scholarly journals Genetic Elucidation of Quorum Sensing and Cobamide Biosynthesis in Divergent Bacterial-Fungal Associations Across the Soil-Mangrove Root Interface

2021 ◽  
Vol 12 ◽  
Author(s):  
Zhengyuan Zhou ◽  
Ruiwen Hu ◽  
Yanmei Ni ◽  
Wei Zhuang ◽  
Zhiwen Luo ◽  
...  

Plant roots in soil host a repertoire of bacteria and fungi, whose ecological interactions could improve their functions and plant performance. However, the potential microbial interactions and underlying mechanisms remain largely unknown across the soil-mangrove root interface. We herein analyzed microbial intra- and inter-domain network topologies, keystone taxa, and interaction-related genes across four compartments (non-rhizosphere, rhizosphere, episphere, and endosphere) from a soil-mangrove root continuum, using amplicon and metagenome sequencing technologies. We found that both intra- and inter-domain networks displayed notable differences in the structure and topology across four compartments. Compared to three peripheral compartments, the endosphere was a distinctive compartment harboring more dense co-occurrences with a higher average connectivity in bacterial-fungal network (2.986) than in bacterial (2.628) or fungal network (2.419), which could be related to three bacterial keystone taxa (Vibrio, Anaerolineae, and Desulfarculaceae) detected in the endosphere as they are known to intensify inter-domain associations with fungi and stimulate biofilm formation. In support of this finding, we also found that the genes involved in cell-cell communications by quorum sensing (rhlI, lasI, pqsH, and lasR) and aerobic cobamide biosynthesis (cobG, cobF, and cobA) were highly enriched in the endosphere, whereas anaerobic cobamide biosynthesis (encoded by cbiT and cbiE) was dominant in three peripheral compartments. Our results provide genetic evidence for the intensified bacterial-fungal associations of root endophytes, highlighting the critical role of the soil-root interface in structuring the microbial inter-domain associations.

2021 ◽  
Author(s):  
Zhengyuan Zhou ◽  
Ruiwen Hu ◽  
Yanmei Ni ◽  
Wei Zhuang ◽  
Zhiwen Luo ◽  
...  

Abstract Background: Plant roots host a repertoire of bacteria and fungi, whose ecological interactions could improve their functions and plant performance. However, potential interactions and underlying mechanisms remain largely unknown in root-associated microbial communities at a continuous fine-scale. Results: We analyzed microbial intra- and inter-domain network topologies, keystone taxa, and interaction-related genes across four compartments (non-rhizosphere, rhizosphere, episphere and endosphere) from a soil-mangrove root continuum, using amplicon and metagenome sequencing technologies. We found that both intra- and inter-domain networks displayed notable differences in the structure and topology across four compartments. Compared to three peripheral compartments, the endosphere was a distinctive compartment with more intensive interactions in bacterial-fungal network than in bacterial or fungal network, which could be related to three bacterial keystone taxa (Vibrio, Anaerolineae and Desulfarculaceae) detected in the endosphere as they are known to intensify inter-domain interactions with fungi and stimulate biofilm formation. Also, high abundances of genes involved in cell-cell communications by quorum sensing (rhlI, lasI, pqsH and lasR) and aerobic cobamide biosynthesis (cobG, cobF and cobA) were detected in the endosphere.Conclusions: Our results reveal intensified inter-domain interactions of endophytes in the mangrove roots, creating a distinct micro-environment to promote a biofilm life-style.


2020 ◽  
Vol 27 (6) ◽  
pp. 955-982 ◽  
Author(s):  
Kyoung Sang Cho ◽  
Jang Ho Lee ◽  
Jeiwon Cho ◽  
Guang-Ho Cha ◽  
Gyun Jee Song

Background: Neuroinflammation plays a critical role in the development and progression of various neurological disorders. Therefore, various studies have focused on the development of neuroinflammation inhibitors as potential therapeutic tools. Recently, the involvement of autophagy in the regulation of neuroinflammation has drawn substantial scientific interest, and a growing number of studies support the role of impaired autophagy in the pathogenesis of common neurodegenerative disorders. Objective: The purpose of this article is to review recent research on the role of autophagy in controlling neuroinflammation. We focus on studies employing both mammalian cells and animal models to evaluate the ability of different autophagic modulators to regulate neuroinflammation. Methods: We have mostly reviewed recent studies reporting anti-neuroinflammatory properties of autophagy. We also briefly discussed a few studies showing that autophagy modulators activate neuroinflammation in certain conditions. Results: Recent studies report neuroprotective as well as anti-neuroinflammatory effects of autophagic modulators. We discuss the possible underlying mechanisms of action of these drugs and their potential limitations as therapeutic agents against neurological disorders. Conclusion: Autophagy activators are promising compounds for the treatment of neurological disorders involving neuroinflammation.


2020 ◽  
Vol 17 (4) ◽  
pp. 498-506 ◽  
Author(s):  
Pavan K. Mujawdiya ◽  
Suman Kapur

: Quorum Sensing (QS) is a phenomenon in which bacterial cells communicate with each other with the help of several low molecular weight compounds. QS is largely dependent on population density, and it triggers when the concentration of quorum sensing molecules accumulate in the environment and crosses a particular threshold. Once a certain population density is achieved and the concentration of molecules crosses a threshold, the bacterial cells show a collective behavior in response to various chemical stimuli referred to as “auto-inducers”. The QS signaling is crucial for several phenotypic characteristics responsible for bacterial survival such as motility, virulence, and biofilm formation. Biofilm formation is also responsible for making bacterial cells resistant to antibiotics. : The human gut is home to trillions of bacterial cells collectively called “gut microbiota” or “gut microbes”. Gut microbes are a consortium of more than 15,000 bacterial species and play a very crucial role in several body functions such as metabolism, development and maturation of the immune system, and the synthesis of several essential vitamins. Due to its critical role in shaping human survival and its modulating impact on body metabolisms, the gut microbial community has been referred to as “the forgotten organ” by O`Hara et al. (2006) [1]. Several studies have demonstrated that chemical interaction between the members of bacterial cells in the gut is responsible for shaping the overall microbial community. : Recent advances in phytochemical research have generated a lot of interest in finding new, effective, and safer alternatives to modern chemical-based medicines. In the context of antimicrobial research various plant extracts have been identified with Quorum Sensing Inhibitory (QSI) activities among bacterial cells. This review focuses on the mechanism of quorum sensing and quorum sensing inhibitors isolated from natural sources.


Biomolecules ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 253
Author(s):  
Xi Guo ◽  
Hong Yi ◽  
Tin Chiu Li ◽  
Yu Wang ◽  
Huilin Wang ◽  
...  

Vascular endothelial growth factor (VEGF) is a well-known angiogenic factor that plays a critical role in various physiological and pathological processes. VEGF also contributes to the process of embryo implantation by enhancing embryo development, improving endometrial receptivity, and facilitating the interactions between the developing embryo and the endometrium. There is a correlation between the alteration of VEGF expression and reproductive failure, including recurrent implantation failure (RIF) and recurrent miscarriage (RM). In order to clarify the role of VEGF in embryo implantation, we reviewed recent literature concerning the expression and function of VEGF in the reproductive system around the time of embryo implantation and we provide a summary of the findings reported so far. We also explored the effects and the possible underlying mechanisms of action of VEGF in embryo implantation.


2013 ◽  
Vol 5 ◽  
pp. BECB.S10886 ◽  
Author(s):  
Brijesh Singh Yadav ◽  
Venkateswarlu Ronda ◽  
Dinesh P. Vashista ◽  
Bhaskar Sharma

The recent advances in sequencing technologies and computational approaches are propelling scientists ever closer towards complete understanding of human-microbial interactions. The powerful sequencing platforms are rapidly producing huge amounts of nucleotide sequence data which are compiled into huge databases. This sequence data can be retrieved, assembled, and analyzed for identification of microbial pathogens and diagnosis of diseases. In this article, we present a commentary on how the metagenomics incorporated with microarray and new sequencing techniques are helping microbial detection and characterization.


2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Daiko Wakita ◽  
Yosuke Kurashima ◽  
Yoshihiro Takasato ◽  
Youngho Lee ◽  
Kenichi Shimada ◽  
...  

Background: KD is the leading cause of acquired heart disease in the US. We have demonstrated the critical role of innate immune responses via IL-1R/MyD88 signaling in the Lactobacillus casei cell wall extract (LCWE)-induced KD mouse model. The diversity and composition of microflora (both bacterial and fungal) have been associated with the regulation and alterations of immune responses and various pathologies. However, the role of gut microbiota in immunopathology of KD has not been investigated. Objective: To evaluate the role of gut microflora in development of coronary arteritis, and vascular abnormalities in KD mouse model. Methods and Results: We investigated the role of gut microflora in the LCWE-induced KD mouse model, using Specific-Pathogen Free (SPF) and Germ Free (GF) mice (C57BL/6). GF mice showed a significant decrease of KD lesions, including coronary arteritis compared with SPF mice. The development of LCWE-induced AAA, which we recently discovered in this mouse model, was also markedly diminished in GF mice. In addition to GF mice, we also investigated the specific role of commensal bacteria and/or fungi, and determined whether altered microorganism burden in this KD mouse model contributes to disease severity. To deplete bacteria and/or fungi in the gut microflora, we exposed pregnant SPF mice and their offspring to antibiotics cocktail (Abx) or antifungal drug (fluconazole; Fluc) in their drinking water for 5 wks and induced KD. The mice treated with Abx or Fluc had significantly reduced coronary arteritis and AAA compared to controls. The Abx plus Fluc administration showed marked decrease of KD vasculitis. Conclusions: We demonstrate here that gut microflora play a critical role in the development of KD vasculitis in LCWE-induced mouse model. Our results suggest that both bacteria and fungi in the intestinal microbiota may control the induction and severity of KD vasculitis. These findings provide a new perspective on the potential role of the microbiome in KD pathogenesis and may offer new diagnostic and therapeutic strategies for KD patients.


2018 ◽  
Vol 19 (11) ◽  
pp. 3390 ◽  
Author(s):  
Sudip Paudel ◽  
Regan Sindelar ◽  
Margaret Saha

Accumulating evidence over the past three decades suggests that altered calcium signaling during development may be a major driving force for adult pathophysiological events. Well over a hundred human genes encode proteins that are specifically dedicated to calcium homeostasis and calcium signaling, and the majority of these are expressed during embryonic development. Recent advances in molecular techniques have identified impaired calcium signaling during development due to either mutations or dysregulation of these proteins. This impaired signaling has been implicated in various human diseases ranging from cardiac malformations to epilepsy. Although the molecular basis of these and other diseases have been well studied in adult systems, the potential developmental origins of such diseases are less well characterized. In this review, we will discuss the recent evidence that examines different patterns of calcium activity during early development, as well as potential medical conditions associated with its dysregulation. Studies performed using various model organisms, including zebrafish, Xenopus, and mouse, have underscored the critical role of calcium activity in infertility, abortive pregnancy, developmental defects, and a range of diseases which manifest later in life. Understanding the underlying mechanisms by which calcium regulates these diverse developmental processes remains a challenge; however, this knowledge will potentially enable calcium signaling to be used as a therapeutic target in regenerative and personalized medicine.


Challenges ◽  
2018 ◽  
Vol 9 (2) ◽  
pp. 40 ◽  
Author(s):  
Jake Robinson ◽  
Jacob Mills ◽  
Martin Breed

Principles of ecology apply at myriad scales, including within the human body and the intertwined macro and microscopic ecosystems that we depend upon for survival. The conceptual principles of dysbiosis (‘life in distress’) also apply to different realms of life—our microbiome, the macro environment and the socioeconomic domain. Viewing the human body as a holobiont—a host plus billions of microbial organisms working symbiotically to form a functioning ecological unit—has the potential to enhance personal and planetary health. We discuss this ecological perspective in our paper. We also discuss the proposals to rewild the microbiome, innovative microbiome-inspired green infrastructure (MIGI) and the basis of prescribing ‘doses of nature’. Particular emphasis is given to MIGI—a collective term for the design and management of innovative living urban features that could potentially enhance public health via health-inducing microbial interactions. This concept builds upon the microbiome rewilding hypothesis. Mounting evidence points to the importance of microbial diversity in maintaining favorable health. Moreover, connecting with nature—both physically and psychologically–has been shown to enhance our health and wellbeing. However, we still need to understand the underlying mechanisms, and optimal types and levels of exposure. This paper adds to other recent calls for the inclusion of the environment-microbiome-health axis in nature–human health research. Recognizing that all forms of life—both the seen and the unseen—are in some way connected (ecologically, socially, evolutionarily), paves the way to valuing reciprocity in the nature–human relationship. It is with a holistic and symbiotic perspective that we can begin to integrate strategies and address connected issues of human and environmental health. The prospective strategies discussed in our paper focus on enhancing our connections with the natural world, and ultimately aim to help address the global challenge of halting and reversing dysbiosis in all its manifestations.


1995 ◽  
Vol 268 (4) ◽  
pp. C1067-C1074 ◽  
Author(s):  
M. E. O'Donnell ◽  
J. D. Brandt ◽  
F. R. Curry

The trabecular meshwork (TM) of the eye plays a critical role in modulating intraocular pressure (IOP) through regulation of aqueous humor outflow, although the underlying mechanisms remain unknown. Ethacrynic acid, an agent known to inhibit Na-K-Cl cotransport of a number of cell types, recently has been reported to increase aqueous outflow and lower IOP through an unknown effect on the TM. In vascular endothelial cells and a variety of other cell types, the Na-K-Cl cotransporter functions to regulate intracellular volume. The present study was conducted to evaluate TM cells for the presence of Na-K-Cl cotransport activity and to test the hypothesis that modulation of cotransport activity alters intracellular volume and, consequently, permeability of the TM. We demonstrate here that bovine and human TM cells exhibit robust Na-K-Cl cotransport activity that is inhibited by bumetanide and by ethacrynic acid. Our studies also show that TM cell Na-K-Cl cotransport is modulated by a variety of hormones and neurotransmitters. Inhibition of the cotransporter either by bumetanide, ethacrynic acid, or inhibitory hormones reduces TM intracellular volume, whereas stimulatory hormones increase cell volume. In addition, shrinkage of the cells by hypertonic media stimulates cotransport activity and initiates a subsequent regulatory volume increase. Permeability of TM cell monolayers, assessed as transmonolayer flux of [14C]sucrose, is increased by hypertonicity-induced cell shrinkage and by bumetanide. These findings suggest that Na-K-Cl cotransport of TM cells is of central importance to regulation of intracellular volume and TM permeability. Defects of Na-K-Cl cotransport may underlie the pathophysiology of glaucoma.


2007 ◽  
Vol 189 (17) ◽  
pp. 6109-6117 ◽  
Author(s):  
Bethany A. Rader ◽  
Shawn R. Campagna ◽  
Martin F. Semmelhack ◽  
Bonnie L. Bassler ◽  
Karen Guillemin

ABSTRACT The genome of the gastric pathogen Helicobacter pylori contains a homologue of the gene luxS, which has been shown to be responsible for production of the quorum-sensing signal autoinducer 2 (AI-2). We report here that deletion of the luxS gene in strain G27 resulted in decreased motility on soft agar plates, a defect that was complemented by a wild-type copy of the luxS gene and by the addition of cell-free supernatant containing AI-2. The flagella of the luxS mutant appeared normal; however, in genetic backgrounds lacking any of three flagellar regulators—the two-component sensor kinase flgS, the sigma factor σ28 (also called fliA), and the anti-sigma factor flgM—loss of luxS altered flagellar morphology. In all cases, the double mutant phenotypes were restored to the luxS + phenotype by the addition of synthetic 4,5-dihydroxy-2,3-pentanedione (DPD), which cyclizes to form AI-2. Furthermore, in all mutant backgrounds loss of luxS caused a decrease in transcript levels of the flagellar regulator flhA. Addition of DPD to luxS cells induced flhA transcription in a dose-dependent manner. Deletion of flhA in a wild-type or luxS mutant background resulted in identical loss of motility, flagella, and flagellar gene expression. These data demonstrate that AI-2 functions as a secreted signaling molecule upstream of FlhA and plays a critical role in global regulation of flagellar gene transcription in H. pylori.


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