Phosphatidylcholine biosynthesis and function in bacteria

Geiger, Otto; López‐Lara, Isabel M.; Sohlenkamp, Christian

doi:10.1016/j.bbalip.2012.08.009

Cited by 186 publications

(168 citation statements)

References 52 publications

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“…PC is important for membrane stability and under stress conditions. PC-deficient S. meliloti and Pseudomonas aeruginosa mutants are more sensitive to freezing than the respective wild type (39,40). Possibly, the N-methylated head group of TMOL is an adaptation to provide membrane stability to S. acidiphila under the changing temperatures (Ϫ20 to 25°C) to which the bacterium is exposed in its natural habitat.…”

Section: Discussionmentioning

confidence: 99%

OlsG (Sinac_1600) Is an Ornithine Lipid N-Methyltransferase from the Planctomycete Singulisphaera acidiphila

Escobedo‐Hinojosa

Vences‐Guzmán

Schubotz

et al. 2015

Journal of Biological Chemistry

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Section: Discussionmentioning

confidence: 99%

OlsG (Sinac_1600) Is an Ornithine Lipid N-Methyltransferase from the Planctomycete Singulisphaera acidiphila

Escobedo‐Hinojosa

Vences‐Guzmán

Schubotz

et al. 2015

Journal of Biological Chemistry

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“…Further, in a study examining plasma carnitine levels in sequential subjects undergoing elective diagnostic cardiac evalusource of choline in omnivores (32)(33)(34), and direct ingestion of PC was shown to result in rises in choline, betaine, and TMAO levels (25). Further, our studies suggested that plasma levels of TMAO showed the strongest positive correlation with CVD risk (25).…”

Section: R E V I E W S E R I E S : G U T M I C R O B I O M Ementioning

confidence: 99%

The contributory role of gut microbiota in cardiovascular disease

2014

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R e v i e w s e R i e s : g u t m i c R o b i o m eSeries Editor: Martin J. Blaser IntroductionCardiovascular disease (CVD) remains the leading cause of death in both the United States and industrialized societies, with growing incidence in developing countries (1). Factors contributing to CVD arise from genetic sources, environmental sources, or a combination of genetic and environmental sources (2). Despite extensive investigations in search of causal genetic variants, such as large-scale GWAS, less than one-fifth of attributable cardiovascular risk has been accounted for from genetic determinants (3, 4). At the same time, major advances in the treatment of atherosclerosis beyond high-potency lipid-lowering agents has not yet materialized (5). Indeed, even with high-potency statin therapy, at least a 50% residual risk remains (6), with the majority of events unchecked. Therefore, there is still ample room for improving our understanding of the processes contributing to CVD pathogenesis, and for improved prevention and treatment of CVD. While the recognizable contribution of genetics to CVD will no doubt significantly increase with time, a reassessment of environmental contributions to CVD pathogenesis and risks for adverse events is certainly worthwhile.Our largest environmental exposure is what we eat. Technically speaking, food is a foreign object that we take into our bodies in kilogram quantities every day. From the latest National Health and Nutrition Examination Survey (NHANES, 2009(NHANES, -2010, the majority of individuals sampled achieved an intermediate or poor Healthy Eating Index (1). However, dietary composition is often difficult to assess, and even precise quantification of dietary intake may not necessarily reveal the many known and unknown factors that may influence the contributions of specific dietary nutrients to disease susceptibility (7). There has also been an overwhelming lack of appreciation at the bedside regarding the intricate and complicated processes that transform ingested food into the myriad metabolites that enter the circulation and fulfill or adversely affect various functional and metabolic processes in the body.Over the past decade we have increasingly begun to appreciate the ecological diversity of microbes living symbiotically within us, a large proportion of which reside within our intestines. We now know that the human gut harbors more than 100 trillion microbial cells, far outnumbering the human host cells of the body (8). Indeed, a sobering fact is that Homo sapiens DNA is estimated to represent less than 10% of the total DNA within our bodies, due to the staggeringly large numbers of microbes that reside in and on us, primarily within our gut (9). Our microbial symbiont guests have coevolved with us and affect a wide range of physiologic and metabolic processes of the body. The major taxa present in gut microbiota consist primarily of 2 major bacterial phyla, Firmicutes and Bacteroidetes, whose proportions appear to remain remarkably stable over time within individu...

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“…While choline is ubiquitous in eukaryotes, the ability to synthesize choline or GB de novo from phosphatidylethanolamine or glycine is less prevalent in bacteria and evidence suggests that it is absent in the pseudomonads (42). While de novo choline synthesis has not been demonstrated in the pseudomonads, transporters for exogenous choline import are ubiquitous within this group based on analyses of current genome sequences (43).…”

Section: Choline and Gb Import Versus De Novo Synthesismentioning

confidence: 99%

“…bPC likely localizes to the inner membrane, but the partitioning of bPC to a specific membrane leaflet has not been determined, and neither has its contribution to the inner leaflet of the outer membrane been examined. bPC has been hypothesized to have a role as an inactive store of choline in the membrane that could be liberated when GB is needed (42,74) (Fig. 1).…”

Section: Figmentioning

confidence: 99%

Homeostasis and Catabolism of Choline and Glycine Betaine: Lessons from Pseudomonas aeruginosa

Wargo

2013

Appl Environ Microbiol

155

121

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Most sequenced bacteria possess mechanisms to import choline and glycine betaine (GB) into the cytoplasm. The primary role of choline in bacteria appears to be as the precursor to GB, and GB is thought to primarily act as a potent osmoprotectant. Choline and GB may play accessory roles in shaping microbial communities, based on their limited availability and ability to enhance survival under stress conditions. Choline and GB enrichment near eukaryotes suggests a role in the chemical relationships between these two kingdoms, and some of these interactions have been experimentally demonstrated. While many bacteria can convert choline to GB for osmoprotection, a variety of soil-and water-dwelling bacteria have catabolic pathways for the multistep conversion of choline, via GB, to glycine and can thereby use choline and GB as sole sources of carbon and nitrogen. In these choline catabolizers, the GB intermediate represents a metabolic decision point to determine whether GB is catabolized or stored as an osmo-and stress protectant. This minireview focuses on this decision point in Pseudomonas aeruginosa, which aerobically catabolizes choline and can use GB as an osmoprotectant and a nutrient source. P. aeruginosa is an experimentally tractable and ecologically relevant model to study the regulatory pathways controlling choline and GB homeostasis in choline-catabolizing bacteria. The study of P. aeruginosa associations with eukaryotes and other bacteria also makes this a powerful model to study the impact of choline and GB, and their associated regulatory and catabolic pathways, on host-microbe and microbe-microbe relationships.

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Phosphatidylcholine biosynthesis and function in bacteria

Cited by 186 publications

References 52 publications

OlsG (Sinac_1600) Is an Ornithine Lipid N-Methyltransferase from the Planctomycete Singulisphaera acidiphila

OlsG (Sinac_1600) Is an Ornithine Lipid N-Methyltransferase from the Planctomycete Singulisphaera acidiphila

The contributory role of gut microbiota in cardiovascular disease

Homeostasis and Catabolism of Choline and Glycine Betaine: Lessons from Pseudomonas aeruginosa

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