Results and Problems in Cell Differentiation最新文献

The human intestinal tract is inhabited by trillions of microorganisms and houses the largest pool of macrophages in the human body. Being a part of the innate immune system, the macrophages, the professional phagocytes, vigorously respond to the microbial and dietary antigens present in the intestine. Because such a robust immune response poses the danger to the survival of the non-harmful and beneficial gut microbiota, the macrophages developed mechanisms of recognition and hyposensitivity toward the non-harmful/beneficial inhabitants of the gut. We will discuss the evolution and identity of some of these mechanisms in the following chapter.

Advances in understanding over the last decade or so highlight the need for a reappraisal of the role of viruses in relation to the origins and evolution of cellular life, as well as in the homeostasis of the biosphere on which all of life depends. The relevant advances have, in particular, revealed an important contribution of viruses to the evolution of the placental mammals, while also contributing key roles to mammalian embryogenesis, genomic evolution, and physiology. Part of this reappraisal will include the origins of viruses, a redefinition of their quintessential nature, and a suggestion as to how we might view viruses in relation to the tree of life.

Symbiogenesis presents the biologist with very different explanatory issues compared to the lineal and selectionist view of evolution based on individual entities, whether genes, organisms or species. A key question is how the co-existence of two or more partners in close association during a given generation can ultimately be stabilized enough to be transmitted to the next, how the ensuing complexity is maintained and how this arrangement impacts the reproductive fitness of the collective over evolutionary time. In this chapter, we highlight some observations gleaned from the microbial world that could shed light on this problem if viewed within the framework of constructive neutral evolution.

Nitrogen-fixing root nodule symbiosis can sustain the development of the host plants under nitrogen-limiting conditions. Such symbiosis occurs only in a clade of angiosperms known as the nitrogen-fixing clade (NFC). It has long been proposed that root nodule symbiosis evolved several times (in parallel) in the NFC. Two recent phylogenomic studies compared the genomes of nodulating and related non-nodulating species across the four orders of the NFC and found that genes essential for nodule formation are lost or pseudogenized in the non-nodulating species. As these symbiosis genes are specifically involved in the symbiotic interaction, it means that the presence of pseudogenes and the loss of symbiosis genes strongly suggest that their ancestor, which still had functional genes, most likely had a symbiosis with nitrogen-fixing bacteria. These findings agree with the hypothesis that nodulation evolved once at the common ancestor of the NFC, and challenge the hypothesis of parallel evolution. In this chapter, we will cover the current understandings on actinorhizal-type and legume nodule development, and discuss the evolution of the legume nodule type.

Many complex diseases are expressed with high incidence only in certain populations. Genealogy studies determine that these diseases are inherited with a high probability. However, genetic studies have been unable to identify the genomic signatures responsible for such heritability, as identifying the genetic variants that make a population prone to a given disease is not enough to explain its high occurrence within the population. This gap is known as the missing heritability problem. We know that the microbiota plays a very important role in determining many important phenotypic characteristics of its host, in particular the complex diseases for which the missing heritability occurs. Therefore, when computing the heritability of a phenotype, it is important to consider not only the genetic variation in the host but also in its microbiota. Here we test this hypothesis by studying an evolutionary model based on gene regulatory networks. Our results show that the holobiont (the host plus its microbiota) is capable of generating a much larger variability than the host alone, greatly reducing the missing heritability of the phenotype. This result strongly suggests that a considerably large part of the missing heritability can be attributed to the microbiome.

The progress of evolutionary biology has revealed that symbiosis played a basic role in the evolution of complex eukaryotic organisms, including humans. Mitochondria are actually simplified endosymbiotic bacteria currently playing the role of cellular organelles. Mitochondrial domestication occurred at the very beginning of eukaryotic evolution. Mitochondria have two different basic functions: they produce energy using oxidative respiration, and they initiate different forms of apoptotic programmed/regulated cell death. Apoptotic programmed cell death may have different cytological forms. Mechanisms of apoptotic programmed cell death exist even in the unicellular organisms, and they play a basic role in the development of complex multicellular organisms, such as fungi, green plants, and animals. Multicellularity was independently established many times among eukaryotes. There are indications that apoptotic programmed cell death is a trait required for the establishment of multicellularity. Regulated cell death is initiated by many different parallel biochemical pathways. It is generally accepted that apoptosis evolved during mitochondrial domestication. However, there are different hypothetical models of the origin of apoptosis. The phylogenetic studies of my group indicate that apoptosis probably evolved during an evolutionary arms race between host ancestral eukaryotic predators and ancestral prey mitochondria (named protomitochondria). Protomitochondrial prey produced many different toxins as a defense against predators. From these toxins evolved extant apoptotic factors. There are indications that aerobic respiration and apoptosis co-evolved and are functionally linked in extant organisms. Perturbations of apoptosis and oxidative respiration are frequently observed during neoplastic transition. Our group showed that perturbations of apoptosis in yeasts also cause perturbations of oxidative respiration.

Prokaryotes commonly undergo genome reduction, particularly in the case of symbiotic bacteria. Genome reductions tend toward the energetically favorable removal of unnecessary, redundant, or nonfunctional genes. However, without mechanisms to compensate for these losses, deleterious mutation and genetic drift might otherwise overwhelm a population. Among the mechanisms employed to counter gene loss and share evolutionary success within a population, gene transfer agents (GTAs) are increasingly becoming recognized as important contributors. Although viral in origin, GTA particles package fragments of their "host" genome for distribution within a population of cells, often in a synchronized manner, rather than selfishly packaging genes necessary for their spread. Microbes as diverse as archaea and alpha-proteobacteria have been known to produce GTA particles, which are capable of transferring selective advantages such as virulence factors and antibiotic resistance. In this review, we discuss the various types of GTAs identified thus far, focusing on a defined set of symbiotic alpha-proteobacteria known to carry them. Drawing attention to the predicted presence of these genes, we discuss their potential within the selective marine and terrestrial environments occupied by mutualistic, parasitic, and endosymbiotic microbes.

Mutualistic symbiosis, in which individuals of different species cooperate and both benefit, has long been an evolutionary puzzle. Why should individuals of two different species cooperate? In this case, as in all others, cooperation is not automatic, but rather requires the mediation of evolutionary conflicts. In chemiosmosis, redox reactions produce a trans-membrane "proton-motive force" that powers energy-requiring reactions in most organisms. Chemiosmosis may also have a role in conflict mediation. Chemiosmosis rapidly produces considerable amounts of products, increasing the risk of end-product inhibition and the formation of dangerous by-products, such as reactive oxygen species. While several mechanisms can modulate chemiosmosis, potential negative effects can also be ameliorated by simply dispersing excess product into the environment. This "free lunch you are forced to make" can attract individuals of other species leading to groups, in which other organisms share the products that are released into the environment by the chemiosmotic cell or organism. Since the time of Darwin, evolutionary biology has recognized that groups are the key to the evolution of cooperation. With many small groups, chance associations of cooperators can arise, even if cooperation is selected against at the individual level. Groups of cooperators can then outcompete groups of defectors, which do not cooperate. Indeed, numerous symbioses may have arisen in this way, perhaps most notably the symbioses of host cells and chemiosmotic bacteria that gave rise to the eukaryotic cell. Other examples in which one partner relies on chemiosmotic products supplied by the other include lichens, corals or other metazoans and dinoflagellates, sap-feeding insects, and plant-rhizobia and plant-mycorrhiza interactions. More problematic are cases of gut microbiomes-for instance, those of termites, ruminants, and even human beings. Under some but not all circumstances, chemiosmosis can be co-opted into punishing defectors and enforcing cooperation, thus leading to mutualistic symbioses.

Wolbachia symbionts, first observed in the 1920s, are now known to be present in about 30-70% of tested arthropod species, in about half of tested filarial nematodes (including the majority of human filarial nematodes), and some plant-parasitic nematodes. In arthropods, they are generally viewed as parasites while in nematodes they appear to be mutualists although this demarcation is not absolute. Their presence in arthropods generally leads to reproductive anomalies, while in nematodes, they are generally required for worm development and reproduction. In mosquitos, Wolbachia inhibit RNA viral infections, leading to populational reductions in human RNA virus pathogens, whereas in filarial nematodes, their requirement for worm fertility and survival has been channeled into their use as drug targets for filariasis control. While much more research on these ubiquitous symbionts is needed, they are viewed as playing significant roles in biological processes, ranging from arthropod speciation to human health.

Tsetse flies (Glossina spp.) act as the sole vectors of the African trypanosome species that cause Human African Trypanosomiasis (HAT or African Sleeping Sickness) and Nagana in animals. These flies have undergone a variety of specializations during their evolution including an exclusive diet consisting solely of vertebrate blood for both sexes as well as an obligate viviparous reproductive biology. Alongside these adaptations, Glossina species have developed intricate relationships with specific microbes ranging from mutualistic to parasitic. These relationships provide fundamental support required to sustain the specializations associated with tsetse's biology. This chapter provides an overview on the knowledge to date regarding the biology behind these relationships and focuses primarily on four bacterial species that are consistently associated with Glossina species. Here their interactions with the host are reviewed at the morphological, biochemical and genetic levels. This includes: the obligate symbiont Wigglesworthia, which is found in all tsetse species and is essential for nutritional supplementation to the blood-specific diet, immune system maturation and facilitation of viviparous reproduction; the commensal symbiont Sodalis, which is a frequently associated symbiont optimized for survival within the fly via nutritional adaptation, vertical transmission through mating and may alter vectorial capacity of Glossina for trypanosomes; the parasitic symbiont Wolbachia, which can manipulate Glossina via cytoplasmic incompatibility and shows unique interactions at the genetic level via horizontal transmission of its genetic material into the genome in two Glossina species; finally, knowledge on recently observed relations between Spiroplasma and Glossina is explored and potential interactions are discussed based on knowledge of interactions between this bacterial Genera and other insect species. These flies have a simple microbiome relative to that of other insects. However, these relationships are deep, well-studied and provide a window into the complexity and function of host/symbiont interactions in an important disease vector.