Dataset Information

Efficient Broad-Spectrum Cyanophage Function Module Mining.

ABSTRACT: Cyanobacterial harmful algal blooms (CyanoHABs) cause health and environmental effects worldwide. Cyanophage is a virus that exclusively infects cyanobacteria. Using cyanophages to control blooms is the latest biological control method. However, little research on the genomics of cyanophages and the presence of numerous proteins with unidentified functions in cyanophage genomes pose challenges for their practical application and comprehensive investigation. We selected the broad-spectrum and efficient cyanophage YongM for our study. On the one hand, through rational analysis, we analyze essential genes, establish the minimal cyanophage genome and single essential gene modules, and examine the impact of essential modules on growth. Additionally, we conducted ultraviolet mutagenesis on YongM to generate more efficient cyanophages' critical modules through random mutagenesis. Then, we sequenced and analyzed the functionality of the mutational gene modules. These findings highlight several gene modules that contribute to a deeper understanding of the functional components within cyanophage genomes.

SUBMITTER: Guo Y

PROVIDER: S-EPMC11356776 | biostudies-literature | 2024 Aug

REPOSITORIES: biostudies-literature

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Efficient Broad-Spectrum Cyanophage Function Module Mining.

Guo Yujing Y Dong Xiaoxiao X Li Huiying H Lin Wei W Cao Lei L Li Dengfeng D Zhang Yiming Y Jin Jin J Tong Yigang Y Liu Zihe Z

Microorganisms 20240802 8

Cyanobacterial harmful algal blooms (CyanoHABs) cause health and environmental effects worldwide. Cyanophage is a virus that exclusively infects cyanobacteria. Using cyanophages to control blooms is the latest biological control method. However, little research on the genomics of cyanophages and the presence of numerous proteins with unidentified functions in cyanophage genomes pose challenges for their practical application and comprehensive investigation. We selected the broad-spectrum and eff ...[more]

PMID: 39203420

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Project description:The phagocytic clearance of apoptotic cells, termed efferocytosis, is essential for both tissue homeostasis and tissue health during cell death-inducing treatments. Failure to efficiently clear apoptotic cells augment the risk of pathological inflammation and has been linked to a myriad of autoimmune and inflammatory diseases. Although past studies have elucidated local molecular signals that regulate homeostatic efferocytosis in a tissue, whether signals arising distally also regulate homeostatic efferocytosis remains elusive. Interestingly, clinical evidence suggests that prolonged use of broad-spectrum antibiotics is associated with an increased risk of autoimmune and inflammatory disease development. We therefore hypothesized that intestinal microbes produce molecular signals that regulate efferocytotic ability in tissue phagocytes beyond the intestines. Here, we find that macrophages, the body’s professional phagocyte, display impaired efferocytosis in the peritoneum of broad-spectrum antibiotics (ABX)-treated, vancomycin-treated, and germ-free mice in vivo, the latter of which could be rescued by fecal microbiota transplantation. Mechanistically, the microbiota-derived short-chain fatty acid butyrate directly boosted efferocytosis efficiency and capacity in mouse and human macrophages, with both intestinal and local delivery of butyrate capable of rescuing ABX-induced large peritoneal macrophage (LPM) efferocytosis defects. Bulk mRNA sequencing of butyrate-treated primary macrophages in vitro and single cell mRNA sequencing of LPMs isolated from ABX-treated and butyrate-rescued mice revealed specific regulation of efferocytosis-supportive transcriptional programs. Specifically, we found that the efferocytosis receptor T-cell immunoglobulin and mucin domain containing 4 (TIM-4, Timd4) was downregulated in LPMs of ABX-treated mice which was rescued by oral butyrate and that TIM-4 was required for the butyrate-induced enhancement of LPM efferocytosis capacity in vivo. Strikingly, LPM efferocytosis was impaired well-beyond withdrawal of ABX and, importantly, ABX-treated mice exhibited significantly worse disease in a mouse model of system lupus erythematosus. Collectively, our results demonstrate that homeostatic efferocytosis relies on distal molecular signals and suggest that a defect in homeostatic efferocytosis may contribute to the clinically observed link between broad-spectrum antibiotics use and inflammatory disease.

Dataset Information

Efficient Broad-Spectrum Cyanophage Function Module Mining.

Publications

Efficient Broad-Spectrum Cyanophage Function Module Mining.

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