The asgE locus is required for cell–cell signalling during Myxococcus xanthus development

In response to starvation, Myxococcus xanthus undergoes a multicellular developmental process that produces a dome‐shaped fruiting body structure filled with differentiated cells called myxospores. Two insertion mutants that block the final stages of fruiting body morphogenesis and reduce sporulatio...

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Veröffentlicht in:Molecular microbiology 2000-02, Vol.35 (4), p.812-824
Hauptverfasser: Garza, Anthony G., Harris, Baruch Z., Pollack, Jeffrey S., Singer, Mitchell
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creator Garza, Anthony G.
Harris, Baruch Z.
Pollack, Jeffrey S.
Singer, Mitchell
description In response to starvation, Myxococcus xanthus undergoes a multicellular developmental process that produces a dome‐shaped fruiting body structure filled with differentiated cells called myxospores. Two insertion mutants that block the final stages of fruiting body morphogenesis and reduce sporulation efficiency were isolated and characterized. DNA sequence analysis revealed that the chromosomal insertions are located in open reading frames ORF2 and asgE, which are separated by 68 bp. The sporulation defect of cells carrying the asgE insertion can be rescued phenotypically when co‐developed with wild‐type cells, whereas the sporulation efficiency of cells carrying the ORF2 insertion was not improved when mixed with wild‐type cells. Thus, the asgE insertion mutant appears to belong to a class of developmental mutants that are unable to produce cell–cell signals required for M. xanthus development, but they retain the ability to respond to them when they are provided by wild‐type cells. Several lines of evidence indicate that asgE cells fail to produce normal levels of A‐factor, a cell density signal. A‐factor consists of a mixture of heat‐stable amino acids and peptides, and at least two heat‐labile extracellular proteases. The asgE mutant yielded about 10‐fold less heat‐labile A‐factor and about twofold less heat‐stable A‐factor than wild‐type cells, suggesting that the primary defect of asgE cells is in the production or release of heat‐labile A‐factor.
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Two insertion mutants that block the final stages of fruiting body morphogenesis and reduce sporulation efficiency were isolated and characterized. DNA sequence analysis revealed that the chromosomal insertions are located in open reading frames ORF2 and asgE, which are separated by 68 bp. The sporulation defect of cells carrying the asgE insertion can be rescued phenotypically when co‐developed with wild‐type cells, whereas the sporulation efficiency of cells carrying the ORF2 insertion was not improved when mixed with wild‐type cells. Thus, the asgE insertion mutant appears to belong to a class of developmental mutants that are unable to produce cell–cell signals required for M. xanthus development, but they retain the ability to respond to them when they are provided by wild‐type cells. Several lines of evidence indicate that asgE cells fail to produce normal levels of A‐factor, a cell density signal. 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Two insertion mutants that block the final stages of fruiting body morphogenesis and reduce sporulation efficiency were isolated and characterized. DNA sequence analysis revealed that the chromosomal insertions are located in open reading frames ORF2 and asgE, which are separated by 68 bp. The sporulation defect of cells carrying the asgE insertion can be rescued phenotypically when co‐developed with wild‐type cells, whereas the sporulation efficiency of cells carrying the ORF2 insertion was not improved when mixed with wild‐type cells. Thus, the asgE insertion mutant appears to belong to a class of developmental mutants that are unable to produce cell–cell signals required for M. xanthus development, but they retain the ability to respond to them when they are provided by wild‐type cells. Several lines of evidence indicate that asgE cells fail to produce normal levels of A‐factor, a cell density signal. A‐factor consists of a mixture of heat‐stable amino acids and peptides, and at least two heat‐labile extracellular proteases. 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Two insertion mutants that block the final stages of fruiting body morphogenesis and reduce sporulation efficiency were isolated and characterized. DNA sequence analysis revealed that the chromosomal insertions are located in open reading frames ORF2 and asgE, which are separated by 68 bp. The sporulation defect of cells carrying the asgE insertion can be rescued phenotypically when co‐developed with wild‐type cells, whereas the sporulation efficiency of cells carrying the ORF2 insertion was not improved when mixed with wild‐type cells. Thus, the asgE insertion mutant appears to belong to a class of developmental mutants that are unable to produce cell–cell signals required for M. xanthus development, but they retain the ability to respond to them when they are provided by wild‐type cells. Several lines of evidence indicate that asgE cells fail to produce normal levels of A‐factor, a cell density signal. 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subjects A-factor
asgE gene
Bacterial Proteins - genetics
Bacterial Proteins - physiology
Culture Media - pharmacology
DNA, Bacterial - chemistry
DNA, Bacterial - genetics
Gene Expression Regulation, Bacterial - drug effects
Genetic Complementation Test - methods
Hot Temperature
Molecular Sequence Data
Morphogenesis - drug effects
Morphogenesis - genetics
Mutagenesis, Insertional
Myxococcus xanthus
Myxococcus xanthus - cytology
Myxococcus xanthus - genetics
Myxococcus xanthus - growth & development
Phenotype
Phosphotransferases
Pronase - pharmacology
Regulatory Sequences, Nucleic Acid
Sequence Analysis, DNA
Signal Transduction
title The asgE locus is required for cell–cell signalling during Myxococcus xanthus development
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