Carbon dioxide and light are two major prerequisites of photosynthesis. Rising CO2 levels in oceanic surface waters in combination with ample light supply are therefore often considered stimulatory to marine primary production(1-3). Here we show that the combination of an increase in both CO2 and light exposure negatively impacts photosynthesis and growth of marine primary producers. When exposed to CO2 concentrations projected for the end of this century(4), natural phytoplankton assemblages of the South China Sea responded with decreased primary production and increased light stress at light intensities representative of the upper surface layer. The phytoplankton community shifted away from diatoms, the dominant phytoplankton group during our field campaigns. To examine the underlying mechanisms of the observed responses, we grew diatoms at different CO2 concentrations and under varying levels (5-100%) of solar radiation experienced by the phytoplankton at different depths of the euphotic zone. Above 22-36% of incident surface irradiance, growth rates in the high-CO2-grown cells were inversely related to light levels and exhibited reduced thresholds at which light becomes inhibitory. Future shoaling of upper-mixed-layer depths will expose phytoplankton to increased mean light intensities(5). In combination with rising CO2 levels, this may cause a widespread decline in marine primary production and a community shift away from diatoms, the main algal group that supports higher trophic levels and carbon export in the ocean.National Basic Research Program of China [2009CB421207, 2011CB200902]; National Natural Science Foundation of China [41120164007, 40930846]; Changjiang Scholars and Innovative Research Team project [IRT0941]; Ministry of Science and Technology [S2012GR0290]; United States National Science Foundation Division of Ocean Sciences [0942379, 0962309, 1043748]; German Ministry of Education and Research; 111 project; State Key Laboratory of Marine Environmental Science (Xiamen University); German Academic Exchange Service (DAAD

A retroviral vector containing the wild-type p53 gene under control of a beta-actin promoter was produced to mediate transfer of wild-type p53 into human non-small cell lung cancers by direct injection. Nine patients whose conventional treatments failed were entered into the study. No clinically significant vector-related toxic effects were noted up to five months after treatment. In situ hybridization and DNA polymerase chain reaction showed vector-p53 sequences in posttreatment biopsies. Apoptosis (programmed cell death) was more frequent in posttreatment biopsies than in pretreatment biopsies. Tumor regression was noted in three patients, and tumor growth stabilized in three other patients.

Southern Ocean primary productivity plays a key role in global ocean biogeochemistry and climate. At the Southern Ocean sea ice edge in coastal McMurdo Sound, we observed simultaneous cobalamin and iron limitation of surface water phytoplankton communities in late Austral summer. Cobalamin is produced only by bacteria and archaea, suggesting phytoplankton-bacterial interactions must play a role in this limitation. To characterize these interactions and investigate the molecular basis of multiple nutrient limitation, we examined transitions in global gene expression over short time scales, induced by shifts in micronutrient availability. Diatoms, the dominant primary producers, exhibited transcriptional patterns indicative of co-occurring iron and cobalamin deprivation. The major contributor to cobalamin biosynthesis gene expression was a gammaproteobacterial population, Oceanospirillaceae ASP10-02a. This group also contributed significantly to metagenomic cobalamin biosynthesis gene abundance throughout Southern Ocean surface waters. Oceanospirillaceae ASP10-02a displayed elevated expression of organic matter acquisition and cell surface attachment-related genes, consistent with a mutualistic relationship in which they are dependent on phytoplankton growth to fuel cobalamin production. Separate bacterial groups, including Methylophaga, appeared to rely on phytoplankton for carbon and energy sources, but displayed gene expression patterns consistent with iron and cobalamin deprivation. This suggests they also compete with phytoplankton and are important cobalamin consumers. Expression patterns of siderophore-related genes offer evidence for bacterial influences on iron availability as well. The nature and degree of this episodic colimitation appear to be mediated by a series of phytoplankton-bacterial interactions in both positive and negative feedback loops.colimitation | Southern Ocean primary productivity | metatranscriptomics | phytoplankton-bacterial interactions | cobalamin P rimary productivity and community composition in the Southern Ocean play key roles in global change (1, 2). The coastal Southern Ocean, particularly its shelf and marginal ice zones, is highly productive, with mean rates approaching 300-450 mg C m −2 ·d −1 (3). As such, identifying factors controlling phytoplankton growth in these regions is essential for understanding the ocean's role in past, present, and future biogeochemical cycles. Although irradiance, temperature, and iron availability are often considered to be the primary drivers of Southern Ocean productivity (1, 4), cobalamin (vitamin B 12 ) availability has also been shown to play a role (5, 6). Cobalamin is produced only by select bacteria and archaea and is required by most eukaryotic phytoplankton, as well as many bacteria that do not produce the vitamin (7). Cobalamin is used for a range of functions, including methionine biosynthesis and one-carbon metabolism. Importantly, phytoplankton that are able to grow without cobalamin preferentially use it when available; growth...

FUS1 is a novel tumor suppressor gene identified in the human chromosome 3p21.3 region that is deleted in many cancers. Using surfaceenhanced laser desorption/ionization mass spectrometric analysis on an anti-Fus1-antibody-capture ProteinChip array, we identified wild-type

BackgroundDrought is a major abiotic stress factors that reduces agricultural productivity. GRAS transcription factors are plant-specific proteins that play diverse roles in plant development. However, the functions of a number of GRAS genes identified in rice are unknown, especially the GRAS genes related to rice drought resistance have not been characterized.ResultsIn this study, a novel GRAS transcription factor gene named OsGRAS23, which is located in a drought-resistant QTL interval on chromosome 4 of rice, was isolated. The expression of OsGRAS23 was induced by drought, NaCl, and jasmonic acid treatments. The OsGRAS23-GFP fused protein was localized in the nucleus of tobacco epidermal cells. A trans-activation assay in yeast cells demonstrated that the OsGRAS23 protein possessed a strong transcriptional activation activity. OsGRAS23-overexpressing rice plants showed improved drought resistance and oxidative stress tolerance as well as less H2O2 accumulation compared with the wild-type plants. Furthermore, microarray analysis showed that several anti-oxidation related genes were up-regulated in the OsGRAS23-overexpressing rice plants. The yeast one hybrid test indicated that OsGRAS23 could bind to the promoters of its potential target genes.ConclusionsOur results demonstrate that OsGRAS23 encodes a stress-responsive GRAS transcription factor and positively modulates rice drought tolerance via the induction of a number of stress-responsive genes.Electronic supplementary materialThe online version of this article (doi:10.1186/s12870-015-0532-3) contains supplementary material, which is available to authorized users.

Acute activation of cells by tumor necrosis factor (TNF) has been well characterized, but little is known about later phases of TNF responses that are relevant for cells exposed to TNF for several days during inflammation. We found that prolonged exposure of human macrophages to TNF resulted in a wave of delayed but sustained activation of c-Jun and nuclear factor κB (NF-κB) proteins and of calcium oscillations that became apparent 1-3 d after TNF stimulation. These signaling events culminated in the induction and activation of the calcium-dependent transcription factor, nuclear factor of activated T cells (NFAT)c1, which mediated a gene expression program leading to cell fusion and osteoclast differentiation. TNF-induced NFATc1 activity primed macrophages for enhanced osteoclastogenesis in response to RANKL. High NFATc1 expression was apparent in synovial macrophages in a subset of patients with TNF-driven inflammatory arthritis. Thus, long-term exposure to TNF activates calcium-dependent signaling and an NFATc1-mediated gene activation program important for cell fusion and osteoclastogenesis. These findings identify a signaling pathway activated by TNF that is important for myeloid cell differentiation and suggest a role for TNF-induced calcium and NFAT signaling in chronic inflammation and associated bone resorption.calcium signaling | polykaryon

Lung cancer is one of the leading causes of death in the world. The underlying cause for lung cancer has been attributed to various factors that include alteration and mutation in the tumor suppressor genes. Restoration of normal function of the tumor suppressor gene is a potential therapeutic strategy. Recent studies have identified a group of candidate tumor suppressor genes on human chromosome 3p21.3 that are frequently deleted in human lung and breast cancers. Among the various genes identified in the 3p21.3 region, we tested the antitumor activity of the FUS1 gene in two human non-small-cell lung cancer (NSCLC) xenografts in vivo. Intratumoral administration of FUS1 gene complexed to DOTAP:cholesterol (DOTAP:Chol) liposome into subcutaneous H1299 and A549 lung tumor xenograft resulted in significant (P ¼ .02) inhibition of tumor growth. Furthermore, intravenous injections of DOTAP:Chol-FUS1 complex into mice bearing experimental A549 lung metastasis demonstrated significant (P ¼ .001) decrease in the number of metastatic tumor nodules. Finally, lung tumor-bearing animals when treated with DOTAP:Chol-FUS1 complex demonstrate prolonged survival (median survival time: 80 days, P ¼ .01) compared to control animals. This result demonstrates the potent tumor suppressive activity of the FUS1 gene and is a promising therapeutic agent for treatment of primary and disseminated human lung cancer.

Oral squamous cell carcinoma (OSCC), with high potential for metastasis, is the most common malignant tumor of the head and neck. Cancer-associated fibroblasts (CAFs) are the main stromal cells in the microenvironment and aggravate tumor progression. However, whether CAFs are associated with the progression of OSCC remains unknown and the underlying mechanism remains unclear. In the present study, the role of CAFs in mediating OSCC cell migration and invasion was investigated, and the participation of exosomal miR-382-5p in this process was elucidated. In this study, according to the α-SMA staining with immunohistochemistry, 47 OSCC patients were divided into CAFs-rich and CAFs poor groups, and association of CAF density and clinicopathologic features of the OSCC patients were analyzed with Pearson χ 2 test. Transwell assay was used for evaluating cell migration and invasion ability of OSCC cells after being co-cultured with NFs or CAFs, or after added exosomes. qPCR was used to detect the expression of miR-382-5p. Western blot analysis was used to measure the expression of migration and invasion-associated proteins. In the present study, the CAF density in tumor tissues was found to be relevant to OSCC lymph node metastasis and TNM stage. Furthermore, we revealed that miR-382-5p was overexpressed in CAFs compared with that in fibroblasts of adjacent normal tissue and miR-382-5p overexpression was responsible for OSCC cell migration and invasion. Finally, we demonstrated that CAF-derived exosomes transported miR-382-5p to OSCC cells. The present study confirmed a new mechanism of CAF-facilitated OSCC progression and may be beneficial for identifying new cancer therapeutic targets.