Host Acid Signal Controls Salmonella Flagella Biogenesis through CadC-YdiV Axis
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA866174 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR22098035_1.fastq.gz | Fastqsanger.gz | |||
| SRR22098035_2.fastq.gz | Fastqsanger.gz | |||
| SRR22098036_1.fastq.gz | Fastqsanger.gz | |||
| SRR22098036_2.fastq.gz | Fastqsanger.gz | |||
| SRR22098037_1.fastq.gz | Fastqsanger.gz |
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Project description:Upon entering host cells, Salmonella quickly turn off flagella biogenesis to avoid recognition by the host immune system. However, it is not clear which host signal(s) Salmonella senses to initiate flagellum control.During the infection of a host,acid pH acts as an important environmental factor to triggers some genes expression. To investigate the effect of environmental acid signaling on the regulation of Salmonella flagella synthesis, we cultivated Salmonella typhimurium ATCC 14028s to an OD600 of 0.4, and then continued to culture for 2 h at pH 7.0 or pH 5.0. We then performed gene expression profiling analysis using data obtained from RNA-seq of cultured cells at different pH condition.
2022-08-06 | GSE210570 | GEO
Project description:Upon entering host cells, Salmonella quickly turns off flagella biogenesis to avoid recognition by the host immune system. However, it is not clear which host signal(s) Salmonella senses to initiate flagellum control. Here, we demonstrate that the acid signal can suppress flagella synthesis and motility of Salmonella, and this occurs after the transcription of master flagellar gene flhDC and depends on the anti-FlhDC factor YdiV. YdiV expression is activated after acid treatment. A global screen with ydiV promoter DNA and total protein from acid-treated Salmonella revealed a novel regulator of YdiV, the acid-related transcription factor CadC. Further studies showed that CadCC, the DNA binding domain of CadC, directly binds to a 33 nt region of the ydiV promoter with a 0.2 μM KD affinity. Furthermore, CadC could separate H-NS-ydiV promoter DNA complex to form CadC-DNA complex at a low concentration. Structural simulation and mutagenesis assays revealed that H43 and W106 of CadC are essential for ydiV promoter binding. No acid-induced flagellum control phenotype was observed in cadC mutant or ydiV mutant strains, suggesting that flagellum control during acid adaption is dependent on CadC and YdiV. The intracellular survival ability of cadC mutant strain decreased significantly compared with WT strain while the flagellin expression could not be effectively controlled in the cadC mutant strain when surviving within host cells. Together, our results demonstrated that acid stress acts as an important host signal to trigger Salmonella flagellum control through the CadC-YdiV-FlhDC axis, allowing Salmonella to sense a hostile environment and regulate flagellar synthesis during infection.
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Project description:The spermatogenesis process is complex and delicate, and any error in any step may cause spermatogenesis arrested and even male infertility. Through mutation screening of patients with clinical azoospermia, we found a heterozygous site of the same mutation on CEP70. The centrosome protein 70 (Cep70) is involved in the regulation of microtubule assembly and shows a high expression trend during human spermatogenesis, but the specific mechanism of this protein in spermatogenesis is still unknown. Therefore, we deleted Cep70 in mice and founded that the deletion of Cep70 causes abnormal spermatogenesis and leads to male sterility. We found that knockout of Cep70 did not affect the prophase of meiosis I, but led to higher levels of thyroid hormone secretion, male germ cell apoptosis and abnormal spermiogenesis. By TEM and SEM analysis, we found that deletion of Cep70 results in abnormal formation of flagella and acrosome during spermiogenesis. TMT-labeled quantitative proteomic analysis revealed that the absence of Cep70 led to the significantly decrease of proteins associated with the formation of the flagella, head and acrosome of sperm and microtubule cytoskeleton according to the proteomic data. Taken together, our results show that Cep70 is essential for the acrosome biogenesis and flagella formation during spermiogenesis.
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Project description:The Rubicon-WIPI axis regulates exosome biogenesis during aging
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Project description:Synthesis of flagella is very energy intensive and, while extensive transcriptional regulation has been described, little is known about the post-transcriptional regulation. Small RNAs (sRNAs) are widespread posttranscriptional regulators; most base pairing with mRNAs to affect their stability and/or translation. Here we describe four UTR-derived sRNAs (UhpU, MotR, FliX and FlgO) whose expression is controlled by the flagella sigma factor, sigma 28 in Escherichia coli. UhpU, MotR and FliX have distinct impacts on flagellin levels, flagella number and swimming, with MotR accelerating flagella synthesis and FliX decelerating flagella synthesis. Interestingly, MotR and FliX are noncanonical in that they base pair within the coding sequences of target genes. We characterize their respective positive and negative effects on genes encoding ribosomal proteins.
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Project description:Campylobacter jejuni produces a single flagellum on one or both poles of the cell, the polar flagella not only confer the bacterium darting motility but also involved in its virulence and metabolic processes. FlhF is a lately defined flagella biosynthesis regulator, but how it regulates flagella assembly isn’t clear at present. Previous research had indicated FlhF was associated with gene expression, to understanding its role in flagella system and its correlation with C. jejuni virulence, the global gene expression profiles of C. jejuni NCTC 11168 after inactivation of FlhF was analyzed. Transcriptome analysis revealed that ten genes were significantly differentially expressed with 6 down-regulated and 4 up-regulated, these genes are involved in diverse cellular functions including bacterial chemotaxis, flagellar assembly and two-component system, significance analysis revealed that the pathway of flagellar assembly was remarkable affected. Further studies were focused on the flagella system, FlhF was found play a global role as 63% (41/65) of the flagella genes were down-regulated, it influences flagella gene transcription from the early stage, this effect persists during the synthesis process and has a remarkable impact on the late part. The results above expand our cognition of this regulator, and also helpful for comprehensively and systematically reveal its role in flagella system.
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Project description:The long external filament of bacterial flagella is composed of several thousand copies of a single protein, flagellin. Here, we explore the role played by lysine methylation of flagellin in Salmonella, which requires the methylase FliB. We show that both flagellins of Salmonella enterica serovar Typhimurium, FliC and FljB, are methylated at surface-exposed lysine residues by FliB. A Salmonella Typhimurium mutant deficient in flagellin methylation is outcompeted for gut colonization in a gastroenteritis mouse model, and methylation of flagellin promotes bacterial invasion of epithelial cells in vitro. Lysine methylation increases the surface hydrophobicity of flagellin and enhances flagella-dependent adhesion of Salmonella to phosphatidylcholine vesicles and epithelial cells.
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Project description:Arachidonic acid (AA) is a polyunsaturated fatty acid present at high concentrations in the ovarian cancer (OC) microenvironment and is associated with poor clinical outcome. In the present study, we elucidate a potential link between AA and pro-tumorigenic macrophage polarization. Methods: AA-triggered signal transduction was studied in primary monocyte-derived macrophages (MDMs) by phosphoproteomics, transcriptional profiling, measurement of intracellular Ca2+ accumulation and reactive oxygen species production in conjunction with bioinformatic analyses. Functional effects were investigated by actin filament staining, quantification of macropinocytosis and analysis of extracellular vesicle release. Results: We identified the ASK1 - p38 (MAPK13/14) axis as a central constituent of signal transduction pathways triggered by non-metabolized AA. This pathway was induced by the Ca2+-triggered activation of calmodulin kinase II, and to a minor extent by ROS generation in a subset of donors. Activated p38 in turn was linked to a transcriptional stress response associated with a poor relapse-free survival. Consistent with the phosphorylation of the p38 substrate HSP27 and the (de)phosphorylation of multiple regulators of Rho family GTPases, AA impaired actin filament organization and inhibited actin-driven macropinocytosis. AA also affected the phosphorylation of proteins regulating vesicle biogenesis, and consistently, AA enhanced the release of tetraspanin-containing exosomes. Finally, we identified phospholipase A2 Group 2A (PLA2G2A) as the clinically most relevant enzyme producing extracellular AA, providing further potentially theranostic options. Conclusion: Our results suggest that AA contributes to an unfavorable clinical outcome of OC by promoting the pro-tumorigenic phenotype of tumor-associated macrophages. Besides critical AA-regulated signal transduction proteins identified in the present study, PLA2G2A might represent a potential prognostic tool and therapeutic target to interfere with OC progression.
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