Academic literature on the topic 'Mutation (Biology) RNA. RNA Phenotype. Evolution (Biology)'

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Journal articles on the topic "Mutation (Biology) RNA. RNA Phenotype. Evolution (Biology)"

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Flamm, Chirstoph, Ivo L. Hofacker, and Peter F. Stadler. "RNA In Silico The Computational Biology of RNA Secondary Structures." Advances in Complex Systems 02, no. 01 (1999): 65–90. http://dx.doi.org/10.1142/s0219525999000059.

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RNA secondary structures provide a unique computer model for investigating the most important aspects of structural and evolutionary biology. The existence of efficient algorithms for solving the folding problem, i.e., for predicting the secondary structure given only the sequence, allows the construction of realistic computer simulations. The notion of a "landscape" underlies both the structure formation (folding) and the (in vitro) evolution of RNA. Evolutionary adaptation may be seen as hill climbing process on a fitness landscape which is determined by the phenotype of the RNA molecule (wi
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Wang, Lili, Dylan Kotliar, Jean Fan, et al. "Integrated Single-Cell Detection of Genotype and Phenotype in SF3B1-Mutated Chronic Lymphocytic Leukemia Cells." Blood 124, no. 21 (2014): 1943. http://dx.doi.org/10.1182/blood.v124.21.1943.1943.

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Abstract Cancer cell phenotype is controlled by both genetic composition and gene expression. Recent large-scale cancer sequencing studies have revealed extensive intratumoral genetic heterogeneity and have demonstrated its potential impact on clonal evolution and clinical outcome. The most direct approach to uncovering the impact of genetic heterogeneity on cellular phenotype requires integration of genetic and transcriptomic profiles of single cells. Currently, however, RNA and DNA cannot be reliably isolated from the same cell. Here, we demonstrate the feasibility for linking single-cell so
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Schaper, Steffen, Iain G. Johnston, and Ard A. Louis. "Epistasis can lead to fragmented neutral spaces and contingency in evolution." Proceedings of the Royal Society B: Biological Sciences 279, no. 1734 (2011): 1777–83. http://dx.doi.org/10.1098/rspb.2011.2183.

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In evolution, the effects of a single deleterious mutation can sometimes be compensated for by a second mutation which recovers the original phenotype. Such epistatic interactions have implications for the structure of genome space—namely, that networks of genomes encoding the same phenotype may not be connected by single mutational moves. We use the folding of RNA sequences into secondary structures as a model genotype–phenotype map and explore the neutral spaces corresponding to networks of genotypes with the same phenotype. In most of these networks, we find that it is not possible to conne
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Inagaki, Ryosaku, Masahiro Marshall Nakagawa, Yasuhito Nannya, et al. "Analysis of Clonal Evolution of AML Using Simultaneous Single-Cell DNA/RNA Analysis." Blood 136, Supplement 1 (2020): 1. http://dx.doi.org/10.1182/blood-2020-143320.

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Background Acute myeloid leukemia (AML) was defined by an increase of immature myeloid cells, or blasts that exceed ≥20% in bone marrow or peripheral blood. Many lines of evidence suggest that the development of AML is shaped by clonal evolution through multiple rounds of positive selection driven by newly acquired mutations, ultimately leading to an increased blast count. This process has been analyzed in detail in the case of progression from myelodysplastic syndromes (MDS) to secondary AML (sAML), which is invariably accompanied by expansion of cells that acquired new driver alterations, ge
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Lim, Huat Chye, and John D. Gordan. "Tumor hepatitis B virus RNA identifies a clinically and molecularly distinct subset of hepatocellular carcinoma." PLOS Computational Biology 17, no. 2 (2021): e1008699. http://dx.doi.org/10.1371/journal.pcbi.1008699.

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Hepatitis B virus (HBV) infection contributes to hepatocellular carcinoma (HCC) initiation and is associated with worse outcomes. Many prior studies of HBV-related HCC have not accounted for potential heterogeneity among HBV-related tumors by assessing whether HBV activity is present in tumor tissue. Here, we measured tumor HBV RNA, a proxy for viral activity, and investigated the association between HBV RNA status and several clinicogenomic characteristics. We obtained clinical, mutation, RNA-Seq and survival data for 439 HCC tumors from The Cancer Genome Atlas and International Cancer Genome
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Dingle, Kamaludin, Steffen Schaper, and Ard A. Louis. "The structure of the genotype–phenotype map strongly constrains the evolution of non-coding RNA." Interface Focus 5, no. 6 (2015): 20150053. http://dx.doi.org/10.1098/rsfs.2015.0053.

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The prevalence of neutral mutations implies that biological systems typically have many more genotypes than phenotypes. But, can the way that genotypes are distributed over phenotypes determine evolutionary outcomes? Answering such questions is difficult, in part because the number of genotypes can be hyper-astronomically large. By solving the genotype–phenotype (GP) map for RNA secondary structure (SS) for systems up to length L = 126 nucleotides (where the set of all possible RNA strands would weigh more than the mass of the visible universe), we show that the GP map strongly constrains the
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Mandary, Masomian, and Poh. "Impact of RNA Virus Evolution on Quasispecies Formation and Virulence." International Journal of Molecular Sciences 20, no. 18 (2019): 4657. http://dx.doi.org/10.3390/ijms20184657.

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RNA viruses are known to replicate by low fidelity polymerases and have high mutation rates whereby the resulting virus population tends to exist as a distribution of mutants. In this review, we aim to explore how genetic events such as spontaneous mutations could alter the genomic organization of RNA viruses in such a way that they impact virus replications and plaque morphology. The phenomenon of quasispecies within a viral population is also discussed to reflect virulence and its implications for RNA viruses. An understanding of how such events occur will provide further evidence about whet
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Lehman, Niles. "Assessing the Likelihood of Recurrence during RNA Evolution in Vitro." Artificial Life 10, no. 1 (2004): 1–22. http://dx.doi.org/10.1162/106454604322875887.

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Recurrence is the possibility of resulting in the same endpoint multiple times when a living system is allowed to evolve repeatedly starting from a given initial point. This concept is of concern to both evolutionary theoreticians and molecular biologists who use nucleic acid selection techniques to mimic biotic and computorial processes in the test tube. Using the continuous in vitro evolution methodology, many replicate experimental evolutionary lineages with populations of catalytic RNA were performed to gain insight into the parameters that could affect recurrence. The likelihood that the
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Kislauskis, E. H., X. Zhu, and R. H. Singer. "Sequences responsible for intracellular localization of beta-actin messenger RNA also affect cell phenotype." Journal of Cell Biology 127, no. 2 (1994): 441–51. http://dx.doi.org/10.1083/jcb.127.2.441.

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We have characterized the structure and function of RNA sequences that direct beta-cytoplasmic actin mRNA to the cell periphery were mapped to two segments of 3'-untranslated region by expression of LacZ/beta-actin chimeric mRNAs in chicken embryo fibroblasts (CEFs). A 54-nt segment, the "RNA zipcode," and a homologous but less active 43-nt segment each localized beta-galactosidase activity to the leading lamellae. This zipcode contains the full activity, and mutations or deletions within it reduce, but do not eliminate, its activity, indicating that several motifs contribute to the activity.
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Barešić, Anja, and Andrew C. R. Martin. "Compensated pathogenic deviations." BioMolecular Concepts 2, no. 4 (2011): 281–92. http://dx.doi.org/10.1515/bmc.2011.025.

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AbstractDeleterious or ‘disease-associated’ mutations are mutations that lead to disease with high phenotype penetrance: they are inherited in a simple Mendelian manner, or, in the case of cancer, accumulate in somatic cells leading directly to disease. However, in some cases, the amino acid that is substituted resulting in disease is the wild-type native residue in the functionally equivalent protein in another species. Such examples are known as ‘compensated pathogenic deviations’ (CPDs) because, somewhere in the second species, there must be compensatory mutations that allow the protein to
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Dissertations / Theses on the topic "Mutation (Biology) RNA. RNA Phenotype. Evolution (Biology)"

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Rendel, Mark D. "The evolutionary dynamics of neutral networks : lessons from RNA." Thesis, University of Oxford, 2008. http://ora.ox.ac.uk/objects/uuid:85107ca7-fada-4582-95e7-17b5bbb038cd.

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The evolutionary options of a population are strongly influenced by the avail- ability of adaptive mutants. In this thesis, I use the concept of neutral networks to show that neutral drift can actually increase the accessibility of adaptive mu- tants, and therefore facilitate adaptive evolutionary change. Neutral networks are groups of unique genotypes which all code for the same phenotype, and are connected by simple point mutations. I calculate the size and shape of the networks in a small but exhaustively enumerated space of RNA genotypes by mapping the sequences to RNA secondary structure
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Diaz, Arenas Carolina. "Evolutionary Dynamics in Molecular Populations of Ligase Ribozymes." PDXScholar, 2010. https://pdxscholar.library.pdx.edu/open_access_etds/44.

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The emergence of life depended on the ability of the first biopolymer populations to thrive and approach larger population sizes and longer sequences. The evolution of these populations likely occurred under circumstances under which Muller's Ratchet in synergism with random drift could have caused large genetic deterioration of the biopolymers. This deterioration can drive the populations to extinction unless there is a mechanism to counteract it. The effect of the mutation rate and the effective population size on the time to extinction was tested on clonal populations of B16-19 ligase riboz
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Dutta, Ranendra Nath. "Experimental Test of Solitary Wave Theory in Viral Populations." University of Toledo Health Science Campus / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=mco1226950654.

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Cowperthwaite, Matthew Cranston 1973. "Mutation: lessons from RNA models." Thesis, 2008. http://hdl.handle.net/2152/3867.

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Mutation is a fundamental process in evolution because affects the amount of genetic variation in evolving populations. Molecular-structure models offer significant advantages over traditional population-genetics models for studying mutation, mainly because such models incorporate simple, tractable genotype-to-phenotype maps. Here, I use RNA secondary structure models to study four basic properties of mutation. The first section of this thesis studies the statistical properties of beneficial mutations. According to population genetics theory, the fitness effects of new beneficial mutations wil
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Book chapters on the topic "Mutation (Biology) RNA. RNA Phenotype. Evolution (Biology)"

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Maynard Smith, John, and Eors Szathmary. "The chicken and egg problem." In The Major Transitions in Evolution. Oxford University Press, 1997. http://dx.doi.org/10.1093/oso/9780198502944.003.0009.

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The most fundamental distinction in biology is between nucleic acids, with their role as carriers of information, and proteins, which generate the phenotype. In existing organisms, nucleic acids and proteins mutually presume one another. The former, owing to their template activity, store the heritable information: the latter, by enzymatic activity, read and express this information. It seems that neither can function without the other. Which came first, nucleic acids or proteins? There are three possible answers: (1) nucleic acids; (2) proteins; (3) neither: they coevolved. In this chapter, we discuss various possible answers to this 'chicken or egg?' problem. In section 5.2, we discuss what seems to us the most likely answer, that at first RNA performed both functions, as replicator and enzyme. In section 5.3, we consider an alternative view, in which protein enzymes existed either before, or alongside, the first nucleic acids. In section 5.4, we ask whether, perhaps, the first replicators were not nucleic acids. Finally, in section 5.5, we ask why, given that the genetic message is carried by nucleic acids, there are only four nucleotides and two base pairs. So far, we have tacitly assumed nucleic acids preceeded proteins, without stating the main reason. Nucleic acids came first because they can perform both functions: they are replicable, and they can have enzymatic activity. For many years, a common opinion was that to be replicable almost amounted to self-replicative ability, but that it was far-fetched to assume enzymatic activity. Today, there is increasing evidence that RNA can act as an enzyme, but we are more aware of the difficulty of self-replication. It should have been expected on theoretical grounds that RNA could act as an enzyme: the possibility was discussed by Woese (1967), Crick (1968) and Orgel (1968). Consider first why proteins can act as enzymes. An enzyme has a well-determined three-dimensional structure of chemical groups that, in most cases, arises automatically from the primary structure. Substrates of the enzyme are bound by the chemical groups on the surface. This means that the reactants will be kept in close proximity, and hence experience a much higher local concentration of each other than in solution. This by itself increases the rate of the reaction.
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Maynard Smith, John, and Eors Szathmary. "The origin of translation and the genetic code." In The Major Transitions in Evolution. Oxford University Press, 1997. http://dx.doi.org/10.1093/oso/9780198502944.003.0010.

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The origin of the code is perhaps the most perplexing problem in evolutionary biology. The existing translational machinery is at the same time so complex, so universal, and so essential that it is hard to see how it could have come into existence, or how life could have existed without it. The discovery of ribozymes has made it easier to imagine an answer to the second of these questions, but the transformation of an ‘RNA world’ into one in which catalysis is performed by proteins, and nucleic acids specialize in the transmission of information, remains a formidable problem. We start, in section 6.1, by discussing changes known to have occurred in the code since its origin. Although these changes are minor, they do shed some light on how the code may have evolved in its very early days. In section 6.2, we ask what can be deduced from the present assignment of codons to amino acids, and from the phytogeny of tRNAs. Finally, in section 6.3, we come to grips with the hardest question: how did a specific association between particular amino acids and particular codons first come into existence? It is this association that is the essence of the code. Today, it plays a role in translation, but we think it first arose to serve quite a different function. If so, this is an example of a common feature of evolution: structures that today serve a complex function arose first to serve a simpler one. For many years the common genetic code was thought to be universal. Recently, some interesting exceptions have been found. These are of two types: either a stop codon is used to code for an amino acid, or a codon has been reassigned to a different amino acid. At first sight it is hard to see how this could happen. To alter the meaning of a codon in one particular gene might be a selective advantage, just as any mutation might be, but to alter its meaning wherever it occurs throughout the genome must surely be disastrous.
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