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Fatty acids from membrane lipids become incorporated into lipid bodies during Myxococcus xanthus differentiation.

Bhat S, Boynton TO, Pham D, Shimkets LJ - PLoS ONE (2014)

Bottom Line: Third, peripheral rods, developing cells that do not produce lipid bodies, fail to shorten.The lipid body regulon involves many developmental genes that are not specifically involved in fatty acid synthesis or degradation.MazF RNA interferase and its target, enhancer-binding protein Nla6, appear to negatively regulate cell shortening and TAG accumulation whereas most cell-cell signals activate these processes.

View Article: PubMed Central - PubMed

Affiliation: Department of Microbiology, University of Georgia, Athens, Georgia, United States of America.

ABSTRACT
Myxococcus xanthus responds to amino acid limitation by producing fruiting bodies containing dormant spores. During development, cells produce triacylglycerides in lipid bodies that become consumed during spore maturation. As the cells are starved to induce development, the production of triglycerides represents a counterintuitive metabolic switch. In this paper, lipid bodies were quantified in wild-type strain DK1622 and 33 developmental mutants at the cellular level by measuring the cross sectional area of the cell stained with the lipophilic dye Nile red. We provide five lines of evidence that triacylglycerides are derived from membrane phospholipids as cells shorten in length and then differentiate into myxospores. First, in wild type cells, lipid bodies appear early in development and their size increases concurrent with an 87% decline in membrane surface area. Second, developmental mutants blocked at different stages of shortening and differentiation accumulated lipid bodies proportionate with their cell length with a Pearson's correlation coefficient of 0.76. Third, peripheral rods, developing cells that do not produce lipid bodies, fail to shorten. Fourth, genes for fatty acid synthesis are down-regulated while genes for fatty acid degradation are up regulated. Finally, direct movement of fatty acids from membrane lipids in growing cells to lipid bodies in developing cells was observed by pulse labeling cells with palmitate. Recycling of lipids released by Programmed Cell Death appears not to be necessary for lipid body production as a fadL mutant was defective in fatty acid uptake but proficient in lipid body production. The lipid body regulon involves many developmental genes that are not specifically involved in fatty acid synthesis or degradation. MazF RNA interferase and its target, enhancer-binding protein Nla6, appear to negatively regulate cell shortening and TAG accumulation whereas most cell-cell signals activate these processes.

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Regulation of lipid body production during M. xanthus fruiting body development.Mutants blocked in synthesis of proteins labeled in in black are deficient in lipid body synthesis (>40%). Those labeled in purple produce intermediate levels of lipid bodies (40–80%). Those in green produce near WT levels or higher (>80%). Red letters indicate developmental signals. Asg, A-signal; Csg, C-signal; Esg, E-signal.
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pone-0099622-g005: Regulation of lipid body production during M. xanthus fruiting body development.Mutants blocked in synthesis of proteins labeled in in black are deficient in lipid body synthesis (>40%). Those labeled in purple produce intermediate levels of lipid bodies (40–80%). Those in green produce near WT levels or higher (>80%). Red letters indicate developmental signals. Asg, A-signal; Csg, C-signal; Esg, E-signal.

Mentions: Figure 5 provides a simplistic model of the lipid body/developmental regulon in M. xanthus illustrating the regulatory points for lipid body production. Development begins with amino acid deprivation. Nla4, an enhancer binding protein, activates expression of relA (synthesis of (p)ppGpp) and initiates the stringent response [37]–[39]. Both mutants exhibit little shortening and little TAG accumulation (Figure 3). Sensing starvation initiates production of the A-signal, a quorum signal composed of specific amino acids designed to determine whether the cell density is sufficient for development [40]. E-signaling also begins about this time [23], [41].


Fatty acids from membrane lipids become incorporated into lipid bodies during Myxococcus xanthus differentiation.

Bhat S, Boynton TO, Pham D, Shimkets LJ - PLoS ONE (2014)

Regulation of lipid body production during M. xanthus fruiting body development.Mutants blocked in synthesis of proteins labeled in in black are deficient in lipid body synthesis (>40%). Those labeled in purple produce intermediate levels of lipid bodies (40–80%). Those in green produce near WT levels or higher (>80%). Red letters indicate developmental signals. Asg, A-signal; Csg, C-signal; Esg, E-signal.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4048283&req=5

pone-0099622-g005: Regulation of lipid body production during M. xanthus fruiting body development.Mutants blocked in synthesis of proteins labeled in in black are deficient in lipid body synthesis (>40%). Those labeled in purple produce intermediate levels of lipid bodies (40–80%). Those in green produce near WT levels or higher (>80%). Red letters indicate developmental signals. Asg, A-signal; Csg, C-signal; Esg, E-signal.
Mentions: Figure 5 provides a simplistic model of the lipid body/developmental regulon in M. xanthus illustrating the regulatory points for lipid body production. Development begins with amino acid deprivation. Nla4, an enhancer binding protein, activates expression of relA (synthesis of (p)ppGpp) and initiates the stringent response [37]–[39]. Both mutants exhibit little shortening and little TAG accumulation (Figure 3). Sensing starvation initiates production of the A-signal, a quorum signal composed of specific amino acids designed to determine whether the cell density is sufficient for development [40]. E-signaling also begins about this time [23], [41].

Bottom Line: Third, peripheral rods, developing cells that do not produce lipid bodies, fail to shorten.The lipid body regulon involves many developmental genes that are not specifically involved in fatty acid synthesis or degradation.MazF RNA interferase and its target, enhancer-binding protein Nla6, appear to negatively regulate cell shortening and TAG accumulation whereas most cell-cell signals activate these processes.

View Article: PubMed Central - PubMed

Affiliation: Department of Microbiology, University of Georgia, Athens, Georgia, United States of America.

ABSTRACT
Myxococcus xanthus responds to amino acid limitation by producing fruiting bodies containing dormant spores. During development, cells produce triacylglycerides in lipid bodies that become consumed during spore maturation. As the cells are starved to induce development, the production of triglycerides represents a counterintuitive metabolic switch. In this paper, lipid bodies were quantified in wild-type strain DK1622 and 33 developmental mutants at the cellular level by measuring the cross sectional area of the cell stained with the lipophilic dye Nile red. We provide five lines of evidence that triacylglycerides are derived from membrane phospholipids as cells shorten in length and then differentiate into myxospores. First, in wild type cells, lipid bodies appear early in development and their size increases concurrent with an 87% decline in membrane surface area. Second, developmental mutants blocked at different stages of shortening and differentiation accumulated lipid bodies proportionate with their cell length with a Pearson's correlation coefficient of 0.76. Third, peripheral rods, developing cells that do not produce lipid bodies, fail to shorten. Fourth, genes for fatty acid synthesis are down-regulated while genes for fatty acid degradation are up regulated. Finally, direct movement of fatty acids from membrane lipids in growing cells to lipid bodies in developing cells was observed by pulse labeling cells with palmitate. Recycling of lipids released by Programmed Cell Death appears not to be necessary for lipid body production as a fadL mutant was defective in fatty acid uptake but proficient in lipid body production. The lipid body regulon involves many developmental genes that are not specifically involved in fatty acid synthesis or degradation. MazF RNA interferase and its target, enhancer-binding protein Nla6, appear to negatively regulate cell shortening and TAG accumulation whereas most cell-cell signals activate these processes.

Show MeSH
Related in: MedlinePlus