR identified possible downstream MYB8-regulated genes. Moreover, MYB8 regulated the expression of iron-regulated transporter 1 (IRT1) by binding to the MYB binding sites motif ('AACAAAC') in its promoter.

Anti-fibrotic effect of extracellular vesicles derived from tea leaves in hepatic stellate cells and liver fibrosis mice.

Background: Activation of hepatic stellate cells (HSCs) is essential for the pathogenesis of liver fibrosis, there is no effective drug used to prevent or reverse the fibrotic process. Methods: With human hepatic stellate cell line LX-2 and mouse model of CCl4-induced liver fibrosis, we investigated the anti-fibrotic effect to liver fibrosis of extracellular vesicles (EVs) extracted from tea leaves through cytological tests such as cell proliferation, cell migration, and cell fibrotic marker. Results: It was found that tea-derived EVs (TEVs) inhibited HSCs activation. In CCl4-induced liver fibrosis model, TEVs treatment can significantly improve the pathological changes of liver tissue, inhibit collagen deposition, reduce the number of lipid droplets in liver tissue, and reduce serum AST and ALT levels. In addition, TEVs inhibited TGF-ß1 signaling and miR-44 in TEVs had the potential inhibitory effect on liver fibrosis. Conclusions: Taken together, our work suggesting that TEVs are novel therapeutic potential for liver fibrosis.

Protein kinase PpCIPK1 modulates plant salt tolerance in Physcomitrella patens.

KEY MESSAGE: This work demonstrates that PpCIPK1, a putative protein kinase, participates in regulating plant salt tolerance in moss Physcomitrella patens. Calcineurin B-Like protein (CBL)-interacting protein kinases (CIPKs) have been reported to be involved in multiple signaling networks and function in plant growth and stress responses, however, their biological functions in non-seed plants have not been well characterized. In this study, we report that PpCIPK1, a putative protein kinase, participates in regulating plant salt tolerance in moss Physcomitrella patens (P. patens). Phylogenetic analysis revealed that PpCIPK1 shared high similarity with its homologs in higher plants. PpCIPK1 transcription level was induced upon salt stress in P. patens. Using homologous recombination, we constructed PpCIPK1 knockout mutant lines (PpCIPK1 KO). Salt sensitivity analysis showed that independent PpCIPK1 KO plants exhibited severe growth inhibition and developmental deficiency of gametophytes under salt stress condition compared to that of wild-type P. patens (WT). Consistently, ionic homeostasis was disrupted in plants due to PpCIPK1 deletion, and high level of H2O2 was accumulated in PpCIPK1 KO than that in WT. Furthermore, PpCIPK1 functions in regulating photosynthetic activity in response to salt stress. Interestingly, we observed that PpCIPK1 could completely rescue the salt-sensitive phenotype of sos2-1 to WT level in Arabidopsis, indicating that AtSOS2 and PpCIPK1 are functionally conserved. In conclusion, our work provides evidence that PpCIPK1 participates in salt tolerance regulation in P. patens.

MYB30 and ETHYLENE INSENSITIVE3 antagonistically modulate root hair growth in Arabidopsis.

Root hair (RH) is essential for plant nutrient acquisition and the plant-environment communication. Here we report that transcription factors MYB30 and ETHYLENE INSENSITIVE3 (EIN3) modulate RH growth/elongation in Arabidopsis in an antagonistic way. The MYB30 loss-of-function mutant displays enhanced RH length, whereas the RH elongation in MYB30-overexpressing plants is highly repressed. MYB30 physically interacts with EIN3, a master transcription factor in ethylene signaling. MYB30 directly binds the promoter region of ROOT HAIR DEFECTIVE SIX-LIKE4 (RSL4) and represses its transcription. RSL4 loss-of-function suppresses the enhanced RH growth in myb30 mutant plants. Ethylene enhances MYB30-EIN3 complex formation, and reduces the association between MYB30 and RSL4 promotor via the action of EIN3. MYB30 and EIN3 antagonistically regulate the expression of RSL4 and a subset of core RH genes in a genome-wide way. Taken together, our work revealed a novel transcriptional network that modulates RH growth in plants.

PpAOX regulates ER stress tolerance in Physcomitrella patens.

Severe environments disturb the folding or assembly of newly synthesized proteins, resulting in accumulation of misfolded or unfolded proteins in the endoplasmic reticulum (ER) as well as cytotoxic aggregation of abnormal proteins. Therefore, ER stress is evoked due to disturbed ER homeostasis. Alternative oxidase (AOX) plays an important role in coping with various abiotic stresses and plant growth. Our previous study has reported that PpAOX is involved in the regulation of salt tolerance in moss Physcomitrella patens (P. patens), but its biological functions in modulating ER stress remain unknown. Here we report that the gametophyte of P. patens displays severe growth inhibition and developmental deficiency under tunicamycin (Tm, an elicitor of ER stress)-induced ER stress conditions. PpAOX and selected ER stress response-like genes in P. patens were induced under Tm treatment. PpAOX knockout (PpAOX KO) plants exhibited decreased resistance to Tm-induced ER stress, whereas PpAOX-overexpressing lines (PpAOX OX) plants were more tolerant to Tm-induced ER stress. Data showed that PpAOX contributes to redox homeostasis under Tm treatment. In addition, we observed that PpAOX completely restores the Tm-sensitive phenotype of Arabidopsis AOX1a mutant (Ataox1a). Taken together, our work reveals a functional link between PpAOX and ER stress tolerance regulation in P. patens.

SUMOylation of MYB30 enhances salt tolerance by elevating alternative respiration via transcriptionally upregulating AOX1a in Arabidopsis.

Salt stress reduces crop growth and productivity globally. Here we report that a R2R3-MYB transcription factor MYB30 participates in salt tolerance in Arabidopsis. MYB30 can be SUMOylated by SIZ1 in response to salt stress and the lysine (K)283 of MYB30 is essential for its SUMOylation. In contrast to wild-type MYB30, the MYB30K283R mutant failed to rescue the salt-sensitive phenotype of the myb30-2 mutant, indicating that SUMOylation of MYB30 is required for the salt-stress response. Through transcriptomic analysis, we identified a MYB30 target, alternative oxidase 1a (AOX1a). MYB30 binds the promoter of AOX1a and upregulates its expression in response to salt stress; however, MYB30K283R cannot bind the promoter of AOX1a. The cyanide (CN)-resistant alternative respiration (Alt) mediated by AOX is significantly reduced in the myb30-2 mutant through the loss of function of MYB30. As a result, the redox homeostasis is disrupted in the myb30-2 mutant compared with that in wild-type seedlings (WT) under salt conditions. The artificial elimination of excess reactive oxygen species partially rescues the salt-sensitive phenotype of the myb30-2 mutant, whereas after the exogenous application of SHAM, an inhibitor of AOXs and Alt respiration, the salt tolerance of Col-0 and the complemented plants decreased to a level similar to that observed in myb30-2. Finally, overexpression of AOX1a in myb30-2 confers WT-like salt tolerance compared with that of the myb30-2 mutant. Taken together, our results revealed a functional link between MYB30 and AOX1a, and indicated that SIZ1-mediated SUMOylation of MYB30 enhances salt tolerance by regulating Alt respiration and cellular redox homeostasis via AOX1a in Arabidopsis.