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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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Lipid body area correlates with cell length in developmental mutants.Lipid body production at 18table 1.
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pone-0099622-g003: Lipid body area correlates with cell length in developmental mutants.Lipid body production at 18table 1.

Mentions: If cell shortening and lipid body production are obligately coupled, then mutants defective in cell shortening should also be defective in lipid body production. We examined over 30 developmental mutants at 18 h, the peak of lipid body production in wild type cells. The mutant set includes most of the commonly studied developmental mutants known to have defects in fruiting body morphogenesis, myxospore differentiation, or both. Lipid body area per cell was averaged from 30 cells at 18 hours of development. The mutants show a wide range of variability from 0% to nearly 140% of wild type levels (Table 1). Average cell length was also calculated for these cells (Table 1). The mutant set reflects a continuum in shape change including those that fail to decrease cell length, those that initiate cell shortening, and those that shorten and ultimately sporulate despite delayed timing. A plot of lipid body area vs. cell length at 18 h shows that lipid body area increases as cell length declines over much of the mutant set (Figure 3). The line describing the best fit to the entire mutant collection passes through the standard deviations for WT cells. The Pearson's correlation coefficient between cell length and lipid body area for the entire mutant collection is 0.76. These results argue that for most mutants, cell length is proportional to lipid body content regardless of the stage at which the mutants are blocked.


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)

Lipid body area correlates with cell length in developmental mutants.Lipid body production at 18table 1.
© Copyright Policy
Related In: Results  -  Collection

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

pone-0099622-g003: Lipid body area correlates with cell length in developmental mutants.Lipid body production at 18table 1.
Mentions: If cell shortening and lipid body production are obligately coupled, then mutants defective in cell shortening should also be defective in lipid body production. We examined over 30 developmental mutants at 18 h, the peak of lipid body production in wild type cells. The mutant set includes most of the commonly studied developmental mutants known to have defects in fruiting body morphogenesis, myxospore differentiation, or both. Lipid body area per cell was averaged from 30 cells at 18 hours of development. The mutants show a wide range of variability from 0% to nearly 140% of wild type levels (Table 1). Average cell length was also calculated for these cells (Table 1). The mutant set reflects a continuum in shape change including those that fail to decrease cell length, those that initiate cell shortening, and those that shorten and ultimately sporulate despite delayed timing. A plot of lipid body area vs. cell length at 18 h shows that lipid body area increases as cell length declines over much of the mutant set (Figure 3). The line describing the best fit to the entire mutant collection passes through the standard deviations for WT cells. The Pearson's correlation coefficient between cell length and lipid body area for the entire mutant collection is 0.76. These results argue that for most mutants, cell length is proportional to lipid body content regardless of the stage at which the mutants are blocked.

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