BACKGROUND: Rhizobium giardinii has been demonstrated to colonize the roots of a variety of legume species, including common beans, and to increase nitrogen fixation. This suggests that Rhizobium giardinii might be a beneficial tool for sustainable agriculture by lowering dependency on synthetic nitrogen fertilizers and enhancing soil fertility. Understanding the regulatory components in the R. giardinii A3AY_RS01 genes might also lead to the creation of innovative ways for increasing the effectiveness of nitrogen fixation in other agriculturally important bacteria. Therefore, this study was aimed to predict regulatory element of R. giardinii DNA-binding response regulator A3AY_RS01 genes.
RESULTS: The locations for 19 % of the Transcriptional start site (TSSs) were within -300 bp relative to the start codon and ten candidate motifs were identified that are shared by at least 50 % of the R. giardinii A3AY_RS01 promoter input sequences from both strands. Motif 1 was revealed as the common promoter motif for all of R. giardinii A3AY_RS01 genes that serves as binding sites for TFs involved in the expression regulation of these genes. Hence, it was revealed that Motif 1 may serve as the binding site chiefly for Ferric uptake regulator (Fur) transcription factor family to regulate expression of A3AY_RS01 genes. High CpG density in the promoter than body regions were observed for most of the genes except for A3AY_RS0102950, A3AY_RS0120195 and A3AY_RS0131150 genes. Nonetheless, promoter areas were richer than body regions in both techniques.
CONCLUSIONS: MV1 motif can serve as a binding site for the Fur transcription factor gene family in R. giardinii to regulate the expression of R. giardinii A3AY_RS01 genes. R. giardinii A3AY_RS01 genes are rich in CpG Islands, and play an important role in the regulation of the gene expression of nitrogen fixing in this bacterium.

In the filamentous ascomycete Aspergillus nidulans, at least three high hierarchy transcription factors are required for growth at extracellular alkaline pH: SltA, PacC and CrzA. Transcriptomic profiles depending on alkaline pH and SltA function showed that pacC expression might be under SltA regulation. Additional transcriptional studies of PacC and the only pH-regulated pal gene, palF, confirmed both the strong dependence on ambient pH and the function of SltA. The regulation of pacC expression is dependent on the activity of the zinc binuclear (C6) cluster transcription factor PacX. However, we found that the ablation of sltA in the pacX- mutant background specifically prevents the increase in pacC expression levels without affecting PacC protein levels, showing a novel specific function of the PacX factor. The loss of sltA function causes the anomalous proteolytic processing of PacC and a reduction in the post-translational modifications of PalF. At alkaline pH, in a null sltA background, PacC72kDa accumulates, detection of the intermediate PacC53kDa form is extremely low and the final processed form of 27 kDa shows altered electrophoretic mobility. Constitutive ubiquitination of PalF or the presence of alkalinity-mimicking mutations in pacC, such as pacCc14 and pacCc700, resembling PacC53kDa and PacC27kDa, respectively, allowed the normal processing of PacC but did not rescue the alkaline pH-sensitive phenotype caused by the null sltA allele. Overall, data show that Slt and PacC/Pal pathways are interconnected, but the transcription factor SltA is on a higher hierarchical level than PacC on regulating the tolerance to the ambient alkalinity in A. nidulans.

The objective of this study was to identify genes associated with the biodegradation of phenol by Acinetobacter sp. strain DF4 through the use of differential display (DD) methodology. The bacteria were grown in YEPG medium, and total RNA was extracted and analyzed using labeled primers to detect gene expression differences. Three distinctively expressed cDNA bands (ph1, ph2, and ph3) were identified, cloned, and sequenced. DNA analysis involved searching for open reading frames (ORFs), verifying results with the NCBI database, predicting promoter regions, and constructing phylogenetic trees using bioinformatics tools. The ph1 gene displayed a 97% identity with the AraC transcriptional regulator, suggesting its potential role in regulating the ortho-catabolic pathway of phenol. The ph2 gene showed a 98% identity with aspartate semialdehyde dehydrogenase, which is involved in phenol degradation. The ph3 gene had a 93% identity with acetyltransferase. Essential transcription factors, such as TATA, GTGTGT, CACA, and CTTTT, were detected, and the three genes promoter regions were predicted. This study successfully identified functional genes involved in the metabolism of cyclic chemicals, particularly phenol, using the DD technique. These findings provide insights into the biodegradation pathways of phenol by Acinetobacter sp. Strain DF4 and may contribute to the development of more efficient bioremediation strategies for phenol-contaminated environments.

One of the most significant environmental challenges to crop growth and yield worldwide is soil salinization. Salinity lowers soil solution water potential, causes ionic disequilibrium and specific ion effects, and increases reactive oxygen species (ROS) buildup, causing several physiological and biochemical issues in plants. Plants have developed biological and molecular methods to combat salt stress. Salt-signaling mechanisms regulated by phytohormones may provide additional defense in salty conditions. That discovery helped identify the molecular pathways that underlie zinc-oxide nanoparticle (ZnO-NP)-based salt tolerance in certain plants. It emphasized the need to study processes like transcriptional regulation that govern plants\' many physiological responses to such harsh conditions. ZnO-NPs have shown the capability to reduce salinity stress by working with transcription factors (TFs) like AP2/EREBP, WRKYs, NACs, and bZIPs that are released or triggered to stimulate plant cell osmotic pressure-regulating hormones and chemicals. In addition, ZnO-NPs have been shown to reduce the expression of stress markers such as malondialdehyde (MDA) and hydrogen peroxide (H2O2) while also affecting transcriptional factors. Those systems helped maintain protein integrity, selective permeability, photosynthesis, and other physiological processes in salt-stressed plants. This review examined how salt stress affects crop yield and suggested that ZnO-NPs could reduce plant salinity stress instead of osmolytes and plant hormones.

Lycopene cyclases (LCYs) are a key branching point in regulating the carotenoid biosynthesis pathway in plants. Bixa orellana L. is characterized by the presence in its seed of bixin, an apocarotenoid of significant importance in the food, pharmaceutical, and cosmetic industries. Gene analysis provides the opportunity to investigate the LCY gene structure in plant species and its relationship with the synthesis of carotenoids. Coding sequences of the LCY genes were retrieved from a B. orellana genome DNA. Boβ-LCY1 and Boβ-LCY2 genes exhibit 100% of identity to their respective cDNA accessions, and exhibit a single coding region of 1512 bp (504 aa) and 1495 bp (498 aa), respectively. In contrast, Boε-LCY gene shows a coding region of 1581 bp (527 aa) with 10 introns of diverse lengths. Putative Transcription Factors (TFs) binding sites were upstream (3000 bp) identified for each LCY gene. TFs cover two groups, one with the categories of photosynthesis, reproduction, and oxidative processes that are frequent. The second one with the categories of defense, cell cycle, signaling, and carbohydrate metabolism, which are poorly represented. Besides, repetitive DNA elements showed motifs and proteins related to LTR from the Ty3/Gypsy family, were associated with the TFs regions. In general, TFs vary in the different BoLCY genes, being more abundant in the Boε-LCY gene. LCY expression analyzed from a transcriptome database, and validated by RT-qPCR, shows an upregulation of the three LCYs, mainly oriented to the synthesis of essential carotenoids in photosynthetic tissues (leaves), as well as an upregulation of the Boβ-LCY2 gene in the non-photosynthetic tissues (firsts seed development stages) related to the bixin accumulation.
UNASSIGNED: The online version contains supplementary material available at 10.1007/s12298-023-01384-8.

BMP2 signaling plays a pivotal role in odontoblast differentiation and maturation during odontogenesis. Teeth lacking Bmp2 exhibit a morphology reminiscent of dentinogenesis imperfecta (DGI), associated with mutations in dentin matrix protein 1 (DMP1) and dentin sialophosphoprotein (DSPP) genes. Mechanisms by which BMP2 signaling influences expressions of DSPP and DMP1 and contributes to DGI remain elusive. To study the roles of BMP2 in dentin development, we generated Bmp2 conditional knockout (cKO) mice. Through a comprehensive approach involving RNA-seq, immunohistochemistry, promoter activity, ChIP, and Re-ChIP, we investigated downstream targets of Bmp2. Notably, the absence of Bmp2 in cKO mice led to dentin insufficiency akin to DGI. Disrupted Bmp2 signaling was linked to decreased expression of Dspp and Dmp1, as well as alterations in intracellular translocation of transcription factors Dlx3 and Sp7. Intriguingly, upregulation of Dlx3, Dmp1, Dspp, and Sp7, driven by BMP2, fostered differentiation of dental mesenchymal cells and biomineralization. Mechanistically, BMP2 induced phosphorylation of Dlx3, Sp7, and histone acetyltransferase GCN5 at Thr and Tyr residues, mediated by Akt and Erk42/44 kinases. This phosphorylation facilitated protein nuclear translocation, promoting interactions between Sp7 and Dlx3, as well as with GCN5 on Dspp and Dmp1 promoters. The synergy between Dlx3 and Sp7 bolstered transcription of Dspp and Dmp1. Notably, BMP2-driven GCN5 acetylated Sp7 and histone H3, while also recruiting RNA polymerase II to Dmp1 and Dspp chromatins, enhancing their transcriptions. Intriguingly, BMP2 suppressed the expression of histone deacetylases. we unveil hitherto uncharted involvement of BMP2 in dental cell differentiation and dentine development through pAkt/pErk42/44/Dlx3/Sp7/GCN5/Dspp/Dmp1.

Transcriptional factors-based biosensors are commonly used in metabolic engineering for inducible control of gene expression and related applications such as high-throughput screening and dynamic pathway regulations. Mining for novel transcriptional factors is essential for expanding the usability of these toolsets. Here, we report the identification, characterization, and engineering of a phenolic acid responsive regulator PadR from Bacillus amyloliquefaciens (BaPadR). This BaPadR-based biosensor system showed a unique ligand preference and exhibited a high output strength comparable to that of commonly used inducible expression systems. Through engineering the DNA binding region of BaPadR, we further enhanced the dynamic range of the biosensor system. The DNA sequences that are responsible for BaPadR recognition were located by promoter truncation and hybrid promoter building. To further explore the tunability of the sensor system, base substitutions were performed on the BaPadR binding region of the phenolic acid decarboxylase promoter (PpadC) and the hybrid promoter. This novel biosensor system can serve as a valuable tool in future synthetic biology applications.

Epigenetics generally involves genetic control by factors other than our own DNA sequence. Recent research has focused on delineating the mechanisms of two major epigenetic phenomena: DNA methylation and histone modification. As epigenetics involves many cellular processes, it is no surprise that it can also influence disease-associated gene expression. A direct link between respiratory infections, host cell epigenetic regulations, and chronic lung diseases is still unknown. Recent studies have revealed bacterium- or virus-induced epigenetic changes in the host cells. In this review, we focused on respiratory pathogens (viruses, bacteria, and fungi) induced epigenetic modulations (DNA methylation and histone modification) that may contribute to lung disease pathophysiology by promoting host defense or allowing pathogen persistence.

One of the adverse outcomes of acute inflammatory response is progressing to the chronic stage or transforming into an aggressive process, which can develop rapidly and result in the multiple organ dysfunction syndrome. The leading role in this process is played by the Systemic Inflammatory Response that is accompanied by the production of pro- and anti-inflammatory cytokines, acute phase proteins, and reactive oxygen and nitrogen species. The purpose of this review that highlights both the recent reports and the results of the authors\' own research is to encourage scientists to develop new approaches to the differentiated therapy of various SIR manifestations (low- and high-grade systemic inflammatory response phenotypes) by modulating redox-sensitive transcription factors with polyphenols and to evaluate the saturation of the pharmaceutical market with appropriate dosage forms tailored for targeted delivery of these compounds. Redox-sensitive transcription factors such as NFκB, STAT3, AP1 and Nrf2 have a leading role in mechanisms of the formation of low- and high-grade systemic inflammatory phenotypes as variants of SIR. These phenotypic variants underlie the pathogenesis of the most dangerous diseases of internal organs, endocrine and nervous systems, surgical pathologies, and post-traumatic disorders. The use of individual chemical compounds of the class of polyphenols, or their combinations can be an effective technology in the therapy of SIR. Administering natural polyphenols in oral dosage forms is very beneficial in the therapy and management of the number of diseases accompanied with low-grade systemic inflammatory phenotype. The therapy of diseases associated with high-grade systemic inflammatory phenotype requires medicinal phenol preparations manufactured for parenteral administration.

Stress is a primary risk factor for psychiatric disorders such as Major Depressive Disorder (MDD) and Post Traumatic Stress Disorder (PTSD). The response to stress involves the regulation of transcriptional programs, which is supposed to play a role in coping with stress. To evaluate transcriptional processes implemented after exposure to unavoidable traumatic stress, we applied microarray expression analysis to the PFC of rats exposed to acute footshock (FS) stress that were sacrificed immediately after the 40 min session or 2 h or 24 h after. While no substantial changes were observed at the single gene level immediately after the stress session, gene set enrichment analysis showed alterations in neuronal pathways associated with glia development, glia-neuron networking, and synaptic function. Furthermore, we found alterations in the expression of gene sets regulated by specific transcription factors that could represent master regulators of the acute stress response. Of note, these pathways and transcriptional programs are activated during the early stress response (immediately after FS) and are already turned off after 2 h-while at 24 h, the transcriptional profile is largely unaffected. Overall, our analysis provided a transcriptional landscape of the early changes triggered by acute unavoidable FS stress in the PFC of rats, suggesting that the transcriptional wave is fast and mild, but probably enough to activate a cellular response to acute stress.