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Abstracts 1985-199129. Dworkin M; Kaiser D. (1985) Cell interactions in myxobacterial growth and development. Science 230:18-24. (UI: 85300525) During their complex life cycle, myxobacteria manifest a number of cell interactions. These include contact-mediated interactions as well as those mediated by soluble extracellular signals. Some of these interactions are well-defined; in addition, the tools for molecular and genetic analysis of these interactions in Myxococcus xanthus are now available. 30. Kaiser D; Kroos L; Kuspa A. (1985) Cell interactions govern the temporal pattern of Myxococcus development. Cold Spring Harbor Symp Quant Biol 50:823-30. (UI: 86163041)
31. Kroos L; Kuspa A; Kaiser D. (1986) A global analysis of developmentally regulated genes in Myxococcus xanthus. Dev Biol 117(1):252-66. (UI: 86301515) Tn5 lac is a transposon that fuses the transcription of lacZ to exogenous promoters. We generated 2374 Tn5 lac insertion-containing strains of Myxococcus xanthus, a soil bacterium that undergoes multicellular development which culminates in the formation of spores. Thirty-six strains were identified that specifically increase beta-galactosidase expression at some particular time during development and these expression times range from minutes after starvation initiates development to 24 hr, when sporulation begins. Different maximum levels of beta-galactosidase expression were also observed and the maximum for many strains that begin beta-galactosidase expression late in development was observed only if spores were disrupted. Seven of the 36 strains display mild to severe defects in aggregation and/or sporulation, as did an additional five strains whose beta-galactosidase expression was not developmentally regulated. Restriction maps of the DNA adjacent to the Tn5 lac insertions that are developmentally regulated and/or cause developmental defects show that most of the 41 insertions are in different regions of the Myxococcus genome. The developmentally regulated Tn5 lac insertions described here provide a set of at least 29 new developmental markers for Myxococcus. 32. Kuspa A; Kroos L; Kaiser D. (1986) Intercellular signaling is required for developmental gene expression in Myxococcus xanthus. Dev Biol 117:267-76. (UI: 86301516) Certain developmental mutants of Myxococcus xanthus can be complemented (extracellularly) by wild-type cells. Insertions of Tn5 lac (a transposon which couples beta-galactosidase expression to exogenous promoters) into developmentally regulated genes were used to investigate extracellular complementation of the A group mutations. A- mutations reduced developmental beta-galactosidase expression from 18 of 21 Tn5 lac insertions tested and that expression was restored to A- Tn5 lac cells by adding wild-type cells. The earliest A-dependent Tn5 lac normally expresses beta-galactosidase at 1.5 hr of development indicating a developmental block at 1-2 hr in A- mutants. A substance which can rescue the expression of this early Tn5 lac is released by wild-type (A+) but not by A- cells. This substance appears in a cell-free wash of wild-type cells or in starvation buffer conditioned by wild-type cells 1-2 hr after development is initiated. The conditioned starvation buffer also restores normal morphological development to an A- mutant. 33. Kaiser D. (1986) Control of multicellular development: Dictyostelium and Myxococcus. Ann Rev Genet 20:539-66. (UI: 87126684)
34. Stephens K; Kaiser, D. (1987). Genetics of gliding motility in Myxococcus xanthus: molecular cloning of the mgl locus. Mol Gen Genet 207:256-66. 35. Kroos L; Kaiser D. (1987) Expression of many developmentally regulated genes in Myxococcus depends on a sequence of cell interactions. Genes and Devel 1:840-54. (UI: 88112825) Certain developmental mutants of Myxococcus xanthus can be complemented extracellularly by wild-type cells. These mutants behave as if they are defective in cell-cell interactions that are required for development. There may be several different interactions because the mutants belong to four extracellular complementation groups (A, B, C, and D). We report here that B- and C- mutations change the pattern of gene expression during Myxococcus development as detected by transcriptional fusions to lacZ mediated by Tn5 lac. The mutant C locus reduced or abolished developmental beta-galactosidase expression from 15 lac fusions that normally begin to be expressed in wild-type cells after 6 hr of development. Expression of these C-dependent lac fusions was restored to C- mutants by adding wild-type cells. The C- mutation did not affect the expression of 10 lac fusions that normally begin to be expressed before 6 hr of development, indicating that the C-mediated cell-cell interaction is required beginning at about 6 hr of development. Cells require the B+ function very early in development because a B- mutation reduced or abolished developmental beta-galactosidase expression from all 26 lac fusions tested, including some that normally begin to be expressed at the onset of development. In a C- mutant and in a B- mutant, some lac fusions responded with reduced beta-galactosidase expression, whereas other fusions, which would normally begin beta-galactosidase expression at about the same time during development, expressed no beta-galactosidase, indicating that developmental genes within a given temporal class display different sensitivities to the absence of cell-cell interactions. Requirements for B+ and C+ function, as well as the previously described A+ function, appear to lie on the same developmental pathway.
36. Kroos L; Hartzell P; Stephens K; Kaiser D. (1988) A link between cell movement and gene expression argues that motility is required for cell-cell signaling during fruiting body development. Genes and Devel 2:1677-85. (UI: 89108001) Nonmotile mutants of Myxococcus xanthus (Myxobacterales) failed to execute the morphogenetic movements required to shape a fruiting body. In addition, nonmotile mutants produced very few spores when plated for fruiting body development at cell densities appropriate for wild-type cells. At higher initial cell densities, the proportion of nonmotile cells that sporulate increased, indicating that one important function of motility in fruiting body development is to increase the local cell density. However, even at 10 times normal cell density, nonmotile cells sporulated at only 1% the wild-type level. This sporulation deficiency of nonmotile mutants accompanies an altered pattern of gene expression, monitored by using transcriptional fusions of lacZ to genes expressed at specific times during fruiting body development. Motility was not required for normal expression of five lac fusions that are expressed within the first 6 hr of fruiting-body development. However, the levels of expression from five lac fusions to later-expressed genes were reduced or abolished in nonmotile strains. beta-Galactosidase expression in these late Tn5 lac insertions was increased, and fruiting body development occurred in certain nonmotile strains that can be stimulated to move when mixed with a donor strain. This shows that motility itself is required because the stimulated cells are nonmotile genotypically. The nonmotile mutations had the same effect on developmental beta-galactosidase expression from these 10 lac fusions as an insertion mutation in the csg (formerly spoC) gene. csg mutants have a cell-cell interaction defect that blocks fruiting body development at approximately 6 hr. The similarity in the pattern of developmental expression of motility mutants and csg mutants suggests that motility is required for this csg-mediated cell-cell interaction.
37. Stephens K; Hartzell P; Kaiser D. (1989) Gliding motility in Myxococcus xanthus: mgl locus, RNA, and predicted protein products. J Bacteriol 171:819-30. (UI: 89123159) Mutants of Myxococcus xanthus that had lost the ability to glide were examined to elucidate the mechanism of gliding motility. Nonmotile mutants resulting from a single mutational step were all defective at the same locus, mgl, which implied an important role for the mgl product(s) in gliding. Deletion experiments, transposon insertion mutagenesis, and genetic rescue of mgl mutants mapped the locus to a 1.6-kilobase segment of Myxococcus DNA. Two species of RNA that hybridized with mgl DNA were found both during vegetative growth and during the starvation-induced development of fruiting bodies, which also requires cell movement. The two RNA species, of 1.5 and 1.3 kilobases, had the same 5' to 3' orientation and overlapped extensively. The DNA sequences of mgl+ and of seven mgl mutants were determined. Each mutant differed from mgl+ by a single-base-pair change in the sequence. Two adjacent open reading frames were found in the sequence hybridizing to both species of mgl RNA. Six of the single-base-pair changes, each of which would result in a single-amino-acid change, and an insertion-produced mgl mutation were located in the downstream open reading frame. This open reading frame (of 195 amino acids) is therefore an mgl gene, called mglA. The function of the upstream open reading frame is not known with certainty, although it does contain one of the mgl mutant sites and could be a second mgl gene. 38. Kaiser D. (1989) Multicellular development in Myxobacteria. In D.A. Hopwood and K.F. Chater (eds.), Genetics of Bacterial Diversity (London: Harcourt Brace), pp. 243-63. 39. Kuspa A; Kaiser D. (1989) Genes required for developmental signalling in Myxococcus xanthus: three asg loci. J Bacteriol 171:2762-72. (UI: 89213968) asg-carrying strains of Myxococcus xanthus arose in a selection for mutants defective in cell-cell signalling during fruiting body development. All 15 asg mutations examined were found to lie in one of three genetic loci, asgA, asgB, or asgC. The loci were defined by linkage to different insertions of transposon Tn5 and molecular cloning of asgA. asg mutants of all three types were deficient in the aggregation of cells into mounds of the sort that normally give rise to fruiting bodies. asg mutants were also deficient in spore formation; sporulation is normally one of the last steps in fruiting body development. Consistent with a requirement for cell-to-cell signalling, at 1 to 2 h asg+-carrying cells release a material called A-factor that can rescue development of asg mutants. asgA, asgB, and asgC mutants released 5% or less of the asg+ level of A-factor, as measured by bioassay. The experimental results are consistent with the hypothesis that a deficiency in A-factor production or release is the primary developmental defect in asg mutants and that aggregation and sporulation depend on A-factor. asg mutations at all three loci also changed the color and morphology of growing colonies, and failure to release A-factor may itself arise from a defect in growing cells. 40. Mayo KA; Kaiser D. (1989) asgB, a gene required early for developmental signalling, aggregation, and sporulation of Myxococcus xanthus. Mol Gen Genet 218:409-18. (UI: 90066344) The asgB genetic locus of Myxococcus xanthus specifies a function which is required early in the developmental pathway leading to aggregation and sporulation in fruiting bodies. The developmental defect of asgB mutants can be compensated by extracellular complementation using either intact wild-type cells or cell-free supernatants conditioned by developing wild-type cells. A Tn5 insertion was isolated closely linked to asgB480 and facilitated the cloning of both the wild-type (asgB+) and the mutant (asgB480) alleles in Escherichia coli plasmid. Tandem duplications of the asgB locus were constructed in M. xanthus; the completely wild-type phenotype of asgB+/asgB480 partial diploids implies that the asgB480 allele is recessive. This finding, along with extracellular complementation by wild-type cells, is consistent with the hypothesis that the asgB+ locus is required to produce a substance with an intercellular signalling function. At least part of the asgB gene was found to lie within a 1.2 kb SmaI DNA fragment. This 1.2 kb fragment, as well as smaller fragments derived from it, were used as DNA probes in RNA/DNA hybrid analyses of transcription in the asgB region. Two small mRNA species were detected, one about 650 bp long, and the other about 500 bp; the two species of mRNAs apparently overlap. Both mRNAs are present in low, but approximately equal amounts, in vegetatively growing cells. This is consistent with the observation that asg mutants display a mutant vegetative phenotype (a change in colony color and spreading behavior) as well as defective development. 41. Cheng Y; Kaiser D. (1989) dsg, a gene required for cell-cell interaction early in Myxococcus development. J Bacteriol 171:3719-26. (UI: 89291715) dsg mutants of Myxococcus xanthus are conditionally defective in fruiting body development, including sporulation. Unable to develop on their own, these mutants can assemble fruiting bodies with spores if they are mixed with wild-type cells. To elucidate the developmental defect in dsg mutants by close comparison with wild type, such mutants have been backcrossed by transduction, using a closely linked insertion of transposon Tn5 for selection. Backcrossed dsg mutants form aggregates that are larger, less compact, and less symmetrical than dsg+ fruiting bodies. Also, the starvation-induced sporulation in dsg aggregates is delayed and reduced. However, dsg mutants can be induced by glycerol or dimethyl sulfoxide to sporulate at levels approaching those of wild type. dsg mutants may thus have a primary defect early in development which diminishes their capacity to aggregate and which indirectly decreases the number of fruiting body spores. The linked insertion of Tn5 also facilitated cloning the dsg gene. The cloned dsg+ allele was shown to be dominant to both the dsg-429 and dsg-439 alleles, and both mutant alleles were shown to belong to the same genetic complementation group. Subcloning of restriction fragments, deletions, and insertions of transposon Tn5 agree in locating the dsg gene to an 850-base-pair segment of the cloned region. 42. Cheng Y; Kaiser D. (1989) dsg, a gene required for Myxococcus development, is necessary for cell viability. J Bacteriol 171:3727-31. (UI: 89291716) Previous work identified the dsg gene as necessary for cell-cell interaction in Myxococcus xanthus. Point mutations of this gene, such as dsg-439, are viable, but insertions of Tn5 within the dsg gene (dsg::Tn5) are lethal. Partial diploids, dsg::Tn5/dsg+ or dsg::Tn5/dsg-429 or dsg::Tn5/dsg-439, are also viable, showing that the lethal effect of the haploid insertions is due to loss of function. Thus the evidence implies that the dsg gene is essential for viability as well as development, but its essential quality differs between growth and development because dsg-429 and dsg-439 mutants grow normally, but are unable to develop. 43. Kuspa A; Vollrath D; Cheng Y; Kaiser D. (1989) Physical mapping of the Myxococcus xanthus genome by random cloning in yeast artificial chromosomes. Proc Natl Acad Sci (USA) 86:8917-21. (UI: 90046900) Random segments of Myxococcus xanthus DNA were cloned in yeast artificial chromosomes (YACs) to construct a physical map of the genome. EcoRI restriction maps of 409 YAC clones with inserts averaging 111 kilobase pairs (kb) were determined. Comparison to the map of a 300-kb region of M. xanthus obtained from clones in Escherichia coli indicates that segments of DNA cloned in YACs are stably maintained in yeast and that their sequences accurately reflect the structure of the Myxococcus genome. The 409 YAC inserts were ordered within 60 map segments (contigs) by aligning their EcoRI restriction maps and by hybridization with 18 gene-specific DNA probes. These 60 map segments may represent the entire Myxococcus genome and could be used to organize its genetic information. This study illustrates the utility of YACs for cloning large segments of DNA and for reliable long-range genomic mapping.
44. Kroos L; Kuspa A; Kaiser D. (1990) Defects in fruiting body development caused by Tn5 lac insertions in Myxococcus xanthus. J Bacteriol 172:484-7. (UI: 90094261) Mutations caused by insertions of Tn5 lac that block development are rare. At least six of the eight mutations examined appeared to be regulatory. Three of these were found to disrupt social motility, suggesting a particular importance for this function. One other occurred in a known cell-cell interaction gene, bsgA, and the remaining two were located in genes operative early in the developmental program. 45. Kim SK; Kaiser D. (1990) C-factor: a cell-cell signaling protein required for fruiting body morphogenesis of M. xanthus. Cell 61:19-26. (UI: 90199893) During fruiting body development, the product of the csgA gene is necessary for cellular aggregation, for spore differentiation, and for gene expression that is initiated after 6 hr of starvation. From nascent wild-type fruiting bodies we have purified a polypeptide of 17 kd called C-factor, which, at approximately 1 to 2 nM, restores normal development to csgA mutant cells. C-factor activity is not recovered from extracts of unstarved, growing cells or csgA mutant cells. The amino acid sequence from purified C-factor demonstrates that it is the product of the csgA gene. C-factor is active over a narrow range of concentration and has properties of a morphogenetic paracrine signal. 46. Kim SK; Kaiser D. (1990) Purification and properties of Myxococcus xanthus C-factor, an intercellular signaling protein. Proc Natl Acad Sci (USA) 87:3635-9. (UI: 90251611) C-factor, a Myxococcus xanthus protein that restores the developmental defects of a class of nonautonomous mutants resulting from mutation of the csgA gene, has been purified approximately 1000-fold from starved wild-type cells. The monomeric form of C-factor is a single polypeptide with a molecular mass of 17 kDa that can be solubilized by detergent from membrane components. Characterization by gel filtration and denaturing gel electrophoresis suggests that biologically active C-factor is a dimer composed of two 17-kDa monomers. Antibodies against a form of the M. xanthus csgA gene product overexpressed in Escherichia coli react with purified C-factor. 47. Kim SK; Kaiser D. (1990) Cell motility is required for the transmission of C-factor, an intercellular signal that coordinates fruiting body morphogenesis of Myxococcus xanthus. Genes and Devel 4:896-904. (UI: 90346289) There are striking similarities between the developmental phenotypes of two different mutant classes of Myxococcus xanthus. The first class, mglA mutants, are nonmotile under all conditions tested. The second class, csgA mutants, are motile but belong to a class of signal-defective developmental mutants that cannot develop alone but will develop when mixed with intact wild-type cells. Nevertheless, both csgA and mglA mutants fail to aggregate properly or to sporulate when induced to form fruiting bodies. An mglA mutation and a csgA mutation affect expression of a panel of lacZ fusions to developmental genes in the same way, indicating that nonmotile cells and csgA cells arrest development at a similar stage. One explanation for the similarity of developmental phenotypes between these mutants is that motility is required for the csgA-mediated cell interaction. In support of this hypothesis, we report that C-factor, a protein purified from nascent wild-type fruiting bodies based on its ability to rescue csgA mutant fruiting body development, also rescues sporulation and expression of beta-galactosidase from developmentally controlled lacZ fusions in mglA strains, apparently without restoring their motility. Wild-type levels of active C-factor can be purified from mglA cells, yet intact mglA cells do not rescue csgA cells upon cell-cell mixing. Intact wild-type cells are unable to restore the sporulation and beta-galactosidase expression of mglA mutants. These results support the hypothesis that donor and responder cell motility is required for C-factor transmission between cells during development.(ABSTRACT TRUNCATED AT 250 WORDS) 48. Kim SK; Kaiser D. (1990) Cell alignment required in differentiation of Myxococcus xanthus. Science 249:926-8. (UI: 90364414) During fruiting body morphogenesis of Myxococcus xanthus, cell movement is required for transmission of C-factor, a short range intercellular signaling protein necessary for sporulation and developmental gene expression. Nonmotile cells fail to sporulate and to express C-factor-dependent genes, but both defects were rescued by a simple manipulation of cell position that oriented the cells in aligned, parallel groups. A similar pattern of aligned cells normally results from coordinated recruitment of wildtype cells into multicellular aggregates, which later form mature fruiting bodies. It is proposed that directed cell movement establishes critical contacts between adjacent cells, which are required for efficient intercellular C-factor transmission.
49. Kaplan HB; Kuspa A; Kaiser D. (1991) Suppressors that permit A-signal-independent developmental gene expression in Myxococcus xanthus. J Bacteriol 173:1460-70. (UI: 91139588) Progression through the early stages of Myxococcus xanthus fruiting body development requires the cell-to-cell transmission of soluble material called A signal. During these early stages, expression from the gene identified by Tn5 lac insertion omega 4521 increases. A DNA probe of the omega 4521 gene was constructed. Use of this probe showed that accumulation of mRNA corresponding to the omega 4521 gene depends upon A signal. A-signal-deficient (asg) mutants fail to accumulate this RNA, and the external addition of A signal restores accumulation. To identify links between A signal and its responsive gene, omega 4521, suppressors of an asg mutation were generated. All of the suppressor alleles restored lacZ expression from omega 4521 in the absence of A signal, and they were demonstrated to be neither reversions of the asgB mutation nor mutations in the promoter of omega 4521. Fifteen suppressor mutations map to two loci, sasA and sasB (for suppressor of asg). sasA and sasB mutants differ phenotypically during growth and development. Mid-logarithmic-phase sasA asgB double mutants, like sas+ asg+ strains, express low levels of lacZ, whereas sasB asgB double mutants express high levels. sasA asg+ mutants form abnormal colonies, are less cohesive than wild type, and are defective in fruiting body formation and sporulation. In contrast, sasB asg+ mutants form normal colonies, are as cohesive as wild type, and appear to develop normally. The characteristics of sasA suppressors implicate the sasA+ product as a negative regulator in the A-signal-dependent regulation of omega 4521. 50. Kim SK; Kaiser D. (1991) C-factor has distinct aggregation and sporulation thresholds during Myxococcus development. J Bacteriol 173:1722-8. (UI: 91154128) C-factor, the protein product of the csgA gene, acts as a short-range morphogenetic signal. It is required for fruiting body development of the gram-negative bacterium Myxococcus xanthus. Aggregation, sporulation, and expression of a set of genes that are C-factor dependent, all of which fail in csgA mutant cells, are completely restored by addition of purified C-factor. We report here that, depending on its concentration, C-factor can elicit two distinct morphogenetic and transcriptional responses from csgA cells. Low levels of C-factor bring about aggregation and expression of an early C-dependent gene, whereas higher levels lead to the same effects plus expression of a late C-dependent gene and spore formation. C-factor positively regulates its own transcription. An approximately fourfold net increase in csgA transcription and C-factor levels during development was measured. We propose that autoregulation and the two distinct activity thresholds allow C-factor to act as a timer, first triggering aggregation, then sporulation, thereby producing the appropriate developmental order. 51. Kimsey HH; Kaiser D. (1991) Targeted disruption of the Myxococcus xanthus orotidine 5'-monophosphate decarboxylase gene: effects on growth and fruiting-body development. J Bacteriol 173:6790-7. (UI: 92041561) The Myxococcus xanthus gene coding for orotidine 5'-monophosphate (OMP) decarboxylase (EC 4.1.1.23) was cloned. The M. xanthus uraA gene efficiently complemented an Escherichia coli OMP decarboxylase mutant, permitting it to grow in the absence of uracil. Electroporation of M. xanthus with a circular plasmid carrying a selectable uraA::kan gene disruption resulted in homologous recombination at the chromosomal uraA locus. Chromosomal integration of the gene disruption plasmid created heterozygous (uraA+/uraA::kan) tandem duplications. These tandem duplications were unstable and segregated auxotrophic uraA::kan daughters at frequencies of 2 x 10(-4) to 8 x 10(-4) per viable cell. Rare uraA::kan segregants were easily obtained by selecting for resistance to the toxic analog 5-fluoroorotic acid. Our experiments suggest that the cloned uraA gene could facilitate the use of gene duplications in the genetic analysis of M. xanthus development. The uraA mutants could utilize uracil, uridine, or uridine 5'-phosphate for growth, indicating that M. xanthus has pyrimidine salvage pathways. During multicellular development, uraA::kan gene disruption mutants sporulated to wild-type levels but formed smaller and more numerous aggregates than did their uraA+ parent, regardless of whether uracil was added to the medium. Pyrimidine deprivation of uraA mutants, under conditions that otherwise supported vegetative growth, failed to induce fruiting-body development or sporulation. 52. Hartzell P; Kaiser D. (1991) Function of MglA, a 22-kilodalton protein essential for gliding in Myxococcus xanthus. J Bacteriol 173:7615-24. (UI: 92041675) Single mutations in the mglA gene in Myxococcus xanthus render cells incapable of gliding. The mglA strains are unique in that all other nonmotile strains of M. xanthus isolated are the result of at least two independent mutations in separate motility system genes. Translational fusions of trpE, or of lacZ, to mglA were constructed, and the resulting fusion polypeptides were used to generate antibodies. Antibodies specific to MglA protein were purified. Antibody-tagged MglA was found localized to the cytoplasm of M. xanthus cells both by fractionation of cell extracts and by electron microscopy of thin sections of whole cells. Four of the five mglA missense mutants tested failed to produce detectable levels of the MglA antigen in whole cell extracts. Nonmotile double mutants (A-S-), which have one mutation in a gene of system A and one mutation in a gene of system S, have the same phenotype as null mglA mutants but produce wild-type levels of MglA protein. MglA protein is conserved in all strains of myxobacteria tested. The amino acid sequence of MglA protein includes three sequence motifs characteristic of GDP/GTP-binding proteins. On the basis of its genetic properties, intracellular location, and amino acid sequence, it is argued that MglA protein is a regulator in the sequence of functions leading to cell movement. 53. Hartzell P; Kaiser D. (1991) Upstream gene of the mgl operon controls the level of MglA protein in Myxococcus xanthus. J Bacteriol 173:7625-35. (UI: 92041676) The mgl operon contains two open reading frames (ORFs) which are transcribed together. A collection of nonmotile mutants helped to define the downstream ORF as the mglA gene. Single mutations at the mglA locus completely abolish motility. A series of deletion mutations was constructed to determine the role of the upstream ORF (now called mglB). A strain carrying a deletion in mglB and with an intact mglA produces small colonies. The cells are motile, but their rate of swarm spreading is reduced. Measurements of cell movement showed that mglB mutant cells advanced, on average, less than 0.1 cell length in 5 min. The mglB+ cells advanced an average of 1.3 cell lengths in the same time. Extracts of delta mglB cells contain 15 to 20% as much of the 22-kDa MglA protein as do mglB+ cells, as measured in Western immunoblots and enzyme-linked immunosorbent assays. However, the amount of mgl transcript is the same in the delta mglB mutants as in the mglB+ strain. Heterozygous partial diploids mglB/mglA with the wild-type alleles in trans have normal motility, demonstrating that the largest of the mglB deletions is not polar on mglA. Like other motility defects, a delta mglB mutation alters fruiting body development and sporulation. The mglB mutants delayed aggregation, produced small immature fruiting bodies, and sporulated at 45 to 50% wild-type levels. All aspects of the mglB mutant phenotype are explained by the reduced levels of mglA protein and the assumption that it limits the amount of gliding. 54. Kim SK. (1991) Intercellular signaling in Myxococcus development: the role of C factor. Trends in Genetics. 7:361-5. 55. Kaiser D. Genetic systems in myxobacteria. Methods in Enzymology, 1991, 204:357-72. (UI: 92048618)
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