Cell Wall Deficient Forms

Mattman, Lida H.

doi:10.1201/b16928

Cited by 31 publications

(20 citation statements)

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“…Their emergence and occurrence has been reported for several Gram-positive and Gram-negative bacterial species. Although conversion to the L-form state may be considered a universal and widespread property of bacteria, it is only poorly understood [1] – [3] . Cell wall-deficiency may be induced in vitro, by exposure to sublethal doses of cell wall-active antibiotics such as β-lactams, but may also occur in vivo [4] .…”

Section: Introductionmentioning

confidence: 99%

Intracellular Vesicles as Reproduction Elements in Cell Wall-Deficient L-Form Bacteria

et al. 2012

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Cell wall-deficient bacteria, or L-forms, represent an extreme example of bacterial plasticity. Stable L-forms can multiply and propagate indefinitely in the absence of a cell wall. Data presented here are consistent with the model that intracellular vesicles in Listeria monocytogenes L-form cells represent the actual viable reproductive elements. First, small intracellular vesicles are formed along the mother cell cytoplasmic membrane, originating from local phospholipid accumulation. During growth, daughter vesicles incorporate a small volume of the cellular cytoplasm, and accumulate within volume-expanding mother cells. Confocal Raman microspectroscopy demonstrated the presence of nucleic acids and proteins in all intracellular vesicles, but only a fraction of which reveals metabolic activity. Following collapse of the mother cell and release of the daughter vesicles, they can establish their own membrane potential required for respiratory and metabolic processes. Premature depolarization of the surrounding membrane promotes activation of daughter cell metabolism prior to release. Based on genome resequencing of L-forms and comparison to the parental strain, we found no evidence for predisposing mutations that might be required for L-form transition. Further investigations revealed that propagation by intracellular budding not only occurs in Listeria species, but also in L-form cells generated from different Enterococcus species. From a more general viewpoint, this type of multiplication mechanism seems reminiscent of the physicochemical self-reproducing properties of abiotic lipid vesicles used to study the primordial reproduction pathways of putative prokaryotic precursor cells.

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Section: Introductionmentioning

confidence: 99%

Intracellular Vesicles as Reproduction Elements in Cell Wall-Deficient L-Form Bacteria

et al. 2012

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“…Although numerous publications exist characterizing their morphologies, growth requirements, and isolation from humans and animals with chronic infections [4], [9]–[11], the role of L-forms in disease has been difficult to ascertain. This, in part, is due to lack of understanding of the basic biology of L-forms and the circumstances favoring the transition of classical bacteria into L-forms.…”

Section: Introductionmentioning

confidence: 99%

“…Since their discovery by Emmy Klieneberger in 1935 [7] , L-forms, named in honor of the Lister Institute where she worked, have been suspected to be causative agents of disease underlying chronic and persistent infections [4] , [6] , [8] . Although numerous publications exist characterizing their morphologies, growth requirements, and isolation from humans and animals with chronic infections [4] , [9] – [11] , the role of L-forms in disease has been difficult to ascertain. This, in part, is due to lack of understanding of the basic biology of L-forms and the circumstances favoring the transition of classical bacteria into L-forms.…”

Section: Introductionmentioning

confidence: 99%

Insights into the Molecular Basis of L-Form Formation and Survival in Escherichia coli

2009

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L-forms have been shown to occur among many species of bacteria and are suspected to be involved in persistent infections. Since their discovery in 1935, numerous studies characterizing L-form morphology, growth, and pathogenic potential have been conducted. However, the molecular mechanisms underlying the formation and survival of L-forms remain unknown. Using unstable L-form colonies of Escherichia coli as a model, we performed genome-wide transcriptome analysis and screened a deletion mutant library to study the molecular mechanisms involved in formation and survival of L-forms. Microarray analysis of L-form versus classical colonies revealed many up-regulated genes of unknown function as well as multiple over-expressed stress pathways shared in common with persister cells and biofilms. Mutant screens identified three groups of mutants which displayed varying degrees of defects in L-form colony formation. Group 1 mutants, which showed the strongest defect in L-form colony formation, belonged to pathways involved in cell envelope stress, DNA repair, iron homeostasis, outer membrane biogenesis, and drug efflux/ABC transporters. Four (Group 1) mutants, rcsB, a positive response regulator of colanic acid capsule synthesis, ruvA, a recombinational junction binding protein, fur, a ferric uptake regulator and smpA a small membrane lipoprotein were selected for complementation. Complementation of the mutants using a high-copy overexpression vector failed, while utilization of a low-copy inducible vector successfully restored L-form formation. This work represents the first systematic genetic evaluation of genes and pathways involved in the formation and survival of unstable L-form bacteria. Our findings provide new insights into the molecular mechanisms underlying L-form formation and survival and have implications for understanding the emergence of antibiotic resistance, bacterial persistence and latent infections and designing novel drugs and vaccines.

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“…The period between 1882 and 1940, after Robert Koch discovered the cause of tuberculosis, was marked by series of papers reporting about the appearance of L-form elements in cultures of mycobacteria, such as filterable forms, branching filaments, syncytial growth, large spheres and "variegated mycelia", all of which characterize mycobacterial growth. Mattman summarized the known data about the ability of M. tuberculosis to convert to cell wall deficient forms and suggested a "L-cycle" for mycobacteria (Mattman et al, 1960;Mattman, , 2001.…”

Section: Historymentioning

confidence: 99%

“…existence without rigid walls, is universal but difficultly recognized phenomenon in nature (Domingue, 1982;Mattman, 2001;Prozorovski et al, 1981). The term "cell wall deficiency" implies alterations in the constitution of bacterial cell wall, resulting from deletion and faulty synthesis of wall components (Mattman, 2001). It is considered that imbalance of cells' ability to degrade and synthesize its classical thick wall results in cell wall deficiency.…”

Section: L-conversion Morphology and Ultrastructurementioning

confidence: 99%

Understanding Tuberculosis - Deciphering the Secret Life of the Bacilli

Cardona¹

2012

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Cell Wall Deficient Forms

Cited by 31 publications

References 0 publications

Intracellular Vesicles as Reproduction Elements in Cell Wall-Deficient L-Form Bacteria

Intracellular Vesicles as Reproduction Elements in Cell Wall-Deficient L-Form Bacteria

Insights into the Molecular Basis of L-Form Formation and Survival in Escherichia coli

Understanding Tuberculosis - Deciphering the Secret Life of the Bacilli

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