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.

Background: Because of the mobile nature of the opd island, identical opd and orf306 sequences are found among soil bacteria. Results: In E. coli, Orf306 suppresses glycolysis and the TCA cycle and promotes up-regulation of alternate carbon catabolic operons. Conclusion:The up-regulated hca and mhp operons contribute to PNP-dependent growth of E. coli. Significance: Together with opd, orf306 contributes to the complete mineralization of OP residues.

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.

AbstractGenome wide expression profiling of

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.