Nature Reviews Microbiology

Published by Springer Nature

Online ISSN: 1740-1534


Print ISSN: 1740-1526


The value of comparison
  • Article

November 2003


45 Reads

Nicholas Thomson



Ana Cerdeño-Tárraga




Julian Parkhill
With the number of published microbial genomes now in excess of 100, any new genome that is sequenced is likely to have a close relative available for comparison. Indeed, it is increasingly difficult to perform any genomic analysis that is not comparative. This should, however, not be seen as a drawback; it is often the case that a large amount of information can be drawn from these comparisons, especially between closely related organisms. Several genome sequences published recently indicate the value of comparisons at the genomic level.

4-in-1 solution

July 2012


26 Reads

A new HIV regimen that combines four medications into one pill, known as Quad, has been shown to be safe and effective, and may increase adherence to anti-HIV treatment.

King GM, Weber CF.. Distribution, diversity and ecology of aerobic CO-oxidizing bacteria. Nat Rev Microbiol 5: 107-118
  • Literature Review
  • Full-text available

March 2007


916 Reads

Numerous studies indicate that carbon monoxide (CO) participates in a broader range of processes than any other single molecule, ranging from subcellular to planetary scales. Despite its toxicity to many organisms, a diverse group of bacteria that span multiple phylogenetic lineages metabolize CO. These bacteria are globally distributed and include pathogens, plant symbionts and biogeochemically important lineages in soils and the oceans. New molecular and isolation techniques, as well as genome sequencing, have greatly expanded our knowledge of the diversity of CO oxidizers. Here, we present a newly emerging picture of the distribution, diversity and ecology of aerobic CO-oxidizing bacteria.

Pyroptosis: host cell death and inflammation. Nat Rev Microbiol 7:99-109

March 2009


394 Reads

Eukaryotic cells can initiate several distinct programmes of self-destruction, and the nature of the cell death process (non-inflammatory or proinflammatory) instructs responses of neighbouring cells, which in turn dictates important systemic physiological outcomes. Pyroptosis, or caspase 1-dependent cell death, is inherently inflammatory, is triggered by various pathological stimuli, such as stroke, heart attack or cancer, and is crucial for controlling microbial infections. Pathogens have evolved mechanisms to inhibit pyroptosis, enhancing their ability to persist and cause disease. Ultimately, there is a competition between host and pathogen to regulate pyroptosis, and the outcome dictates life or death of the host.

Figure 1: Global distribution of known hydrothermal vents.Temperature and chemical anomalies hint that many more sites exist throughout the world's oceans. Data courtesy of D. Fornari and T. Shank, Woods Hole Oceanographic Institute, Massachusetts, USA.
Figure 3: Chemical and biochemical reactions.A schematic of the H2-dependent conversions of CO2 to CH4 without cofactors (a) and with cofactors (b,c) in acetogens (to acetate) and methanogens growing on H2 and CO2. The numbers next to the arrows indicate the approximate change in free energy (G0) at 25°C and pH 7 (G0') in kJ per mole. The thermodynamic values are taken from Refs 55,56. For details of the biologically catalysed reactions, see the review by Maden55. For details of the reactions without cofactors under hydrothermal conditions, in which the thermodynamic values provided do not directly apply, see Ref. 101. The dotted oval represents bifunctional CO dehydrogenase/acetyl-coenzyme A (acetyl CoA) synthase (CODH/ACS), a conserved enzyme that is common to the acetyl-CoA pathway of CO2 reduction in both acetogens and methanogens. The enzymes that are involved in methyl synthesis in acetogens and methanogens are not evolutionary related, even though similar chemical steps are involved55, 63. This has been interpreted to mean that the overall exergonic chemical conversions are more ancient than the enzymes that catalyse them in modern cells. Although all reactions shown are reversible, arrows are shown in only one direction for simplicity. The asterisks at the methyl-H4MPT to CH4 conversion and the acetyl-CoA to acetate conversion54 indicate that several enzymes and cofactors that are not shown here are involved55. In both acetogens54 and methanogens53, net energy conservation (ATP gain) involves the generation of ion gradients using the overall reaction shown. This chemiosmotic potential is then harnessed by an ATPase. The coupling site in methanogenesis (not shown) entails the conversion of methyl-H4MPT to CH4 (Ref. 53); the coupling site in acetogenesis (not shown) has recently been suggested to involve a ferredoxin–NAD+ oxidoreductase102. The formate to formyl-H4F conversion in acetogens involves ATP hydrolysis (not shown), which lowers G0' for the reaction to -10 kJ per mole55; the chemiosmotic potential is required for the synthesis of formyl-MF in methanogens53. For both acetogens and methanogens, black arrows indicate reactions that are involved in core ATP synthesis, whereas grey arrows indicate that a portion of the total carbon flux is used to satisfy the carbon needs of the cell. H4F, tetrahydrofolate; H4MPT, tetrahydromethanopterin; HSCoA, coenzyme A; MF, methanofuran; Ni[E], an Fe–Ni–S cluster in CODH/ACS. Part a adapted, with permission, from Ref. 101 © (2006) National Academy of Sciences. Parts b,c adapted, with permission, from Ref. 55 © (2000) Portland Press.
Hydrothermal vents and the origin of life. Nat Rev Micro 6(11): 805-814

October 2008


3,112 Reads

Submarine hydrothermal vents are geochemically reactive habitats that harbour rich microbial communities. There are striking parallels between the chemistry of the H(2)-CO(2) redox couple that is present in hydrothermal systems and the core energy metabolic reactions of some modern prokaryotic autotrophs. The biochemistry of these autotrophs might, in turn, harbour clues about the kinds of reactions that initiated the chemistry of life. Hydrothermal vents thus unite microbiology and geology to breathe new life into research into one of biology's most important questions - what is the origin of life?

Zhao L.. The gut microbiota and obesity: from correlation to causality. Nat Rev Microbiol 11: 639-647

August 2013


997 Reads

The gut microbiota has been linked with chronic diseases such as obesity in humans. However, the demonstration of causality between constituents of the microbiota and specific diseases remains an important challenge in the field. In this Opinion article, using Koch's postulates as a conceptual framework, I explore the chain of causation from alterations in the gut microbiota, particularly of the endotoxin-producing members, to the development of obesity in both rodents and humans. I then propose a strategy for identifying the causative agents of obesity in the human microbiota through a combination of microbiome-wide association studies, mechanistic analysis of host responses and the reproduction of diseases in gnotobiotic animals.

Brakhage, A. A. Regulation of fungal secondary metabolism. Nat. Rev. Microbiol. 11, 21-32

November 2012


687 Reads

Fungi produce a multitude of low-molecular-mass compounds known as secondary metabolites, which have roles in a range of cellular processes such as transcription, development and intercellular communication. In addition, many of these compounds now have important applications, for instance, as antibiotics or immunosuppressants. Genome mining efforts indicate that the capability of fungi to produce secondary metabolites has been substantially underestimated because many of the fungal secondary metabolite biosynthesis gene clusters are silent under standard cultivation conditions. In this Review, I describe our current understanding of the regulatory elements that modulate the transcription of genes involved in secondary metabolism. I also discuss how an improved knowledge of these regulatory elements will ultimately lead to a better understanding of the physiological and ecological functions of these important compounds and will pave the way for a novel avenue to drug discovery through targeted activation of silent gene clusters.

Hughes DT, Sperandio V.. Inter-kingdom signalling: communication between bacteria and their hosts. Nat Rev Microbiol 6: 111-120

March 2008


281 Reads

Microorganisms and their hosts communicate with each other through an array of hormonal signals. This cross-kingdom cell-to-cell signalling involves small molecules, such as hormones that are produced by eukaryotes and hormone-like chemicals that are produced by bacteria. Cell-to-cell signalling between bacteria, usually referred to as quorum sensing, was initially described as a means by which bacteria achieve signalling in microbial communities to coordinate gene expression within a population. Recent evidence shows, however, that quorum-sensing signalling is not restricted to bacterial cell-to-cell communication, but also allows communication between microorganisms and their hosts.

Hiscox, JA. RNA viruses: hijacking the dynamic nucleolus. Nat Rev Microbiol 5: 119-127

March 2007


102 Reads

The nucleolus is a dynamic subnuclear structure with roles in ribosome subunit biogenesis, mediation of cell-stress responses and regulation of cell growth. The proteome and structure of the nucleolus are constantly changing in response to metabolic conditions. RNA viruses interact with the nucleolus to usurp host-cell functions and recruit nucleolar proteins to facilitate virus replication. Investigating the interactions between RNA viruses and the nucleolus will facilitate the design of novel anti-viral therapies, such as recombinant vaccines and therapeutic molecular interventions, and also contribute to a more detailed understanding of the cell biology of the nucleolus.

Cary SC, McDonald IR, Barrett JE, Cowan DA.. On the rocks: the microbiology of Antarctic dry valley soils. Nat Rev Microbiol 8: 129-138

February 2010


1,025 Reads

The arid soils of the Antarctic Dry Valleys constitute some of the oldest, coldest, driest and most oligotrophic soils on Earth. Early studies suggested that the Dry Valley soils contained, at best, very low levels of viable microbiota. However, recent applications of molecular methods have revealed a dramatically contrasting picture - a very wide diversity of microbial taxa, many of which are uncultured and taxonomically unique, and a community that seems to be structured solely by abiotic processes. Here we review our understanding of these extreme Antarctic terrestrial microbial communities, with particular emphasis on the factors that are involved in their development, distribution and maintenance in these cold desert environments.

Figure 1: Legionella pneumophila modulates the trafficking of its vacuole to establish a replicative niche.a | Formation of the replication vacuole. After uptake into target amoebae or macrophages, the Legionella-containing vacuole (LCV) evades transport to the lysosomal network and is sequestered in a compartment that is different from those observed for non-pathogens6, 7. Within minutes of uptake, vesicles derived from the endoplasmic reticulum (ER; yellow compartments) and mitochondria appear in close proximity to the LCV surface. The identity of the ER-derived vesicles is based on the presence of proteins that are known to be associated with the early secretory apparatus. The vesicles that surround the LCV appear to be docked and extend out onto the surface, and eventually, the membranes that surround the bacterium become similar to rough ER in appearance and become studded with ribosomes. Within this ER-like compartment, the bacterium replicates to high numbers and eventually lyses the host cell. b | Default pathway of trafficking a non-pathogen. After bacterial uptake, the membrane-bound compartment acquires the character of early endosomes and late endosomes before entering the lysosomal network. Dot/Icm, defect in organelle trafficking/intracellular multiplication.
Figure 2: The Legionella-containing vacuole.Legionella pneumophila proteins secreted via the Dot/Icm (defect in organelle trafficking/intracellular multiplication) translocation system associate with the Legionella-containing vacuole (LCV) and recruit host proteins that are involved in vesicle trafficking through the early secretory pathway. To simplify the components, the Dot/Icm apparatus is depicted as a tube that extends from the bacterial cytoplasm into the host cytosol, but there is no mechanistic support for this simplistic view. Sec22b, which is involved in the docking of endoplasmic reticulum (ER)-derived vesicles at the Golgi, is recruited to the LCV, although the mechanism of recruitment is unclear12. Rab1, another vesicle docking and fusion protein, is recruited to the LCV by the L. pneumophila protein SidM76 (also known as DrrA77), which functions as both a Rab1 GDF (guanine nucleotide-dissociation inhibitor (GDI) dissociation factor78, 83) and a Rab1 GEF (guanine nucleotide exchange factor76, 77). LidA acts in conjunction with SidM to sequester activated Rab1 at the LCV membrane76. LepB is a RabGAP (Rab GTPase activating protein78), and may be involved in the dissociation of Rab1 from the vacuolar membrane. ADP-ribosylation factor 1 (Arf1), which is involved in vesicle budding and recycling at the Golgi, is recruited to the LCV by RalF, which functions as an Arf1 GEF33. Host membrane recruitment to the LCV might involve an autophagy process, as both the host autophagy proteins Atg7 and Atg8 also localize to the LCV21.
Figure 3: The Dot/Icm translocation apparatus.The presumed locations and topological relationships of the various Dot/Icm (defect in organelle trafficking/intracellular multiplication) components in the Legionella pneumophila envelope are shown based on a study of the stability of individual proteins in the presence of defined deletion mutations46. Individual letters represent Dot protein names, whereas letters preceded by an 'i' indicate Icm protein names.
Figure 4: Legionella pneumophila manipulates host cell death and survival pathways.After uptake into mammalian cells, a response to L. pneumophila that threatens to terminate intracellular growth by causing host cell death occurs. The cell death pathways have both a necrotic as well as an apoptotic character, and require an intact Dot/Icm (defect in organelle trafficking/intracellular multiplication) translocation system. The individual L. pneumophila components or translocated substrates that cause cell death have not been identified. In addition, there are at least two translocated substrates that interfere with host cell death. SdhA (sidH paralogue A) is required to inhibit multiple pathways that lead to cell death after L. pneumophila contact with host cells, and its absence causes a defect in intracellular replication within macrophages59. L. pneumophila also activates the host transcription factor nuclear factor-B (NF-B) to promote expression of anti-apoptotic genes to delay host cell death102, 103. However, the mechanism by which this occurs has not yet been determined. At later stages of infection, SidF directly inhibits an apoptotic pathway by interfering with pro-death proteins in the rambo family91. Bcl2, B-cell lymphoma 2; LCV, Legionella-containing vacuole; Nod, nodulation; Sid, substrates of Icm/Dot.
Isberg RR, O’Connor TJ, Heidtman M.. The Legionella pneumophila replication vacuole: making a cosy niche inside host cells. Nat Rev Microbiol 7: 13-24

December 2008


2,646 Reads

The pathogenesis of Legionella pneumophila is derived from its growth within lung macrophages after aerosols are inhaled from contaminated water sources. Interest in this bacterium stems from its ability to manipulate host cell vesicular-trafficking pathways and establish a membrane-bound replication vacuole, making it a model for intravacuolar pathogens. Establishment of the replication compartment requires a specialized translocation system that transports a large cadre of protein substrates across the vacuolar membrane. These substrates regulate vesicle traffic and survival pathways in the host cell. This Review focuses on the strategies that L. pneumophila uses to establish intracellular growth and evaluates why this microorganism has accumulated an unprecedented number of translocated substrates that are targeted at host cells.

Figure 1: Schematic representation of the different type-IV-dependent mechanisms.The three subfamilies of type IV secretion (T4S) systems are shown. Conjugation machines deliver DNA to recipient bacteria and other cell types by cell-to-cell contact. DNA-uptake and -release systems exchange DNA with the extracellular milieu independently of contact with target cells. Effector translocators deliver DNA or protein substrates to eukaryotic cells during infection. The effector translocators contribute in markedly different ways to the infection processes of the bacterial pathogens shown. PT, pertussis toxin.
Table 1 | Type IV secretion (T4S) systems and disease manifestations
Table 3 | Type IV secretion substrates and host interacting partner proteins*
Figure 4: Schematic representation of the cellular consequences of type IV secretion (T4S) system effector translocation.T4S effector translocation alters various eukaryotic cellular processes, as illustrated for the four systems in which effector molecules have been identified so far. Agrobacterium tumefaciens delivery of T-DNA and effector proteins induces synthesis of opine food substrates and also induces tumour production through modulation of phytohormone levels. Helicobacter pylori CagA modulates various pathways associated with eukaryotic-cell differentiation, proliferation and motility. Bordetella pertussis pertussis toxin (PT) interferes with G-protein-dependent signalling pathways, and Legionella pneumophila RalF recruits the ARF (ADP ribosylation factor) family of guanosine triphosphatases to the phagosome to promote intracellular survival.
Cascales E, Christie PJ. The versatile bacterial type IV secretion systems. Nat Rev Microbiol 1: 137-149

December 2003


332 Reads

Bacteria use type IV secretion systems for two fundamental objectives related to pathogenesis--genetic exchange and the delivery of effector molecules to eukaryotic target cells. Whereas gene acquisition is an important adaptive mechanism that enables pathogens to cope with a changing environment during invasion of the host, interactions between effector and host molecules can suppress defence mechanisms, facilitate intracellular growth and even induce the synthesis of nutrients that are beneficial to bacterial colonization. Rapid progress has been made towards defining the structures and functions of type IV secretion machines, identifying the effector molecules, and elucidating the mechanisms by which the translocated effectors subvert eukaryotic cellular processes during infection.

Travers, A. & Muskhelishvili, G. DNA supercoiling-a global transcriptional regulator for enterobacterial growth? Nature Rev. Microbiol. 3, 157-169
A fundamental principle of exponential bacterial growth is that no more ribosomes are produced than are necessary to support the balance between nutrient availability and protein synthesis. Although this conclusion was first expressed more than 40 years ago, a full understanding of the molecular mechanisms involved remains elusive and the issue is still controversial. There is currently agreement that, although many different systems are undoubtedly involved in fine-tuning this balance, an important control, and in our opinion perhaps the main control, is regulation of the rate of transcription initiation of the stable (ribosomal and transfer) RNA transcriptons. In this review, we argue that regulation of DNA supercoiling provides a coherent explanation for the main modes of transcriptional control - stringent control, growth-rate control and growth-phase control - during the normal growth of Escherichia coli.

Levin BR, Bull JJ.. Population and evolutionary dynamics of phage therapy. Nat Rev Micro 2: 166-173
Following a sixty-year hiatus in western medicine, bacteriophages (phages) are again being advocated for treating and preventing bacterial infections. Are attempts to use phages for clinical and environmental applications more likely to succeed now than in the past? Will phage therapy and prophylaxis suffer the same fates as antibiotics--treatment failure due to acquired resistance and ever-increasing frequencies of resistant pathogens? Here, the population and evolutionary dynamics of bacterial-phage interactions that are relevant to phage therapy and prophylaxis are reviewed and illustrated with computer simulations.

Cegelski L, Marshall GR, Eldridge GR, Hultgren SJ.. The biology and future prospects of antivirulence therapies. Nat Rev Microbiol 6: 17-28

February 2008


448 Reads

The emergence and increasing prevalence of bacterial strains that are resistant to available antibiotics demand the discovery of new therapeutic approaches. Targeting bacterial virulence is an alternative approach to antimicrobial therapy that offers promising opportunities to inhibit pathogenesis and its consequences without placing immediate life-or-death pressure on the target bacterium. Certain virulence factors have been shown to be potential targets for drug design and therapeutic intervention, whereas new insights are crucial for exploiting others. Targeting virulence represents a new paradigm to empower the clinician to prevent and treat infectious diseases.

Figure 1: The effects of biodegradation on oil composition.a | Composition of a light North Sea crude oil (top panel) and a slightly biodegraded (heavy) oil (bottom panel). The resins and asphaltenes are complex mixtures of polar compounds. The degraded oil is characterized as being slightly biodegraded on the basis of its detailed molecular composition. Most resolvable saturated hydrocarbons have been biodegraded, as have the non-cyclic terpenoids pristane and phytane. The cyclic terpenoids, however, are intact, and only the two- and three-ring aromatic hydrocarbons have been extensively degraded. b | Gas-chromatogram traces showing separation of the components of whole oil that is increasingly biodegraded (from top to bottom). The main peaks that are lost are the resolvable saturated hydrocarbons. The large peaks on the right that do not decrease with biodegradation are internal standards that are added to the oil before analysis for quantification of individual components of the oil.
Head IM, Jones DM, Röling WF.. Marine microorganisms make a meal of oil. Nat Rev Microbiol 4: 173-182

April 2006


2,045 Reads

Hundreds of millions of litres of petroleum enter the environment from both natural and anthropogenic sources every year. The input from natural marine oil seeps alone would be enough to cover all of the world's oceans in a layer of oil 20 molecules thick. That the globe is not swamped with oil is testament to the efficiency and versatility of the networks of microorganisms that degrade hydrocarbons, some of which have recently begun to reveal the secrets of when and how they exploit hydrocarbons as a source of carbon and energy.

Harms H, Schlosser D, Wick LY.. Untapped potential: exploiting fungi in bioremediation of hazardous chemicals. Nat Rev Microbiol 9: 177-192

March 2011


990 Reads

Fungi possess the biochemical and ecological capacity to degrade environmental organic chemicals and to decrease the risk associated with metals, metalloids and radionuclides, either by chemical modification or by influencing chemical bioavailability. Furthermore, the ability of these fungi to form extended mycelial networks, the low specificity of their catabolic enzymes and their independence from using pollutants as a growth substrate make these fungi well suited for bioremediation processes. However, despite dominating the living biomass in soil and being abundant in aqueous systems, fungi have not been exploited for the bioremediation of such environments. In this Review, we describe the metabolic and ecological features that make fungi suited for use in bioremediation and waste treatment processes, and discuss their potential for applications on the basis of these strengths.

Table 2 | Comparison of pandemic HA with avian consensus sequences
Table 3 | Comparison of pandemic NA with avian consensus sequences
Evidence of an absence: The genetic origins of the 1918 pandemic influenza virus

December 2004


279 Reads

Annual outbreaks of influenza A infection are an ongoing public health threat and novel influenza strains can periodically emerge to which humans have little immunity, resulting in devastating pandemics. The 1918 pandemic killed at least 40 million people worldwide and pandemics in 1957 and 1968 caused hundreds of thousands of deaths. The influenza A virus is capable of enormous genetic variation, both by continuous, gradual mutation and by reassortment of genome segments between viruses. Both the 1957 and 1968 pandemic strains are thought to have originated as reassortants in which one or both human-adapted viral surface proteins were replaced by proteins from avian influenza strains. Analyses of the genes of the 1918 pandemic virus, however, indicate that this strain might have had a different origin. The haemagglutinin and nucleoprotein genome segments in particular are unlikely to have come directly from an avian source that is similar to those that are currently being sequenced. Determining whether a pandemic influenza virus can emerge by different mechanisms will affect the scope and focus of surveillance and prevention efforts.

VerBerkmoes NC, Denef VJ, Hettich RL, Banfield JF.. SYSTEMS BIOLOGY functional analysis of natural microbial consortia using community proteomics. Nat Rev Microbiol 7: 196-205
We know very little about the metabolic functioning and evolutionary dynamics of microbial communities. Recent advances in comprehensive, sequencing-based methods, however, are laying a molecular foundation for new insights into how microbial communities shape the Earth's biosphere. Here we explore the convergence of microbial ecology, genomics, biological mass spectrometry and informatics that form the new field of microbial community proteogenomics. We discuss the first applications of proteogenomics and its potential for studying the physiology, ecology and evolution of microbial populations and communities.

Entropy as the driver of chromosome segregation. Nature Reviews Microbiology 2010 + Supplementary Information on polymer physics
We present a new physical biology approach to understanding the relationship between the organization and segregation of bacterial chromosomes. We posit that replicated Escherichia coli daughter strands will spontaneously demix as a result of entropic forces, despite their strong confinement within the cell; in other words, we propose that entropy can act as a primordial physical force which drives chromosome segregation under the right physical conditions. Furthermore, proteins implicated in the regulation of chromosome structure and segregation may in fact function primarily in supporting such an entropy-driven segregation mechanism by regulating the physical state of chromosomes. We conclude that bacterial chromosome segregation is best understood in terms of spontaneous demixing of daughter strands. Our concept may also have important implications for chromosome segregation in eukaryotes, in which spindle-dependent chromosome movement follows an extended period of sister chromatid demixing and compaction.

Bartenschlager R, Lohmann V, Penin F. The molecular and structural basis of advanced antiviral therapy for hepatitis C virus infection. Nat Rev Microbiol. 2013;11(7):482-96
The availability of the first molecular clone of the hepatitis C virus (HCV) genome allowed the identification and biochemical characterization of two viral enzymes that are targets for antiviral therapy: the protease NS3-4A and the RNA-dependent RNA polymerase NS5B. With the advent of cell culture systems that can recapitulate either the intracellular steps of the viral replication cycle or the complete cycle, additional drug targets have been identified, most notably the phosphoprotein NS5A, but also host cell factors that promote viral replication, such as cyclophilin A. Here, we review insights into the structures of these proteins and the mechanisms by which they contribute to the HCV replication cycle, and discuss how these insights have facilitated the development of new, directly acting antiviral compounds that have started to enter the clinic.

Knipe, D.M. & Cliffe, A. Chromatin control of herpes simplex virus lytic and latent infection. Nat. Rev. Microbiol. 6, 211-221
Herpes simplex viruses (HSV) can undergo a lytic infection in epithelial cells and a latent infection in sensory neurons. During latency the virus persists until reactivation, which leads to recurrent productive infection and transmission to a new host. How does HSV undergo such different types of infection in different cell types? Recent research indicates that regulation of the assembly of chromatin on HSV DNA underlies the lytic versus latent decision of HSV. We propose a model for the decision to undergo a lytic or a latent infection in which HSV encodes gene products that modulate chromatin structure towards either euchromatin or heterochromatin, and we discuss the implications of this model for the development of therapeutics for HSV infections.

Angert ER.. Alternatives to binary fission in bacteria. Nat Rev Microbiol 3: 214-224
Whereas most prokaryotes rely on binary fission for propagation, many species use alternative mechanisms, which include multiple offspring formation and budding, to reproduce. In some bacterial species, these eccentric reproductive strategies are essential for propagation, whereas in others the programmes are used conditionally. Although there are tantalizing images and morphological descriptions of these atypical developmental processes, none of these reproductive structures are characterized at the molecular genetic level. Now, with newly available analytical techniques, model systems to study these alternative reproductive programmes are being developed.

Top-cited authors