The banana (Musa spp.) industry experiences dramatic annual losses from Fusarium wilt of banana disease, which is caused by the fungus Fusarium oxysporum f. sp. cubense (FOC). Pisang Awak banana ‘Fenza No. 1’ (Musa spp. cultivar Fenza No. 1), a major banana cultivar with high resistance to F. oxysporum f. sp. cubense race 4, is considered to be ideal for growth in problematic areas. However, ‘Fenza No. 1’ is still affected by F. oxysporum f. sp. cubense race 1 in the field. TR21 is an endophytic Bacillus subtilis strain isolated from orchids (Dendrobium sp.). Axillary spraying of banana plants with TR21 controls Fusarium wilt of banana, decreasing the growth period and increasing yields in the field. In this study, we established that TR21 increases root growth in different monocotyledonous plant species. By axillary inoculation, TR21 induced a similar transcriptomic change as that induced by F. oxysporum f. sp. cubense race 1 but also upregulated the biosynthetic pathways for the phytohormones brassinosteroid and jasmonic acid in ‘Fenza No. 1’ root tissues, indicating that TR21 increases Fusarium wilt of banana resistance, shortens growth period, and increases yield of banana by inducing specific transcriptional reprogramming and modulating phytohormone levels. These findings will contribute to the identification of candidate genes related to plant resistance against fungi in a nonmodel system and facilitate further study and exploitation of endophytic biocontrol agents.

Background: Several WRKY transcription factors (TFs), including CaWRKY6, CaWRKY22, CaWRKY27, and CaWRKY40 are known to govern the resistance of pepper (Capsicum annuum L.) plants to Ralstonia solanacearum infestation (RSI) and other abiotic stresses. However, the molecular mechanisms underlying these processes remain elusive. Methods: This study functionally described CaWRKY3 for its role in pepper immunity against RSI. The roles of phytohormones in mediating the expression levels of CaWRKY3 were investigated by subjecting pepper plants to 1 mM salicylic acid (SA), 100 µM methyl jasmonate (MeJA), and 100 µM ethylene (ETH) at 4-leaf stage. A virus-induced gene silencing (VIGS) approach based on the Tobacco Rattle Virus (TRV) was used to silence CaWRKY3 in pepper, and transiently over-expressed to infer its role against RSI. Results: Phytohormones and RSI increased CaWRKY3 transcription. The transcriptions of defense-associated marker genes, including CaNPR1, CaPR1, CaDEF1, and CaHIR1 were decreased in VIGS experiment, which made pepper less resistant to RSI. Significant hypersensitive (HR)-like cell death, H₂O₂ buildup, and transcriptional up-regulation of immunological marker genes were noticed in pepper when CaWRKY3 was transiently overexpressed. Transcriptional activity of CaWRKY3 was increased with overexpression of CaWRKY6, CaWRKY22, CaWRKY27, and CaWRKY40, and vice versa. In contrast, Pseudomonas syringae pv tomato DC3000 (Pst DC3000) was easily repelled by the innate immune system of transgenic Arabidopsis thaliana that overexpressed CaWRKY3. The transcriptions of defense-related marker genes like AtPR1, AtPR2, and AtNPR1 were increased in CaWRKY3-overexpressing transgenic A. thaliana plants. Conclusion: It is concluded that CaWRKY3 favorably regulates phytohormone-mediated synergistic signaling, which controls cell death in plant and immunity of pepper plant against bacterial infections.

Lung adenocarcinoma (LUAD) accounts for ~40% of lung cancer cases, and the 5‐year relative survival rate is no more than 1%. Dysregulation of components of striatin‐interacting phosphatase and kinase (STRIPAK) complexes is associated with various diseases, including cancer. Striatin‐interacting protein 2 (STRIP2), also called Fam40b, has been reported to regulate tumor cell growth and migration. Here, we investigated the role of STRIP2 in LUAD growth, migration and the underlying mechanisms. Analysis of data from The Cancer Genome Atlas database revealed that STRIP2 is highly expressed and predicted poor outcomes in patients with LUAD. Moreover, quantitative RT‐PCR (qRT‐PCR) analysis revealed that the mRNA expression of STRIP2 is greater in all tested LUAD cells than in a normal lung cell line. To investigate the function of STRIP2, we overexpressed STRIP2 in SPC‐A1 cells and depleted STRIP2 in Calu‐3 cells. Cell proliferation was evaluated by Cell Counting Kit‐8 and colony‐forming assays, and Transwell assay was employed to test cell invasion and migration. Our results indicate that STRIP2 depletion suppressed cell proliferation, invasion and migration in Calu‐3 cells, and overexpression of STRIP2 had the opposite effects in SPC‐A1 cells. Moreover, we discovered that STRIP2 depletion reduced the protein levels of p‐Akt and phosphorylated‐mammalian target of rapamycin (p‐mTOR) in Calu‐3 cells, whereas STRIP2 overexpression increased levels of these proteins in SPC‐A1 cells. Furthermore, we found that silencing of STRIP2 clearly enhanced protein levels of E‐cadherin and reduced levels of N‐cadherin, Vimentin and matrix metalloproteinase‐9 in Calu‐3 cells, whereas overexpression of STRIP2 had the opposite effect in SPC‐A1 cells. Our data indicate that STRIP2 promotes the proliferation and motility of LUAD cells, and this may be mediated through the regulation of the Akt/mTOR pathway and epithelial–mesenchymal transition. These results may facilitate the development of therapeutic strategies to treat LUAD.