Fox transcription factor AccGRF1 in response to glyphosate stress in Apis cerana cerana.

Glyphosate is an herbicide commonly used in agriculture, and its widespread use has adversely affected the survival of nontarget organisms. Among these organisms, bees in particular are important pollinators, and declining bee populations have severely affected crop yields around the world. However, the molecular mechanism by which glyphosate harms bees remains unclear. In our experiment, we screened and cloned a glyphosate-induced gene in Apis cerana cerana (A. c. cerana) and named glyphosate response factor 1 (AccGRF1). Sequence analysis showed that AccGRF1 contains a winged-helix DNA binding domain, which suggests that it belongs to the Forkhead box (Fox) protein family. qRT-PCR and heterologous expression in Escherichia coli and yeast showed that AccGRF1 can respond to glyphosate and oxidative stress. After AccGRF1 knockdown by means of RNA interference (RNAi), the resistance of A. c. cerana to glyphosate stress improved. The results suggested that AccGRF1 is involved in A. c. cerana glyphosate stress tolerance. This study reveals the functions of Fox transcription factors in response to glyphosate stress and provides molecular insights into the regulation of glyphosate responses in honeybees.

STRIP2, a member of the striatin-interacting phosphatase and kinase complex, is implicated in lung adenocarcinoma cell growth and migration.

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.

Profile of Chest Injuries and Oxygen Therapy in Trauma Patients with Acute Respiratory Failure after the Jiangsu Tornado in China: A Retrospective Study.

BACKGROUND: The aim of this study was to analyze the profile of chest injuries, oxygen therapy for respiratory failure, and the outcomes of victims after the Jiangsu tornado, which occurred on June 23, 2016 in Yancheng City, Jiangsu Province, China. METHODS: The clinical records of 144 patients referred to Yancheng City No.1 People's Hospital from June 23 through June 25 were retrospectively investigated. Of those patients, 68 (47.2%) sustained major chest injuries. The demographic details, trauma history, details of injuries and Abbreviated Injury Scores (AIS), therapy for respiratory failure, surgical procedures, length of intensive care unit (ICU) and hospital stay, and mortality were analyzed. RESULTS: Of the 68 patients, 41 (60.3%) were female and 27 (39.7%) were male. The average age of the injured patients was 57.1 years. Forty-six patients (67.6%) suffered from polytrauma. The mean thoracic AIS of the victims was calculated as 2.85 (SD = 0.76). Rib fracture was the most common chest injury, noted in 56 patients (82.4%). Pulmonary contusion was the next most frequent injury, occurring in 12 patients (17.7%). Ten patients with severe chest trauma were admitted to ICU. The median ICU stay was 11.7 (SD = 8.5) days. Five patients required intubation and ventilation, one patient was treated with noninvasive positive pressure ventilation (NPPV), and four patients were treated with high-flow nasal cannula (HFNC). Three patients died during hospitalization. The hospital mortality was 4.41%. CONCLUSIONS: Chest trauma was a common type of injury after tornado. The most frequent thoracic injuries were rib fractures and pulmonary contusion. Severe chest trauma is usually associated with a high incidence of respiratory support requirements and a long length of stay in the ICU. Early initiation of appropriate oxygen therapy was vital to restoring normal respiratory function and saving lives. Going forward, HFNC might be an effective and well-tolerated therapeutic addition to the management of acute respiratory failure in chest trauma.

The phytopathogenic virulent effector protein RipI induces apoptosis in budding yeast Saccharomyces cerevisiae.

Virulent protein toxins secreted by the bacterial pathogens can cause cytotoxicity by various molecular mechanisms to combat host cell defense. On the other hand, these proteins can also be used as probes to investigate the defense pathway of host innate immunity. Ralstonia solanacearum, one of the most virulent bacterial phytopathogens, translocates more than 70 effector proteins via type III secretion system during infection. Here, we characterized the cytotoxicity of effector RipI in budding yeast Saccharomyce scerevisiae, an alternative host model. We found that over-expression of RipI resulted in severe growth defect and arginine (R) 117 within the predicted integrase motif was required for inhibition of yeast growth. The phenotype of death manifested the hallmarks of apoptosis. Our data also revealed that RipI-induced apoptosis was independent of Yca1 and mitochondria-mediated apoptotic pathways because Δyca1 and Δaif1 were both sensitive to RipI as compared with the wild type. We further demonstrated that RipI was localized in the yeast nucleus and the N-terminal 1-174aa was required for the localization. High-throughput RNA sequencing analysis showed that upon RipI over-expression, 101 unigenes of yeast ribosome presented lower expression level, and 42 GO classes related to the nucleus or recombination were enriched with differential expression levels. Taken together, our data showed that a nuclear-targeting effector RipI triggers yeast apoptosis, potentially dependent on its integrase function. Our results also provided an alternative strategy to dissect the signaling pathway of cytotoxicity induced by the protein toxins.