Identification of prognostic hub genes and therapeutic targets for selenium deficiency in chicks model through transcriptome profiling.

Selenium deficiency is a prevalent micronutrient deficiency that poses a major health concern worldwide. This study aimed to shed light on the molecular mechanisms underlying selenium deficiency using a chick model. Chickens were divided into control and selenium deficient groups. Plasma samples were collected to measure selenium concentration and transcriptome analyse were performed on oviduct samples. The results showed that selenium deficiency led to a significant reduction in plasma selenium levels and altered the expression of 10,266 differentially expressed genes (DEGs). These DEGs primarily regulated signal transduction and cell motility. The molecular function includes GTPase regulatory activity, and KEGG pathway analysis showed that they were mainly involved in the signal transduction. By using Cytoscape and CancerGeneNet tool, we identified 8 modules and 10 hub genes (FRK, JUN, PTPRC, ACTA2, MST1R, SDC4, SDC1, CXCL12, MX1 and EZR) associated with receptor tyrosine kinase pathway, Wnt and mTOR signaling pathways that may be closely related to cancer. These hub genes could be served as precise diagnostic and prognostic candidate biomarkers of selenium deficiency and potential targets for treatment strategies in both animals and humans. This study sheds light on the molecular basis of selenium deficiency and its potential impact on public health.

Outer Membrane Vesicles of Acinetobacter baumannii DS002 Are Selectively Enriched with TonB-Dependent Transporters and Play a Key Role in Iron Acquisition.

Outer membrane vesicles (OMVs) of Acinetobacter baumannii DS002 carry proteins which perform selective biological functions. The proteins involved in cell wall/membrane biogenesis and inorganic ion transport and metabolism occupied a significant portion of the 302 proteins associated with OMVs. Interestingly, the TonB-dependent transporters (TonRs), linked to the active transport of nutrients across the energy-deprived outer membrane, are predominant among proteins involved in inorganic ion transport and metabolism. The OMVs of DS002 contain TonRs capable of transporting iron complexed to catecholate, hydroximate, and mixed types of siderophores. Consistent with this observation, the OMVs were firmly bound to ferric-enterobactin (55Fe-Ent) and successfully transported iron into A. baumannii DS002 cells grown under iron-limiting conditions. In addition to the TonRs, OMVs also carry proteins known to promote pathogenesis, immune evasion, and biofilm formation. Our findings provide conclusive evidence for the role of OMVs in the transport of nutrients such as iron and show the presence of proteins with proven roles in pathogenicity and immune response. IMPORTANCE TonB-dependent transporters (TonRs) play a crucial role in transporting nutrients such as iron, nickel, copper, and complex carbohydrates across the energy-deprived outer membrane. Due to their unique structural features, TonRs capture nutrients in an energy-independent manner and transport them across the outer membrane by harvesting energy derived from the inner membrane-localized Ton-complex. In this study, we report the presence of TonRs capable of transporting various nutrients in OMVs and demonstrate their role in capturing and transporting ferric iron complexed with enterobactin into A. baumannii DS002 cells. The OMV-associated TonRs appear to play a critical role in the survival of A. baumannii, listed as a priority pathogen, under nutrient-deprived conditions.

Metabolic remodeling in Escherichia coli MG1655. A prophage e14-encoded small RNA, co293, post-transcriptionally regulates transcription factors HcaR and FadR.

In previous studies, we have shown the existence of metabolic remodeling in glucose-grown Escherichia coli MG1655 cells expressing the esterase Orf306 from the opd island of Sphingobium fuliginis. We now show that Orf306-dependent metabolic remodeling is due to regulation of a novel small RNA (sRNA). Endogenous propionate, produced due to the esterase/lipase activity of Orf306, repressed expression of a novel E. coli sRNA, co293. This sRNA post-transcriptionally regulates expression of the transcription factors HcaR and FadR either by inhibiting translation or by destabilizing their transcripts. Hence, repression of co293 expression elevates the levels of HcaR and FadR with consequent activation of alternative carbon catabolic pathways. HcaR activates the hca and MHP operons leading to upregulation of the phenyl propionate and hydroxy phenyl propionate (HPP) degradation pathways. Similarly, FadR stimulates the expression of the transcription factor IclR which negatively regulates the glyoxylate bypass pathway genes, aceBAK.

Proteomics of Sphingobium indicum B90A for a deeper understanding of hexachlorocyclohexane (HCH) bioremediation.

Genome wide expression profiling of Sphingobium indicum B90A revealed induction of lin genes, linA and linB, involved in dechlorination of hexachlorocyclohexane (HCH), in the presence of all four isomers of HCH. Supporting proteomics data, the qPCR and promoter assay showed upregulation of linA transcription in the presence of HCH isomers. Analysis of the upstream region of the linA gene revealed the existence of the GntR binding site overlapping the -10 hexamer of the putative promoter motif. As GntR is a known transcription repressor its dissociation from the linA promoter is expected to induce lin genes in the presence of HCH isomers. Comparison of in situ and in-culture proteomics indicated expression lin genes at the dumpsite, an indication for the in situ HCH degradation.

The Organophosphate Degradation (opd) Island-borne Esterase-induced Metabolic Diversion in Escherichia coli and Its Influence on p-Nitrophenol Degradation.

In previous studies of the organophosphate degradation gene cluster, we showed that expression of an open reading frame (orf306) present within the cluster in Escherichia coli allowed growth on p-nitrophenol (PNP) as sole carbon source. We have now shown that expression of orf306 in E. coli causes a dramatic up-regulation in genes coding for alternative carbon catabolism. The propionate, glyoxylate, and methylcitrate cycle pathway-specific enzymes are up-regulated along with hca (phenylpropionate) and mhp (hydroxyphenylpropionate) degradation operons. These hca and mhp operons play a key role in degradation of PNP, enabling E. coli to grow using it as sole carbon source. Supporting growth experiments, PNP degradation products entered central metabolic pathways and were incorporated into the carbon backbone. The protein and RNA samples isolated from E. coli (pSDP10) cells grown in (14)C-labeled PNP indicated incorporation of (14)C carbon, suggesting Orf306-dependent assimilation of PNP in E. coli cells.