scholarly journals The evolution of spherical cell shape; progress and perspective

2019 ◽  
Vol 47 (6) ◽  
pp. 1621-1634 ◽  
Author(s):  
Paul Richard Jesena Yulo ◽  
Heather Lyn Hendrickson
Keyword(s):  
Cell Wall ◽  
Bacterial Cell ◽  
Cell Shape ◽  
Shape Change ◽  
Spherical Cell ◽  
Shape Evolution ◽  
Penicillin Binding Proteins ◽  
Cell Shape Change ◽  
Peptidoglycan Cell Wall ◽  
Bacterial Cell Shape

Bacterial cell shape is a key trait governing the extracellular and intracellular factors of bacterial life. Rod-like cell shape appears to be original which implies that the cell wall, division, and rod-like shape came together in ancient bacteria and that the myriad of shapes observed in extant bacteria have evolved from this ancestral shape. In order to understand its evolution, we must first understand how this trait is actively maintained through the construction and maintenance of the peptidoglycan cell wall. The proteins that are primarily responsible for cell shape are therefore the elements of the bacterial cytoskeleton, principally FtsZ, MreB, and the penicillin-binding proteins. MreB is particularly relevant in the transition between rod-like and spherical cell shape as it is often (but not always) lost early in the process. Here we will highlight what is known of this particular transition in cell shape and how it affects fitness before giving a brief perspective on what will be required in order to progress the field of cell shape evolution from a purely mechanistic discipline to one that has the perspective to both propose and to test reasonable hypotheses regarding the ecological drivers of cell shape change.

scholarly journals Bacterial Cell Wall Quality Control during Environmental Stress

mBio ◽  
2020 ◽  
Vol 11 (5) ◽  
Author(s):  
Elizabeth A. Mueller ◽  
Petra Anne Levin
Keyword(s):  
Quality Control ◽  
Cell Wall ◽  
Cell Surface ◽  
Environmental Stress ◽  
Environmental Conditions ◽  
Bacterial Cell ◽  
Cell Shape ◽  
Bacterial Cell Wall ◽  
Peptidoglycan Synthesis ◽  
Peptidoglycan Cell Wall

ABSTRACT Single-celled organisms must adapt their physiology to persist and propagate across a wide range of environmental conditions. The growth and division of bacterial cells depend on continuous synthesis of an essential extracellular barrier: the peptidoglycan cell wall, a polysaccharide matrix that counteracts turgor pressure and confers cell shape. Unlike many other essential processes and structures within the bacterial cell, the peptidoglycan cell wall and its synthesis machinery reside at the cell surface and are thus uniquely vulnerable to the physicochemical environment and exogenous threats. In addition to the diversity of stressors endangering cell wall integrity, defects in peptidoglycan metabolism require rapid repair in order to prevent osmotic lysis, which can occur within minutes. Here, we review recent work that illuminates mechanisms that ensure robust peptidoglycan metabolism in response to persistent and acute environmental stress. Advances in our understanding of bacterial cell wall quality control promise to inform the development and use of antimicrobial agents that target the synthesis and remodeling of this essential macromolecule. IMPORTANCE Nearly all bacteria are encased in a peptidoglycan cell wall, an essential polysaccharide structure that protects the cell from osmotic rupture and reinforces cell shape. The integrity of this protective barrier must be maintained across the diversity of environmental conditions wherein bacteria replicate. However, at the cell surface, the cell wall and its synthesis machinery face unique challenges that threaten their integrity. Directly exposed to the extracellular environment, the peptidoglycan synthesis machinery encounters dynamic and extreme physicochemical conditions, which may impair enzymatic activity and critical protein-protein interactions. Biotic and abiotic stressors—including host defenses, cell wall active antibiotics, and predatory bacteria and phage—also jeopardize peptidoglycan integrity by introducing lesions, which must be rapidly repaired to prevent cell lysis. Here, we review recently discovered mechanisms that promote robust peptidoglycan synthesis during environmental and acute stress and highlight the opportunities and challenges for the development of cell wall active therapeutics.

scholarly journals FtsEX-mediated regulation of inner membrane fusion and cell separation reveals morphogenetic plasticity inCaulobacter crescentus

2017 ◽  
Author(s):  
Elizabeth L. Meier ◽  
Qing Yao ◽  
Allison K. Daitch ◽  
Grant J. Jensen ◽  
Erin D. Goley
Keyword(s):  
Cell Wall ◽  
Membrane Fusion ◽  
Bacterial Cell ◽  
Cell Separation ◽  
Cell Shape ◽  
Caulobacter Crescentus ◽  
Inner Membrane ◽  
Bacterial Cell Shape ◽  
Late Stages ◽  
Shape Changes

AbstractDuring its life cycle,Caulobacter crescentusundergoes a series of coordinated shape changes, including generation of a polar stalk and reshaping of the cell envelope to produce new daughter cells through the process of cytokinesis. The mechanisms by which these morphogenetic processes are coordinated in time and space remain largely unknown. Here we demonstrate that the conserved division complex FtsEX controls both the early and late stages of cytokinesis inC. crescentus, namely initiation of constriction and final cell separation. ΔftsEcells display a striking phenotype: cells are chained, with skinny connections between cell bodies resulting from defects in inner membrane fusion and cell separation. Surprisingly, the thin connections in ΔftsEcells share morphological and molecular features withC. crescentusstalks. Our data uncover unanticipated morphogenetic plasticity inC. crescentus, with loss of FtsE causing a stalk-like program to take over at failed division sites and yield novel cell morphology.Author SummaryBacterial cell shape is genetically hardwired and is critical for fitness and, in certain cases, pathogenesis. In most bacteria, a semi-rigid structure called the cell wall surrounds the inner membrane, offering protection against cell lysis while simultaneously maintaining cell shape. A highly dynamic macromolecular structure, the cell wall undergoes extensive remodeling as bacterial cells grow and divide. We demonstrate that a broadly conserved cell division complex, FtsEX, relays signals from the cytoplasm to the cell wall to regulate key developmental shape changes in the α-proteobacteriumCaulobacter crescentus. Consistent with studies in diverse bacteria, we observe strong synthetic interactions betweenftsEand cell wall hydrolytic factors, suggesting that regulation of cell wall remodeling is a conserved function of FtsEX. Loss of FtsE causes morphological defects associated with both the early and late stages of division. Intriguingly, without FtsE, cells frequently fail to separate and instead elaborate a thin, tubular structure between cell bodies, a growth mode observed in other α-proteobacteria. Overall, our results highlight the plasticity of bacterial cell shape and demonstrate how altering the activity of one morphogenetic program can produce diverse morphologies resembling those of other bacteria in nature.

scholarly journals Bacterial Cell Wall Synthesis: New Insights from Localization Studies

2005 ◽  
Vol 69 (4) ◽  
pp. 585-607 ◽  
Author(s):  
Dirk-Jan Scheffers ◽  
Mariana G. Pinho
Keyword(s):  
Cell Wall ◽  
Bacterial Cell ◽  
Cell Shape ◽  
Fluorescent Protein ◽  
Model Organisms ◽  
Live Cells ◽  
Cell Wall Synthesis ◽  
A Cell ◽  
Green Fluorescent ◽  
Bacterial Cell Shape

SUMMARY In order to maintain shape and withstand intracellular pressure, most bacteria are surrounded by a cell wall that consists mainly of the cross-linked polymer peptidoglycan (PG). The importance of PG for the maintenance of bacterial cell shape is underscored by the fact that, for various bacteria, several mutations affecting PG synthesis are associated with cell shape defects. In recent years, the application of fluorescence microscopy to the field of PG synthesis has led to an enormous increase in data on the relationship between cell wall synthesis and bacterial cell shape. First, a novel staining method enabled the visualization of PG precursor incorporation in live cells. Second, penicillin-binding proteins (PBPs), which mediate the final stages of PG synthesis, have been localized in various model organisms by means of immunofluorescence microscopy or green fluorescent protein fusions. In this review, we integrate the knowledge on the last stages of PG synthesis obtained in previous studies with the new data available on localization of PG synthesis and PBPs, in both rod-shaped and coccoid cells. We discuss a model in which, at least for a subset of PBPs, the presence of substrate is a major factor in determining PBP localization.

Induction of L-form-like cell shape change of Bacillus subtilis under microculture conditions

Microbiology ◽  
2003 ◽  
Vol 149 (9) ◽  
pp. 2501-2511 ◽  
Author(s):  
Ryuji Shingaki ◽  
Yasuhiro Kasahara ◽  
Megumi Iwano ◽  
Masayoshi Kuwano ◽  
Tomomasa Takatsuka ◽  
...  
Keyword(s):  
Cell Wall ◽  
Bacillus Subtilis ◽  
Cell Shape ◽  
Shape Change ◽  
Cell Protein ◽  
Nitrate Respiration ◽  
Cover Glass ◽  
Whole Cell ◽  
Cell Shape Change ◽  
Whole Cell Protein

A remarkable cell shape change was observed in Bacillus subtilis strain 168 under microculture conditions on CI agar medium (Spizizen's minimal medium supplemented with a trace amount of yeast extract and Casamino acids). Cells cultured under a cover glass changed in form from rod-shaped to spherical, large and irregular shapes that closely resembled L-form cells. The cell shape change was observed only with CI medium, not with Spizizen's minimum medium alone or other rich media. The whole-cell protein profile of cells grown under cover glass and cells grown on CI agar plates differed in several respects. Tandem mass analysis of nine gel bands which differed in protein expression between the two conditions showed that proteins related to nitrate respiration and fermentation were expressed in the shape-changed cells grown under cover glass. The cell shape change of CI cultures was repressed when excess KNO3 was added to the medium. Whole-cell protein analysis of the normal rod-shaped cells grown with 0·1 % KNO3 and the shape-changed cells grown without KNO3 revealed that the expression of the branched-chain α-keto acid dehydrogenase complex (coded by the bfmB gene locus) was elevated in the shape-changed cells. Inactivation of the bfmB locus resulted in the repression of cell shape change, and cells in which bfmB expression was induced by IPTG did show changes in shape. Transmission electron microscopy of ultrathin sections demonstrated that the shape-changed cells had thin walls, and plasmolysis of cells fixed with a solution including 0·1 M sucrose was observed. Clarifying the mechanism of thinning of the cell wall may lead to the development of a new type of cell wall biosynthetic inhibitor.

The role of microtubules in chick blastoderm expansion—a quantitative study using colchicine

Development ◽  
1975 ◽  
Vol 34 (1) ◽  
pp. 265-277
Author(s):  
J. R. Downie
Keyword(s):  
Cell Division ◽  
Cell Shape ◽  
Shape Change ◽  
Cell Sheet ◽  
Cell Movement ◽  
Vitelline Membrane ◽  
General Context ◽  
Chick Blastoderm ◽  
Cell Shape Change ◽  
Cytoplasmic Microtubules

Since their discovery, cytoplasmic microtubules have been much studied in the context of cell movement and cell shape change. Much of the work has used drugs, particularly colchicine and its relatives, which break down microtubules — the so-called anti-tubulins. Colchicine inhibits the orientated movements of many cell types in vitro, and disrupts cell shape change in several morphogenetic situations. The investigation reported here used chick blastoderm expansion in New culture in an attempt to quantify the colchicine effect on orientated cell movement. However, although colchicine could halt blastoderm expansion entirely, a simple interpretation was not possible. (1) Colchicine at concentrations capable of blocking mitosis, and of disrupting all or most of the cytoplasmic microtubules of the cells studied, inhibited blastoderm expansion, often resulting in an overall retraction of the cell sheet. (2) Though blastoderm expansion does normally involve considerable cell proliferation, the colchicine effect could not be ascribed to a block on cell division since aminopterin, which stops cell division without affecting microtubules, did not inhibit expansion. (3) Blastoderm expansion is effected by the locomotion of a specialized band of edge cells at the blastoderm periphery. These are the only cells normally attached to the vitelline membrane — the substrate for expansion. When most of the blastoderm was excised, leaving the band of edge cells, and the cultures then treated with colchicine, expansion occurred normally. The colchicine effect on blastoderm expansion could not therefore be ascribed to a direct effect on the edge cells. (4) An alternative site of action of the drug is the remaining cells of the blastoderm. These normally become progressively flatter as expansion proceeds. If flattening in these cells is even partially dependent on their cytoplasmic microtubules, disruption of these microtubules might result in the inherent contractility of the cells resisting and eventually halting edge cell migration. That cell shape in these cells is dependent on microtubules was demonstrated by treating flat blastoderm fragments with colchicine. On incubation, the area occupied by these fragments decreased by 25–30 % more than controls. The significance of these results in the general context of orientated cell movements and cell shape determination is discussed, with particular emphasis on the analogous system of Fundulus epiboly.

Autonomy and non-autonomy in Drosophila mesoderm determination and morphogenesis

Development ◽  
1994 ◽  
Vol 120 (4) ◽  
pp. 853-859 ◽  
Author(s):  
M. Leptin ◽  
S. Roth
Keyword(s):  
Cell Shape ◽  
Shape Change ◽  
Developmental Program ◽  
Cell Shape Change ◽  
Ventral Furrow ◽  
Large Numbers ◽  
The Individual ◽  
Mutant Cells ◽  
Transplantation Experiments ◽  
Shape Changes

The mesoderm in Drosophila invaginates by a series of characteristic cell shape changes. Mosaics of wild-type cells in an environment of mutant cells incapable of making mesodermal invaginations show that this morphogenetic behaviour does not require interactions between large numbers of cells but that small patches of cells can invaginate independent of their neighbours' behaviour. While the initiation of cell shape change is locally autonomous, the shapes the cells assume are partly determined by the individual cell's environment. Cytoplasmic transplantation experiments show that areas of cells expressing mesodermal genes ectopically at any position in the egg form an invagination. We propose that ventral furrow formation is the consequence of all prospective mesodermal cells independently following their developmental program. Gene expression at the border of the mesoderm is induced by the apposition of mesodermal and non-mesodermal cells.

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