Academic literature on the topic 'Selfish DNA element'

Abstract Biologists seek functional explanations for the attributes of organisms. Such explanations show the advantage that the attribute gives to the organism. Any attribute, including components of the genome, can potentially be explained in this way. The belief that such functional explanations are appropriate rests on the tenet of the Neo-Darwinian evolutionary theory that states that the only systematic mechanism by which genes or other DNA sequences can spread through populations is through differences in the fitnesses of their carriers. Transposable elements, however, increase in number either directly or indirectly during transposition, and thus could potentially spread without increasing the fitness of their hosts. This non-Darwinian behaviour illegitimizes functional explanations and requires us to seek causal explanations for the presence of transposable elements in genomes, incorporating both their own molecular properties and their effects on their hosts. One class of explanations are those in which the effects of transposable elements on their hosts are negative. In other words, they are ‘selfish DNAs’ (1, 2). In this chapter, I will discuss some of the ideas and experiments indicating the selfishness or otherwise of transposable genetic elements. For details of the structures of various classes of transposable elements and the mechanisms of their transposition, the reader should consult other chapters in this volume. I will concentrate mainly on the elements in sexually reproducing diploid eukaryotes, for which the data sets of the distributions and frequencies of elements are often more complete, and for which the Neo-Darwinian population genetics synthesis provides a framework for considerations of transposable element evolution. I will strive, however, to highlight the ways in which the evolutionary process affecting prokaryotic transposable elements shows important similarities to and differences from the diploid paradigm.

Abstract Simple sequence repeats (SSRs) are highly mutable sites that are distributed throughout eukaryotic genomes. They often occur as functional elements within genes and gene-regulatory regions where mutational changes in repeat number provide extensive variation with minimal genetic load. Implicit in this mutability is the potential for rapid and reversible adjustment of quantitative traits. Although these repetitive elements have been regarded as “junk” or “selfish” DNA, their unique properties are consistent with indirect selection for a “tuning knob” function that facilitates efficient evolutionary adaptation.

Abstract Gene selfishness is not in itself a barrier to cooperation; in fact, it is the reverse. We have seen repeatedly how self-interested cooperation evolves because of the benefits it brings to team players. But cooperation does not just produce benefits; it also creates opportunities for cheats. Cheating reaches its most extreme in the genomic parasites that exploit the replication machinery of the cell. Viruses are a familiar example, and they are arguably nature’s oldest professional cheats. Another class of genomic parasites is the transposable elements (TEs), which comprise over half our DNA. The variety of TEs is enormous and their nefarious strategies various—some are even parasitic within other TEs. Eukaryote genomes are not alone in containing TEs; bacterial chromosomes also have them, but in bacteria they are usually deleted and not allowed by natural selection to accumulate. The exceptions are TEs that team up with genes that are of positive advantage to their bacterial host, for example in conferring antibiotic resistance. In contrast to bacteria, it is clear from the sheer numbers of TEs that accumulate in eukaryotes that deletion is not so ready an option. The reason boils down to the difference in generation time between bacteria (c. 20 minutes) and most eukaryotes (25 years in humans). Short generation time and huge population size in bacteria sharpen the blade of natural selection, but the reverse blunts its ability to remove TEs from eukaryote genomes.

Error and chance events, random mutations, are necessary prerequisites for evolution to happen. In a perfect world with no mutations there would be no evolution because no genetic variation would be generated that natural selection or genetic drift could work upon. This chapter first reviews how DNA is organized into genomes and genes in bacteria, archaea, and, in greater detail, eukaryotes. A surprising finding is that only a small fraction of the eukaryote genome consists of coding sequence. Evolutionary processes that can explain the presence of large amounts of noncoding DNA and the repetitive structure of the genome are reviewed, with emphasis on the roles that selfish genetic elements and unequal crossing over play. The chapter further explores the mechanisms that cause mutation and how new genes and protein functions originate.

This chapter discusses how open reading frames (ORFs) of some RNAs can be altered after transcription by RNA editing. The chapter highlights the important role RNA editing plays in keeping selfish DNA elements in the genome in check. It also mentions the significant role RNA editing plays in enabling tRNAs to translate mRNAs efficiently, which is a process that is conserved between bacteria and eukaryotes. The chapter explains how RNA editing changes the sequence of RNAs once they have already been transcribed. It analyses RNA editing through base modification that changes the chemical identity of nucleotides already present within the transcript.

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