scholarly journals Muller’s Ratchet and Ribosome Degeneration in the Obligate Intracellular Parasites Microsporidia

2018 ◽  
Vol 19 (12) ◽  
pp. 4125 ◽  
Author(s):  
Sergey Melnikov ◽  
Kasidet Manakongtreecheep ◽  
Keith Rivera ◽  
Arthur Makarenko ◽  
Darryl Pappin ◽  
...  
Keyword(s):  
Ribosomal Proteins ◽  
Evolutionary Process ◽  
Obligate Intracellular ◽  
Muller's Ratchet ◽  
Automated Annotation ◽  
Intracellular Parasites ◽  
Genome Decay ◽  
Muller’S Ratchet ◽  
Forms Of Life ◽  
Cellular Components

Microsporidia are fungi-like parasites that have the smallest known eukaryotic genome, and for that reason they are used as a model to study the phenomenon of genome decay in parasitic forms of life. Similar to other intracellular parasites that reproduce asexually in an environment with alleviated natural selection, Microsporidia experience continuous genome decay that is driven by Muller’s ratchet—an evolutionary process of irreversible accumulation of deleterious mutations that lead to gene loss and the miniaturization of cellular components. Particularly, Microsporidia have remarkably small ribosomes in which the rRNA is reduced to the minimal enzymatic core. In this study, we analyzed microsporidian ribosomes to study an apparent impact of Muller’s ratchet on structure of RNA and protein molecules in parasitic forms of life. Through mass spectrometry of microsporidian proteome and analysis of microsporidian genomes, we found that massive rRNA reduction in microsporidian ribosomes appears to annihilate the binding sites for ribosomal proteins eL8, eL27, and eS31, suggesting that these proteins are no longer bound to the ribosome in microsporidian species. We then provided an evidence that protein eS31 is retained in Microsporidia due to its non-ribosomal function in ubiquitin biogenesis. Our study illustrates that, while Microsporidia carry the same set of ribosomal proteins as non-parasitic eukaryotes, some ribosomal proteins are no longer participating in protein synthesis in Microsporidia and they are preserved from genome decay by having extra-ribosomal functions. More generally, our study shows that many components of parasitic cells, which are identified by automated annotation of pathogenic genomes, may lack part of their biological functions due to continuous genome decay.

scholarly journals Muller’s Ratchet and Ribosome Degeneration in the Obligate Intracellular Parasites Microsporidia

2018 ◽  
Author(s):  
Sergey Melnikov ◽  
Kasidet Manakongtreecheep ◽  
Keith Rivera ◽  
Arthur Makarenko ◽  
Darryl Pappin ◽  
...  
Keyword(s):  
Ribosomal Proteins ◽  
Evolutionary Process ◽  
Mass Spectrometry Analysis ◽  
Spectrometry Analysis ◽  
Muller's Ratchet ◽  
Ribosome Structure ◽  
Intracellular Parasites ◽  
Genome Decay ◽  
Muller’S Ratchet ◽  
The Impact

Microsporidia are fungi-like parasites that have the smallest known eukaryotic genome, and for that reason they are used as a model to study the phenomenon of genome decay in parasitic forms of life. Similar to other intracellular parasites that reproduce asexually in an environment with alleviated natural selection, Microsporidia experience continuous genome decay driven by Muller's ratchet - an evolutionary process of irreversible accumulation of deleterious mutations, which leads to gene loss and miniaturization of cellular components. Particularly, Microsporidia have remarkably small ribosomes in which the rRNA is reduced to the minimal enzymatic core. To better understand the impact of Muller's ratchet on RNA and protein molecules in parasitic organisms, particularly regarding their ribosome structure, we have explored an apparent effect of Muller's ratchet on microsporidian ribosomal proteins. Through mass spectrometry, analysis of microsporidian genome sequences and analysis of ribosome structure from non-parasitic eukaryotes, we found that massive rRNA reduction in microsporidian ribosomes appears to annihilate binding sites for ribosomal proteins eL8, eL27, and eS31, suggesting that these proteins are no longer bound to the ribosome in microsporidian species. We then provided an evidence that protein eS31 is retained in Microsporidia due to its non-ribosomal function in ubiquitin biogenesis. To sum up, our study illustrates that while Microsporidia carry the same set of ribosomal proteins as non-parasitic eukaryotes, some of ribosomal proteins are no longer participating in protein synthesis in Microsporidia and they are preserved from genome decay by having extra-ribosomal functions.

scholarly journals Genotypic Males Play an Important Role in the Creation of Genetic Diversity in Gynogenetic Gibel Carp

2021 ◽  
Vol 12 ◽  
Author(s):  
Xin Zhao ◽  
Zhi Li ◽  
Miao Ding ◽  
Tao Wang ◽  
Ming-Tao Wang ◽  
...  
Keyword(s):  
Genetic Diversity ◽  
Sex Determination ◽  
Common Carp ◽  
Evolutionary Process ◽  
Gibel Carp ◽  
Temperature Dependent ◽  
Muller's Ratchet ◽  
Genotypic Sex Determination ◽  
Muller’S Ratchet ◽  
The Creation

Unisexual lineages are commonly considered to be short-lived in the evolutionary process as accumulation of deleterious mutations stated by Muller’s ratchet. However, the gynogenetic hexaploid gibel carp (Carassius gibelio) with existence over 0.5 million years has wider ecological distribution and higher genetic diversity than its sexual progenitors, which provides an ideal model to investigate the underlying mechanisms on countering Muller’s ratchet in unisexual taxa. Unlike other unisexual lineages, the wild populations of gibel carp contain rare and variable proportions of males (1–26%), which are determined via two strategies including genotypic sex determination and temperature-dependent sex determination. Here, we used a maternal gibel carp from strain F to be mated with a genotypic male from strain A+, a temperature-dependent male from strain A+, and a male from another species common carp (Cyprinus carpio), respectively. When the maternal individual was mated with the genotypic male, a variant of gynogenesis was initiated, along with male occurrence, accumulation of microchromosomes, and creation of genetic diversity in the offspring. When the maternal individual was mated with the temperature-dependent male and common carp, typical gynogenesis was initiated that all the offspring showed the same genetic information as the maternal individual. Subsequently, we found out that the genotypic male nucleus swelled and contacted with the female nucleus after fertilization although it was extruded from the female nucleus eventually, which might be associated with the genetic variation in the offspring. These results reveal that genotypic males play an important role in the creation of genetic diversity in gynogenetic gibel carp, which provides insights into the evolution of unisexual reproduction.

scholarly journals 'Lose-to-gain' adaptation to genome decay in the structure of the smallest eukaryotic ribosomes

2021 ◽  
Author(s):  
David Nicholson ◽  
Marco Salamina ◽  
Johan Panek ◽  
Karla Helena-Bueno ◽  
Charlotte R Brown ◽  
...  
Keyword(s):  
Evolutionary Process ◽  
Building Blocks ◽  
Structural Features ◽  
Molecular Structures ◽  
Evolutionary Pattern ◽  
Gain Adaptation ◽  
Intracellular Parasites ◽  
Genome Decay ◽  
The One ◽  
Genetic Drifts

The evolution of microbial parasites involves the interplay of two opposing forces. On the one hand, the pressure to survive drives parasites to improve through Darwinian natural selection. On the other, frequent genetic drifts result in genome decay, an evolutionary process in which an ever-increasing burden of deleterious mutations leads to gene loss and gradual genome reduction. Here, seeking to understand how this interplay occurs at the scale of individual macromolecules, we describe cryo-EM and evolutionary analyses of ribosomes from Encephalitozoon cuniculi, a eukaryote with one of the most reduced genomes in nature. We show that E. cuniculi ribosomes, the smallest eukaryotic cytoplasmic ribosomes to be structurally characterized, employ unparalleled structural innovations that allow extreme rRNA reduction without loss of ribosome integrity. These innovations include the evolution of previously unknown rRNA features such as molten rRNA linkers and bulgeless rRNA. Furthermore, we show that E. cuniculi ribosomes withstand the loss of rRNA and protein segments by evolving a unique ability to effectively trap small molecules and use them as ribosomal building-blocks and structural mimics of degenerated rRNA and protein segments. Overall, our work reveals a recurrent evolutionary pattern, which we term 'lose-to-gain' evolution, where it is only through the loss of rRNA and protein segments that E. cuniculi ribosomes evolve their major innovations. Our study shows that the molecular structures of intracellular parasites long viewed as reduced, degenerated, and suffering from various debilitating mutations instead possess an array of systematically overlooked and extraordinary structural features. These features allow them to not only adapt to molecular reduction but evolve new activities that parasites can possibly use to their advantage.

scholarly journals Small-world networks decrease the speed of Muller's ratchet

2007 ◽  
Vol 89 (1) ◽  
pp. 7-18 ◽  
Author(s):  
JAIME COMBADÃO ◽  
PAULO R. A. CAMPOS ◽  
FRANCISCO DIONISIO ◽  
ISABEL GORDO
Keyword(s):  
Evolutionary Process ◽  
Small World ◽  
Structured Populations ◽  
Stepping Stone ◽  
Muller's Ratchet ◽  
Structured Population ◽  
Muller’S Ratchet ◽  
Spatially Structured Population ◽  
Disease Epidemics ◽  
Regular Networks

Muller's ratchet is an evolutionary process that has been implicated in the extinction of asexual species, the evolution of non-recombining genomes, such as the mitochondria, the degeneration of the Y chromosome, and the evolution of sex and recombination. Here we study the speed of Muller's ratchet in a spatially structured population which is subdivided into many small populations (demes) connected by migration, and distributed on a graph. We studied different types of networks: regular networks (similar to the stepping-stone model), small-world networks and completely random graphs. We show that at the onset of the small-world network – which is characterized by high local connectivity among the demes but low average path length – the speed of the ratchet starts to decrease dramatically. This result is independent of the number of demes considered, but is more pronounced the larger the network and the stronger the deleterious effect of mutations. Furthermore, although the ratchet slows down with increasing migration between demes, the observed decrease in speed is smaller in the stepping-stone model than in small-world networks. As migration rate increases, the structured populations approach, but never reach, the result in the corresponding panmictic population with the same number of individuals. Since small-world networks have been shown to describe well the real contact networks among people, we discuss our results in the light of the evolution of microbes and disease epidemics.

scholarly journals Special Issue: “Viral Replication Complexes”

Viruses ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 1902
Author(s):  
Núria Verdaguer ◽  
Diego S. Ferrero
Keyword(s):  
Viral Replication ◽  
Special Issue ◽  
Obligate Intracellular ◽  
Intracellular Parasites ◽  
Biological Entities ◽  
Cellular Components

Viruses are extraordinary biological entities that can only thrive as obligate intracellular parasites, exploiting other living cellular components in order to reproduce [...]

scholarly journals Untargeted Metabolomics Uncovers the Essential Lysine Transporter in Toxoplasma gondii

Metabolites ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 476
Author(s):  
Joachim Kloehn ◽  
Matteo Lunghi ◽  
Emmanuel Varesio ◽  
David Dubois ◽  
Dominique Soldati-Favre
Keyword(s):  
Amino Acids ◽  
Toxoplasma Gondii ◽  
Rna Degradation ◽  
Major Facilitator Superfamily ◽  
Untargeted Metabolomics ◽  
Apicomplexan Parasites ◽  
Obligate Intracellular ◽  
Intracellular Parasites ◽  
Major Facilitator ◽  
Plasma Membrane Transporter

Apicomplexan parasites are responsible for devastating diseases, including malaria, toxoplasmosis, and cryptosporidiosis. Current treatments are limited by emerging resistance to, as well as the high cost and toxicity of existing drugs. As obligate intracellular parasites, apicomplexans rely on the uptake of many essential metabolites from their host. Toxoplasma gondii, the causative agent of toxoplasmosis, is auxotrophic for several metabolites, including sugars (e.g., myo-inositol), amino acids (e.g., tyrosine), lipidic compounds and lipid precursors (cholesterol, choline), vitamins, cofactors (thiamine) and others. To date, only few apicomplexan metabolite transporters have been characterized and assigned a substrate. Here, we set out to investigate whether untargeted metabolomics can be used to identify the substrate of an uncharacterized transporter. Based on existing genome- and proteome-wide datasets, we have identified an essential plasma membrane transporter of the major facilitator superfamily in T. gondii—previously termed TgApiAT6-1. Using an inducible system based on RNA degradation, TgApiAT6-1 was depleted, and the mutant parasite’s metabolome was compared to that of non-depleted parasites. The most significantly reduced metabolite in parasites depleted in TgApiAT6-1 was identified as the amino acid lysine, for which T. gondii is predicted to be auxotrophic. Using stable isotope-labeled amino acids, we confirmed that TgApiAT6-1 is required for efficient lysine uptake. Our findings highlight untargeted metabolomics as a powerful tool to identify the substrate of orphan transporters.

Encystment and germination of the parasitic chytrid Rozella allomycis on host hyphae

1973 ◽  
Vol 51 (10) ◽  
pp. 1825-1835 ◽  
Author(s):  
Abraham A. Held
Keyword(s):  
Cyst Wall ◽  
Germ Tube ◽  
Light And Electron Microscopy ◽  
Multivesicular Bodies ◽  
Cell Periphery ◽  
General Sequence ◽  
Obligate Intracellular ◽  
Host Cytoplasm ◽  
Intracellular Parasites ◽  
Three Stages

Zoospores of the obligately parasitic chytrid Rozella allomycis which settle upon hyphae of the water mold host, Allomyces arbuscula, encyst and germinate before their protoplasts penetrate into the host cytoplasm. This process has been examined by light and electron microscopy. Three stages which follow the attachment to the host and the retraction of the zoospore's flagellum are described: (1) the early cyst lacks a wall; it is discoid, and its shape is maintained by the coil of the retracted axoneme which forms its rim; (2) a cyst wall is formed while multivesicular bodies occur at the cell periphery and eventually disappear; a germ tube starts to grow at the point of attachment; and (3) the firm-walled cyst is spheroidal; it has a fully developed germ tube with a specialized class of vesicles; it also forms a distal, flattened vacuole whose swelling eventually injects the Rozella protoplast into the host; at this stage the retracted axoneme has disappeared and the cell's organelles have undergone extensive changes. Electron-dense, "gamma-like" granules enclosed in vacuoles may play a major role in the formation of both the cyst wall and the distal vacuole. These granules appear to give rise to small vesicles, and thus to multivesicular bodies; the distal vacuole appears to form by coalescense of gamma-like vacuoles.The general sequence of encystment and germination resembles that found in other Chytridiomycetes, both saprophytic and parasitic. However, the distal vacuole and the vesicles in the germ tube appear to be parasitic adaptations and are shared by obligate intracellular parasites from several unrelated groups of zoosporic fungi.

Round Table Discussion

PEDIATRICS ◽  
1948 ◽  
Vol 2 (4) ◽  
pp. 469-479
Author(s):  
RUSSELL J. BLATTNER
Keyword(s):  
Inclusion Bodies ◽  
Cellular Response ◽  
Infectious Agent ◽  
Round Table ◽  
Chemotherapeutic Agents ◽  
Tissue Response ◽  
Round Table Discussion ◽  
Obligate Intracellular ◽  
Form Of Life ◽  
Intracellular Parasites

Chairman Blattner: During recent years, there has been increasing interest shown in diseases caused by filterable viruses, and significant work has been accomplished in this comparatively new and absorbing field of endeavor. With the advent of chemotherapeutic agents and antibiotics, the presence and action of these infectious agents has become more apparent. Viral diseases, therefore, have assumed increasing importance in medical literature in general and in pediatric literature in particular. By way of review, it is well to bear in mind that viruses are filter-passing agents, obligate intracellular parasites, capable of reproducing themselves and of producing disease in plants and animals, including man. While these agents cannot be seen except by the most elaborate methods, their presence can be detected by their injurious effects. The pathologic picture produced by viral agents is rather characteristic and can be recognized readily by experienced observers acquainted with tissue response. In some instances, inclusion bodies are produced which may be intranuclear or intracytoplasmic, and represent cytologic changes which are considered typical of the pathologic response to viral invasion. When inclusion bodies are present they may serve as sign posts for the recognition of the type of infectious agent. The nature of a filterable virus is as yet unknown. Viruses may be a form of life similar to bacteria, but infinitely smaller in size. It is conceivable that viruses are enzymes capable of reproducing themselves and capable of producing cellular response. They may be non-living, crystallizable substances, such as the Stanley tobacco-mosaic virus; or a form of life, the definite nature of which is as yet unrecognized. Dr. Thomas M. Rivers has stated : "Viruses are a heterogeneous collection of diverse agents which happen to induce a state of broad similarity." He points out that the reaction of the tissues in general, and of the cells in particular, determines the nature of the pathologic process about as much as the infectious agent itself.

Muller’s ratchet of the Y chromosome with gene conversion

Genetics ◽  
2021 ◽  
Author(s):  
Takahiro Sakamoto ◽  
Hideki Innan
Keyword(s):  
Gene Duplication ◽  
Gene Conversion ◽  
Y Chromosome ◽  
Conversion Rate ◽  
Single Copy ◽  
Duplicated Genes ◽  
Fitness Effect ◽  
Muller's Ratchet ◽  
Y Chromosomes ◽  
Muller’S Ratchet

Abstract Muller’s ratchet is a process in which deleterious mutations are fixed irreversibly in the absence of recombination. The degeneration of the Y chromosome, and the gradual loss of its genes, can be explained by Muller’s ratchet. However, most theories consider single-copy genes, and may not be applicable to Y chromosomes, which have a number of duplicated genes in many species, which are probably undergoing concerted evolution by gene conversion. We developed a model of Muller’s ratchet to explore the evolution of the Y chromosome. The model assumes a non-recombining chromosome with both single-copy and duplicated genes. We used analytical and simulation approaches to obtain the rate of gene loss in this model, with special attention to the role of gene conversion. Homogenization by gene conversion makes both duplicated copies either mutated or intact. The former promotes the ratchet, and the latter retards, and we ask which of these counteracting forces dominates under which conditions. We found that the effect of gene conversion is complex, and depends upon the fitness effect of gene duplication. When duplication has no effect on fitness, gene conversion accelerates the ratchet of both single-copy and duplicated genes. If duplication has an additive fitness effect, the ratchet of single-copy genes is accelerated by gene duplication, regardless of the gene conversion rate, whereas gene conversion slows the degeneration of duplicated genes. Our results suggest that the evolution of the Y chromosome involves several parameters, including the fitness effect of gene duplication by increasing dosage and gene conversion rate.

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