Search

The WRKY transcription factors (TFs) play multifaceted roles in plant growth, development, and stress response. Previously, we found that SlWRKY81 negatively regulates tomato tolerance to drought; however, the mechanisms of stomatal regulation in response to drought remain largely unclear. Here, we showed that droughtinduced upregulation in the SlWRKY81 transcripts induced photoinhibition and reduced the net photosynthetic rate in tomato leaves. However, silencing SlWRKY81 alleviated those inhibitions and minimized the drought-induced damage. A timecourse of water loss showed that SlWRKY81 silencing significantly and consistently reduced leaf water loss, suggesting a role for SlWRKY81 in stomatal movement. Further analysis using light microscopy revealed that SlWRKY81 silencing significantly decreased stomatal aperture and increased the ratio of length to width of stomata under drought. Both biochemical assay and confocal laser scanning microscopy demonstrated that drought-induced upregulation in SlWRKY81 expression inhibited the nitric oxide (NO) accumulation in the guard cells, which was attributed to the simultaneous declines in the activity of nitrate reductase (NR) and NR expression in tomato leaves. The inspection of 3-kb sequences upstream of the predicted transcriptional start site of the NR identified three copies of the core W-box (TTGACC/T) sequence in the promoter region, indicating possible targets of SlWRKY81. Taken together, these data suggest that SlWRKY81 potentially represses NR transcription and thus reduces NO accumulation to attenuate stomatal closure and subsequent drought tolerance. These findings provide an improved understanding of the mechanism of WRKY-induced regulation of stomatal closure, which can be exploited in the future to enhance drought tolerance in crops. [ABSTRACT FROM AUTHOR]

Leaf senescence is an integral part of plant development, during which, nutrients are remobilized from senescent leaves to fast-growing organs. The initiation and progression dynamics of leaf senescence is therefore vital not only to the maximal accumulation of assimilates but also to the efficient remobilization of nutrients. Senescence is a finely tuned process that involves the action of a large number of transcription factors (TFs). The NAC TFs play critical roles in regulating leaf senescence in Arabidopsis, wheat, rice and tomato. Here, we identified a NAC TF, ZmNAC126 that is responsive to leaf senescence in maize. Ectopic overexpression of ZmNAC126 in Arabidopsis and maize enhanced chlorophyll degradation and promoted leaf senescence. Electrophoretic mobility shift and chromatin immunoprecipitation assays revealed that ZmNAC126 could directly bind to the promoters of major chlorophyll catabolic genes in maize. Dual-luciferase assay in maize protoplasts indicated that ZmNAC126 positively regulates these chlorophyll catabolic genes in maize. Moreover, ZmNAC126 could be induced by ethylene, and ZmEIN3, a major TF of ethylene signalling, could bind to its promoter to transactivate its expression. Taken together, ZmNAC126 may play a pivotal role in regulating natural and ethylene-triggered leaf senescence in maize. [ABSTRACT FROM AUTHOR]

Wearing titanium particle‐induced osteoclastogenesis, accompanied by peri‐implant osteolysis, is the main cause of long‐term failure of hip prosthesis. Currently, medications used for the prevention and treatment of peri‐implant osteolysis show serious side effects. Therefore, development for more effective new drugs with less side effects is extremely urgent. Vaccarin is a natural flavonoid extracted from Vaccaria segetalis, with various biological functions, including antioxidantory, anti‐inflammatory, and promotion of angiogenesis. However, the putative role of vaccarin in the inhibition of titanium particle‐induced osteolysis has not been reported. In this study, it was indicated that vaccarin could effectively inhibit RANKL‐induced osteoclastogenesis, fusion of F‐actin rings, bone resorption, and expression of osteoclast marker genes in a dose‐dependent manner in vitro. Moreover, vaccarin could also inhibit RANKL‐induced osteoclastogenesis via the inhibition of NF‐κB and MAPK (p38, ERK, and JNK) signaling pathways, and inhibit the transcription of downstream transcription factors, such as c‐Fos and NFATc1. Consistent with in vitro results, this in vivo study showed that vaccarin exhibited an inhibitory effect on titanium particle‐induced osteolysis by antiosteoclastogenesis. In conclusion, vaccarin could be a promising agent for preventing and treating peri‐implant osteolysis. [ABSTRACT FROM AUTHOR]

Background: ING5 is the last member of the Inhibitor of Growth (ING) candidate tumor suppressor family that has been implicated in multiple cellular functions, including cell cycle regulation, apoptosis, and chromatin remodeling. Our previous study showed that ING5 overexpression inhibits lung cancer aggressiveness and epithelial–mesenchymal transition (EMT), with unknown mechanisms. Methods: Western blotting was used to detect total and phosphorylated levels of β‐catenin and EMT‐related proteins. Immunofluorescent staining was used to observe E‐cadherin expression. Proliferation and colony formation, wound healing, and Transwell migration and invasion assays were performed to study the proliferative and invasive abilities of cancer cells. Results: ING5 overexpression promotes phosphorylation of β‐catenin at Ser33/37, leading to a decreased β‐catenin protein level. Small hairpin RNA‐mediated ING5 knockdown significantly increased the β‐catenin level and inhibited phosphorylation of β‐catenin S33/37. Treatment with the WNT/β‐catenin inhibitor XAV939 inhibited ING5‐knockdown promoted proliferation, colony formation, migration, and invasion of lung cancer A549 cells, with increased phosphorylation of β‐catenin S33/37 and a decreased β‐catenin level. XAV939 also impaired ING5‐knockdown‐induced EMT, as indicated by upregulated expression of the EMT marker E‐cadherin, an epithelial marker; and decreased expression of N‐cadherin, a mesenchymal marker, and EMT‐related transcription factors, including Snail, Slug, Twist, and Smad3. Furthermore, XAV939 could inhibit the activation of both IL‐6/STAT3 and PI3K/Akt signaling pathways. Conclusion: ING5 inhibits lung cancer invasion and EMT by inhibiting the WNT/β‐catenin pathway. [ABSTRACT FROM AUTHOR]

NPR1 is required for systemic acquired resistance, and there are five NPR1 paralogs in Arabidopsis. Here we report knockout analysis of two of these, NPR3 and NPR4. npr3 single mutants have elevated basal PR-1 expression and the npr3 npr4 double mutant shows even higher expression. The double mutant plants also display enhanced resistance against virulent bacterial and oomycete pathogens. This enhanced disease resistance is partially dependent on NPR1, can be in part complemented by either wild-type NPR3 or NPR4, and is not associated with an elevated level of salicylic acid. NPR3 and NPR4 interact with TGA2, TGA3, TGA5 and TGA6 in yeast two-hybrid assays. Using bimolecular fluorescence complementation analysis, we show that NPR3 interacts with TGA2 in the nucleus of onion epidermal cells and Arabidopsis mesophyll protoplasts. Combined with our previous finding that basal PR-1 levels are also elevated in the tga2 tga5 tga6 triple mutant, we propose that NPR3 and NPR4 negatively regulate PR gene expression and pathogen resistance through their association with TGA2 and its paralogs. [ABSTRACT FROM AUTHOR]