bioRxiv Science⌕ Search

Biology subjects

Elsayed, E. M.

Publications and source records attributed to Elsayed, E. M..

2 recordsLinked to original sources

Dynamic expression range expansion of ECF sigma factor-dependent synthetic regulons by promoter context engineering

Alternative {sigma} factors enable bacteria to reprogram transcription in response to environmental cues and provide powerful tools for synthetic gene regulation. Extracytoplasmic function (ECF) {sigma} factors have recently been implemented as orthogonal transcriptional switches in several bacteria, including the -proteobacterium Sinorhizobium meliloti. Here, we investigated how promoter sequence context influences the activity and specificity of heterologous ECF-dependent core promoters. Combining ECF core promoters from Pseudomonas syringae and Escherichia coli with flanking sequences derived from strong promoters of S. meliloti and other proteobacteria increased promoter activity by up to 45-fold while preserving {sigma} factor specificity. We identified a short upstream AT motif, resembling a minimal UP element, as a key determinant of promoter strength. Targeted mutagenesis confirmed its role in supporting transcription initiation. Engineering promoter-flanking sequences together with the AT motif generated promoter libraries spanning up to a 75-fold range of activities. Importantly, promoter activity hierarchies were maintained within synthetic multi-gene regulons controlled by a single ECF master regulator, demonstrating modular and predictable gene expression. Our results establish promoter environment engineering as a robust strategy for expanding the dynamic range of orthogonal ECF regulatory systems and facilitate the scalable design of synthetic transcriptional programs in bacteria.

synthetic biology↗

NAD+ metabolism is a key modulator of bacterial respiratory epithelial infections

1.Lower respiratory tract infections caused by StreptococcusOpneumoniae (Spn) are a leading cause of death globally. Here we investigate the bronchial epithelial response to Spn infection on a transcriptomic, proteomic and metabolic level. We found the NAD+ salvage pathway to be dysregulated upon infection in a cell line model, primary human lung tissue and in vivo in rodents, leading to a reduced production of NAD+. Knockdown of NAD+ salvage enzymes (NAMPT, NMNAT1) increased bacterial replication. NAD+ treatment of Spn inhibited its growth while growth of other respiratory pathogens improved. Boosting NAD+ production increased NAD+ levels in immortalized and primary cells and decreased bacterial replication upon infection. NAD+ treatment of Spn dysregulated the bacterial metabolism and reduced intrabacterial ATP. Enhancing the bacterial ATP metabolism abolished the antibacterial effect of NAD+. Thus, we identified the NAD+ salvage pathway as an antibacterial cascade in Spn infections, predicting a novel antibacterial mechanism of NAD+.

immunology↗