Search Results (5)

We study how small harmful mutations spread in populations that reproduce asexually. This process is known as Muller’s ratchet—it means that even though these mutations are damaging, they can still build up over generations. To explore this, we use a mathematical model that describes how such mutations move through a population living in an environment with limited resources. We model Muller’s ratchet deterministically using differential equations, incorporating modifications that account for extinction risk of small mutation classes. We analyze two modifications: a published cutoff modification and a more flexible exponential modification. We show that the exponential modification better matches stochastic simulations over specific parameter ranges. Full article

Uniparental inheritance of mitochondria enables organisms to avoid the costs of intracellular competition among potentially selfish organelles. By preventing recombination, uniparental inheritance may also render a mitochondrial lineage effectively asexual and expose mitochondria to the deleterious effects of Muller’s ratchet. Even among animals and plants, the evolutionary dynamics of mitochondria remain obscure, and less is known about mitochondrial inheritance among fungi. To understand mitochondrial inheritance and test for mitochondrial recombination in one species of filamentous fungus, we took a population genomics approach. We assembled and analyzed 88 mitochondrial genomes from natural populations of the invasive death cap Amanita phalloides, sampling from both California (an invaded range) and Europe (its native range). The mitochondrial genomes clustered into two distinct groups made up of 57 and 31 mushrooms, but both mitochondrial types are geographically widespread. Multiple lines of evidence, including negative correlations between linkage disequilibrium and distances between sites and coalescent analysis, suggest low rates of recombination among the mitochondria (ρ = 3.54 × 10⁻⁴). Recombination requires genetically distinct mitochondria to inhabit a cell, and recombination among A. phalloides mitochondria provides evidence for heteroplasmy as a feature of the death cap life cycle. However, no mushroom houses more than one mitochondrial genome, suggesting that heteroplasmy is rare or transient. Uniparental inheritance emerges as the primary mode of mitochondrial inheritance, even as recombination appears as a strategy to alleviate Muller’s ratchet. Full article

Some debilitating mutations in RNA viruses are repairable; however, the triggering factors of mutation repair remain largely unknown. In this study, multiple triggering factors of mutation repair are identified based on genetic damage to the TLS in CMV. TLS mutations in different RNAs distinctively impact viral pathogenicity and present different types of mutation repair. RNA2 relative reduction level or RNA3 sequence change resulting from TLS mutation is correlated with a high rate of mutation repair, and the TLS mutation of RNA1 fails to be repaired at the high inoculum dose. However, the TLS mutation of RNA1 can be repaired at a low dose of inoculation, particularly around the dilution end-point or in the mixed inoculation with RNA2 having a pre-termination mutation of the 2b gene, an RNAi suppressor. Taken together, TLS mutations resulting in quality or quantity defects of the viral genome or TLS mutations at low doses around the dilution end-point are likely to be repaired. Different levels of TLS mutation repair necessarily require cell-to-cell movement, therefore implying its obligated effect on the evolution of low-fitness viruses and providing a new insight into Muller’s ratchet. This study provides important information on virus evolution and the application of mild viral vaccines. Full article

The circulation in Europe of novel reassortant strains of infectious bursal disease virus (IBDV), containing a unique genetic background composition, represents a serious problem for animal health. Since the emergence of this novel IBDV mosaic was first described in Poland, this scenario has become particularly attractive to uncover the evolutionary forces driving the genetic diversity of IBDV populations. This study additionally addressed the phenotypic characterization of these emergent strains, as well as the main features affecting the viral fitness during the competition process of IBDV lineages in the field. Our results showed how different evolutionary mechanisms modulate the genetic diversity of co-existent IBDV lineages, leading to the error catastrophe effect, Muller ratchet effect, or prevalence, depending on their genetic compositions. We also determined that the action of the positive selection pressure, depending on the genomic segment on which it is acting, can drive two main phenotypes for IBDV: immune-escaping strains from the selection on segment A or strains with functional advantages from the selection on segment B. This last group seems to possess an increased fitness landscape in the viral quasispecies composition, presenting better adaptability to dissimilar environmental conditions and likely becoming the dominant population. The reassortant strains also exhibited a lower mortality rate compared with the well-known vvIBDV strains, which can facilitate their spreading. Full article

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. Full article