BackgroundThe ultimate goal of this work was to detect the role of transcription factors (TFs) concordantly expressed with genes related to programmed cell death (PCD) during PCD and salt stress. This work was based on the hypothesis that TFs and their driven genes likely co-express under different stimuli. The conserved superfamily ethylene responsive factor (AP2/ERF) draw attention of the present study as it participates in the response to biotic and abiotic stimuli as well as to program cell death (PCD).ResultsRNA-Seq analysis was done for tobacco (N. benthamiana) leaves exposed to oxalic acid (OA) at 20 mM for 0, 2, 6, 12 and 24 h to induce PCD. Genes up-regulated after 2 h of OA treatment with known function during PCD were utilized as landmarks to select TFs with concordant expression. Knockdown mutants of these TFs were generated in tobacco via virus induced gene silencing (VIGS) in order to detect their roles during PCD. Based on the results of PCD assay, knockout (KO) T-DNA insertion mutants of Arabidopsis as well as over-expression lines of two selected TFs, namely ERF109 and TFIID5, analogs to those in tobacco, were tested under salt stress (0, 100, 150 and 200 mM NaCl).ConclusionsResults of knockdown mutant tobacco cells confirmed the influence of these two TFs during PCD. Knockout insertion mutants and over-expression lines indicated the role of ERF109 in conferring salt tolerance in Arabidopsis.Electronic supplementary materialThe online version of this article (doi:10.1186/s12870-016-0908-z) contains supplementary material, which is available to authorized users.

Hypoxia most often occurs in cancer and the occurrence of hypoxia helps the cells in adapting different responses than the normal such as the activation of of those signaling pathways which regulate proliferation, angiogenesis, and cell death. There are large number of genes which are known to be associated with diverse biological processes and their control and coordination and in different cancers, the hypoxia-response differs. In this study our goal is to understand the impact of alteration in expression of hypoxia and immune systems related genes and its survival in breast cancer and analyzed the hallmarks of molecular signatures. For this purpose we have collected the hypoxia-associated genes based on the literature related with diverse biological processes and functions. For all these genes, we have studied the survival analysis, breast cancer gene expression profiling, and relevant hypoxic genes alterations. Based on our study, we conclude that there are 17 critical pathways and 40 genes from hypoxic gene list appear to play the major roles in case of breast cancer and overall we observe that immune signaling pathways and its components are highly altered in case of breast cancer. Among the top raked hallmarks of molecular signatures are apoptosis, hypoxia, DNA repair, E2F targets, MYC targets, androgen and estrogen response, and TNFa signaling.

Background Calotropis procera is a wild plant species in the family Apocynaceae that is able to grow in harsh, arid and heat stressed conditions. Understanding how this highly adapted plant persists in harsh environments should inform future efforts to improve the hardiness of crop and forage plant species. To study the plant response to droμght and osmotic stress, we treated plants with polyethylene glycol and NaCl and carried out transcriptomic and metabolomics measurements across a time-course of five days.ResultsWe identified a highly dynamic transcriptional response across the time-course including dramatic changes in inositol signaling, stress response genes and cytokinins. The resulting metabolome changes also involved sharp increases of myo-inositol, a key signaling molecule and elevated amino acid metabolites at later times.ConclusionsThe data generated here provide a first glimpse at the expressed genome of C. procera, a plant that is exceptionally well adapted to arid environments. We demonstrate, through transcriptome and metabolome analysis that myo-inositol signaling is strongly induced in response to drought and salt stress and that there is elevation of amino acid concentrations after prolonged osmotic stress. This work should lay the foundations of future studies in adaptation to arid environments.Electronic supplementary materialThe online version of this article (10.1186/s12870-017-1155-7) contains supplementary material, which is available to authorized users.

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This study was conducted to identify the regulation of the expression of the cEbf1-3 (chick early B-cell factor 1-3) genes in the pharyngeal arches (PAs), cranial sensory ganglia and placodes. cEbf1 and cEbf3 were mainly expressed in the cranial neural crest cells (NCCs) occupying the PAs, but cEbf2 was expressed in the mesenchymal core. cEbf1-3 were prominently expressed in the olfactory placodes, but cEbf1 and cEbf3 were only expressed in the otic vesicle. cEbf1 was expressed in all cranial sensory ganglia, cEbf2 (only) in the dorsolateral ganglia and cEbf3 in the trigeminal and vestibular ganglia. The removal of the source (the cranial neural tube) of the cranial NCCs before their migration to the PAs led to downregulation of cEbf1 and cEbf3 and upregulation of cEbf2 expression. Gain- and loss-of-function experiments showed that sonic hedgehog did not regulate cEbf1-3 expression in the PAs or associated ganglia. Bone morphogenetic protein 2 (Bmp2) can, however, directly and indirectly regulate cEbf1 and cEbf3 expression in the PAs and the proximal (NCC-derived) portion, but not the distal (placodal-derived) portion of the cranial sensory ganglia. Conversely, cEbf2 expression was upregulated following injection of Noggin before the migration of NCCs, but did not change after the overexpression of either Noggin or Bmp2 in the arch after NCC migration. In conclusion, Bmp2 regulates cEbf1 and cEbf3 expression in PAs and cranial sensory ganglia both directly and indirectly, via the migration of cranial NCCs. However, cEbf2 expression in the mesenchymal core of PAs is controlled by other undetermined signals.

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Transferrin receptor protein 1 (TfR1) is an important molecule in anti-cancer therapy. Targeted delivery of such therapeutic compounds improves their cellular uptake and circulation time, thereby enhancing therapeutic efficacy. Drug designing is therefore used to engineer molecules with structures that facilitate specific interactions. However, this process requires a thorough knowledge of all the interactions, including the three-dimensional (3D) and quaternary structures (QS) of the interacting molecules. Since structural information is available for only a part of the full TfR1 sequence, in the present study, we predicted the whole structure of TfR1 using homology modelling, docking, and molecular dynamics simulations. Homology modelling is used to generate 3D structures of TfR1 using MODELLER, I-TASSER, and RaptorX programs. Verify3D and Rampage server evaluated the quality of the resultant models. According to this evaluation, the model built by the RaptorX server and validated by Verify3D (compatibility: 83.82%) had the highest number of residues (95.5%) within the favoured regions of the Ramachandran plot, making it the most reliable 3D protein structure for TfR1 compared with others. The QS of TfR1 was built using HADDOCK and SymmDock docking software, and the results were evaluated by the ligand root mean square deviation (l-RMSD) value computed using the ProFit software. This showed that both HADDOCK and SymmDock gave acceptable results. However, the HADDOCK result was more stable and closest to the native complex structure with disulfide bonds. Therefore, the HADDOCK complex was further refined using both SymmRef and GalaxyRefineComplex until the medium l-RMSD rank was reached. This QS was successfully verified using nanoscale molecular dynamics (NAMD) energy minimization. This model could pave the way for further functional, structural, and therapeutic studies on TfR1.

Solitary unilateral lung cyst is an unusual finding in preterm infants. It may be difficult to distinguish acquired from congenital lung cysts clinically. The definitive diagnosis is histological; however, CT scan of the chest is a useful diagnostic tool. We present an extremely preterm infant with solitary lung cyst and background chronic lung disease. The initial chest x-rays showed solitary right lung cyst. At 6 weeks he required an escalation of ventilator support coupled with x-ray evidence of increased size of the cyst. CT scan confirmed large solitary cyst of the right lower lobe with evidence of compression and mediastinal shift, suspicious of congenital cystic adenomatoid malformation. The cyst was surgically removed in view of clinical deterioration. However, histology showed persistent pulmonary interstitial emphysema (PPIE). This case illustrates that in the context of prematurity PPIE can present as a solitary lung cyst and may require surgery.