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Introduction to Genomics
Published in Altuna Akalin, Computational Genomics with R, 2020
DNA methylation is usually associated with gene silencing. DNA methyltransferase enzyme catalyzes the addition of a methyl group to cytosine of CpG dinucleotides (while in mammals the addition of methyl group is largely restricted to CpG dinucleotides, methylation can occur in other bases as well). This covalent modification either interferes with transcription factor binding on the region, or methyl-CpG binding proteins induce the spread of repressive chromatin domains, thus the gene is silenced if its promoter has methylated CG dinucleotides. DNA methylation usually occurs in repeat sequences to repress transposable elements. These elements, when active, can jump around and insert them to random parts of the genome, potentially disrupting the genomic functions.
Mobile DNA Sequences and Their Possible Role in Evolution
Published in S. K. Dutta, DNA Systematics, 2019
Georgii P. Georgiev, Yurii V. Ilyin, Alexei P. Ryskov, Tatiana I. Gerasimova
Amplification of mobile elements themselves increases the amount of genetic material in the genome. This extra material may be used for the formation of new genes in evolution. We have already mentioned that almost any part of the genome may act as a passive transposable element mobilized through reverse transcription of RNA-polymerase II or III transcripts. Such novel construction may appear in any region of the genome. In this way, the complete genes, their parts, larger sequences of DNA, or small signal sequences can be spread throughout the genome. As a result, new genes or some novel constructions consisting of parts of different genes or of their regulatory elements can appear.
The Concept of Health
Published in Dien Ho, A Philosopher Goes to the Doctor, 2019
The example of a “selfish” DNA can help illustrate the gap between a gene’s interests and our interests. Approximately two-thirds of the human genome consists of transposable elements (Graur, 2015, p. 417). These elements mostly reside in the parts of our DNA that have no effect on our physiology. However, these transposable elements, or transposons, can move around, replicate, and slice and dice our genes, inserting themselves in various segments of our DNA. Very rarely, when transposons alter our DNA, can they confer positive effects on the host. Most of the time, the changes are either benign or have negative effects on the host. The origins of many of these transposons date back millions of years, and they are now a majority of our genome. When they are benign, they are free-riders, changing our gametes and passing themselves along. When they are harmful, they are not just selfish genes but nasty genes, risking the health of the host in their evolutionary track. From the point of view of our evolutionary fitness (and even health), most selfish genes seem to be useless. However, from the point of view of the genes’ evolutionary fitness, they are doing quite well, for they somehow have managed to ride along in our genome for millions of years.
The effects of transpositions of functional I retrotransposons depend on the conditions and dose of parental exposure
Published in International Journal of Radiation Biology, 2023
Transposable elements (TEs) act as ‘stress receptors’ and induce a large amount of DNA damages which cause various genetic rearrangements. The ability of TEs to move in genome produces the genetic instability in the offspring of animals not only of the first generation, but also of subsequent generations (Harms-Ringdahl 1998; Yushkova 2019). P- and hobo transposons are widely studied in this aspect and I retroelements are largely understudied (Zainullin et al. 2000; Zakharenko et al. 2006; Zainullin and Yushkova 2012; Yushkova 2017). Despite these TEs differ in molecular structure, mutability, and sensitivity to stressors, any of them have two main features as participation in formation of genetic systems in Drosophila melanogaster and the specific movement accompanied by formation of double breaks in cellular DNA (Ivashchenko and Grishaeva 2002; Vasil’eva et al. 2007; Orsi et al. 2010).
RNA A-to-I editing, environmental exposure, and human diseases
Published in Critical Reviews in Toxicology, 2021
Retrotransposons (or “jumping genes,” via RNA intermediates) comprise almost half of the human genome. They are the discrete sequences of DNA that can move from region to region across genomes under environmental stress. By affecting human genomic structures, transposable elements contribute to genomic evolution. Besides, they modify the risks for various diseases, including cancer, by generating chromosome mutations (insertion/deletion), genomic instability, and disorder in gene expression. Retrotransposons include the widely studied LINE-1 and Alu elements that are defined as short interspersed nuclear elements (SINEs) and common in the primate genome (Bazak et al. 2014). In Alu elements, intramolecular double strand RNA occurs in introns and 3′ untranslated region which are subject to RNA editing (Nishikura 2016). Recent advances in deep sequencing accelerate our understanding of how RNA editing is common in Alu double stranded RNAs. Now, we have substantial evidence from various studies that RNA editing sites are commonly available in Alu elements. Approximately 1.6 million RNA editing sites were demonstrated in Alu elements which are much higher than is anticipated (Bazak et al. 2014). In another human transcriptome study, the authors reported that A-to-I RNA editing was common in human mRNAs containing 14,500 sites and located in untranslated regions and introns (Athanasiadis et al. 2004; Levanon et al. 2004).
Stress-induced strain and brain region-specific activation of LINE-1 transposons in adult mice
Published in Stress, 2018
Ugo Cappucci, Giulia Torromino, Assunta Maria Casale, Jeremy Camon, Fabrizio Capitano, Maria Berloco, Andrea Mele, Sergio Pimpinelli, Arianna Rinaldi, Lucia Piacentini
Transposable elements (TEs) are highly abundant mobile genetic elements that constitute a large fraction of most eukaryotic genomes and are emerging as novel modulators of gene expression (Goodier & Kazazian, 2008). In the early 1950s, Barbara McClintock first suggested that TEs are capable of actively reprograming host genetic regulatory network and fine-tuning the host response to specific environmental stress stimuli (Fedoroff, 2012; McClintock, 1951, 1984); since then, the release of the epigenetic TEs silencing has been reported in Drosophila and other organisms in response to different types of stress as temperature, UV exposure, radiations, wounding, cell culture, pathogen infection, and polyploidization (Fanti, Piacentini, Cappucci, Casale, & Pimpinelli, 2017; Natt & Thorsell, 2016; Piacentini et al., 2014). Stress-induced TEs expression could increase the genome ability to flexibly cope with environmental changes through two different mechanisms. First, the mutagenic activity of TEs might directly trigger genomic variability by creating mutations, chromosome rearrangements and new functional regulatory elements (Wheeler, 2013). Second, transposons transcripts per se might widely influence the transcriptome by producing regulatory small-RNAs that could modulate intrans the expression profiles of non-neighboring genes (Wheeler, 2013). Therefore, although functional roles and mobilization mechanisms remain poorly understood, it is now clear that TEs coevolved with their host genomes.