<i>Myxococcus xanthus dif</i>
            Genes Are Required for Biogenesis of Cell Surface Fibrils Essential for Social Gliding Motility

Yang, Zhaomin; Ma, Xiaoyuan; Tong, Lili; Kaplan, Heidi B.; Shimkets, Lawrence J.; Shi, Wenyuan

doi:10.1128/jb.182.20.5793-5798.2000

Cited by 122 publications

(175 citation statements)

References 42 publications

(71 reference statements)

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“…Four of these five genes, rfaA (MXAN4623), rfaB (MXAN4622), rfaC (MXAN4621), and wbgB (MXAN4619), are known to be required for LPS biosynthesis (Bowden and Kaplan 1998;Yang et al 2000a) (Figure 3, top). Also, one magellan-4 insertion interrupts MXAN4620, predicted to encode a hypothetical protein with unknown function.…”

Section: Resultsmentioning

confidence: 99%

Transposon Insertions ofmagellan-4That Impair Social Gliding Motility inMyxococcus xanthus

Youderian

Hartzell

2006

Genetics

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Myxococcus xanthus has two different mechanisms of motility, adventurous (A) motility, which permits individual cells to glide over solid surfaces, and social (S) motility, which permits groups of cells to glide. To identify the genes involved in S-gliding motility, we mutagenized a DaglU (A ÿ ) strain with the defective transposon, magellan-4, and screened for S ÿ mutants that form nonmotile colonies. Sequence analysis of the sites of the magellan-4 insertions in these mutants and the alignment of these sites with the M. xanthus genome sequence show that two-thirds of these insertions lie within 27 of the 37 nonessential genes known to be required for social motility, including those necessary for the biogenesis of type IV pili, exopolysaccharide, and lipopolysaccharide. The remaining insertions also identify 31 new, nonessential genes predicted to encode both structural and regulatory determinants of S motility. These include three tetratricopeptide repeat proteins, several regulators of transcription that may control the expression of genes involved in pilus extension and retraction, and additional enzymes involved in polysaccharide metabolism. Three insertions that abolish S motility lie within genes predicted to encode glycolytic enzymes, suggesting that the signal for pilus retraction may be a simple product of exopolysaccharide catabolism.

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Section: Resultsmentioning

confidence: 99%

Transposon Insertions ofmagellan-4That Impair Social Gliding Motility inMyxococcus xanthus

Youderian

Hartzell

2006

Genetics

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“…To distinguish between these two possibilities, PilA-A32V was introduced into a DpilA DdifA double mutation background. In the DdifA background, all assembled pili remain on the cell surface because the cells are defective in EPS production and therefore lack the trigger for retraction (Yang et al, 1998(Yang et al, , 2000. The addition of purified EPS from wild-type cells or the EPS analogue chitin was found to trigger TFP retraction and abolish the overpiliation phenotype (Li et al, 2003).…”

Section: A32v Tfp Has Eps-binding Ability But Is Unable To Retractmentioning

confidence: 99%

Alanine 32 in PilA is important for PilA stability and type IV pili function in Myxococcus xanthus

Yang

Chen

et al. 2011

Microbiology

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Type IV pili (TFP) are membrane-anchored filaments with a number of important biological functions. In the model organism Myxococcus xanthus, TFP act as molecular engines that power social (S) motility through cycles of extension and retraction. TFP filaments consist of several thousand copies of a protein called PilA or pilin. PilA contains an N-terminal α-helix essential for TFP assembly and a C-terminal globular domain important for its activity. The role of the PilA sequence and its structure–function relationship in TFP-dependent S motility remain active areas of research. In this study, we identified an M. xanthus PilA mutant carrying an alanine to valine substitution at position 32 in the α-helix, which produced structurally intact but retraction-defective TFP. Characterization of this mutant and additional single-residue variants at this position in PilA demonstrated the critical role of alanine 32 in PilA stability, TFP assembly and retraction.

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“…2, Right). To eliminate the possibility that stimulation was caused by extracellular complementation of exopolysaccharide (EPS) molecules, we tested whether a dsp/dif mutant, which is defective in EPS production (25,26), could be stimulated for motility. Using the same procedure, we observed that motility was not stimulated in this strain (Fig.…”

Section: Ome Rescues the Motility And Development Of O-antigen Mutantsmentioning

confidence: 99%

Cell rejuvenation and social behaviors promoted by LPS exchange in myxobacteria

Vassallo

Pathak

Cao

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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Bacterial cells in their native environments must cope with factors that compromise the integrity of the cell. The mechanisms of coping with damage in a social or multicellular context are poorly understood. Here we investigated how a model social bacterium, Myxococcus xanthus, approaches this problem. We focused on the social behavior of outer membrane exchange (OME), in which cells transiently fuse and exchange their outer membrane (OM) contents. This behavior requires TraA, a homophilic cell surface receptor that identifies kin based on similarities in a polymorphic region, and the TraB cohort protein. As observed by electron microscopy, TraAB overexpression catalyzed a prefusion OM junction between cells. We then showed that damage sustained by the OM of one population was repaired by OME with a healthy population. Specifically, LPS mutants that were defective in motility and sporulation were rescued by OME with healthy donors. In addition, a mutant with a conditional lethal mutation in lpxC, an essential gene required for lipid A biosynthesis, was rescued by Tradependent interactions with a healthy population. Furthermore, lpxC cells with damaged OMs, which were more susceptible to antibiotics, had resistance conferred to them by OME with healthy donors. We also show that OME has beneficial fitness consequences to all cells. Here, in merged populations of damaged and healthy cells, OME catalyzed a dilution of OM damage, increasing developmental sporulation outcomes of the combined population by allowing it to reach a threshold density. We propose that OME is a mechanism that myxobacteria use to overcome cell damage and to transition to a multicellular organism.Myxococcus xanthus | outer membrane | lipopolysaccharide | lpxC | fusion A fundamental question in biology is how cells cope with damage. Microbes occupy diverse habitats fraught with physical, biological, and chemical insults (1, 2). UV radiation, desiccation, predation, extracellular enzymes, antimicrobial compounds, pH, temperature, and osmolarity changes are all stresses to the individual cell. In addition, when cells are in nutrient-poor environments, cell division can be rare, taking days to months to complete (3). In a slow-growing state, cell-surface components that may not be undergoing active repair can accumulate damage through natural aging processes such as oxidation (4, 5) and protein denaturation. Although internal cell stress response pathways are known (6), mechanisms to cope with cell surface damage are less well understood.Although cell damage threatens the fitness of the individual, social organisms have strength in numbers. The strategy of kin selection allows evolutionarily viable cooperation between individuals in a closely related population (7). Communication between individuals and sharing of resources establishes the potential for assistance between individual population members. Social support can be beneficial when the fitness of individuals in a group depends on collaborative behaviors such as prey hunting or the developm...

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Myxococcus xanthus dif Genes Are Required for Biogenesis of Cell Surface Fibrils Essential for Social Gliding Motility

Cited by 122 publications

References 42 publications

Transposon Insertions ofmagellan-4That Impair Social Gliding Motility inMyxococcus xanthus

Transposon Insertions ofmagellan-4That Impair Social Gliding Motility inMyxococcus xanthus

Alanine 32 in PilA is important for PilA stability and type IV pili function in Myxococcus xanthus

Cell rejuvenation and social behaviors promoted by LPS exchange in myxobacteria

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