In contrast, the CI binding site is a short target (166 bp), but mutations in this region are likely to be dominant because they will lead to nonrepressible, constitutive TetA production.įig. The repressor gene provides a large target (714 bp), but mutations inactivating cI should be recessive since in trans copies of wild-type CI will still be able to repress tetA. Derepression can be achieved through mutations that either inactivate the cI gene or disrupt the CI binding site upstream of tetA ( Fig. This system provides tetracycline resistance when tetA transcription is derepressed. This construct consists of a cI gene, encoding the bacteriophage λ CI repressor, in control of the expression of a contiguous tetA gene, which encodes a tetracycline efflux pump (ref. Monod used to investigate the regulation of the Lac operon ( 18). To test whether genetic dominance determines the emergence of mutations in MGE-encoded genes, we used a two-gene synthetic system conceptually similar to the one that F. Results and Discussion Genetic Dominance Shapes the Emergence of Mutations in MGE-Encoded Genes. In light of these evidences, genetic dominance should strongly affect both the emergence of new mutations in MGE-encoded genes and the phenotypic effects of horizontally transferred alleles. Moreover, HGT in bacteria mostly occurs between close relatives ( 16, 17), and genes encoded on mobile elements can therefore create allelic redundancy with chromosomal genes. Extrachromosomal MGEs thus produce an island of local polyploidy in the bacterial genome ( 14, 15). Many MGEs, including plasmids and filamentous phages, replicate independently of the bacterial chromosome and are generally present at more than one copy per cell, with copy number ranging from a handful to several hundred ( 12, 13). However, the bacterial genome consists of more than the single chromosome a myriad of MGEs populate bacterial cells. Therefore, the role of genetic dominance in bacterial evolution has generally been overlooked. In haploid organisms like these, new alleles are able to produce a phenotype regardless of the degree of genetic dominance of the underlying mutations. Most bacteria of human interest carry a single copy of their chromosome. In diploid or polyploid organisms, the evolution of new traits encoded by recessive mutations is therefore constricted because the presence of a dominant allele will always block the phenotypic contribution of the recessive allele. Genetic dominance is the relationship between alleles of the same gene in which one allele (dominant) masks the phenotypic contribution of a second allele (recessive). Moreover, our findings offer a framework to forecast the spread and evolvability of MGE-encoded genes, which encode traits of key human interest, such as virulence or antibiotic resistance. Our results help to understand how MGEs evolve and spread, uncovering the neglected influence of genetic dominance on bacterial evolution. ![]() ![]() The combination of these two effects governs the catalog of genes encoded on MGEs. In addition, genetic dominance also determines the phenotypic effects of horizontally acquired MGE-encoded genes, silencing recessive alleles if the recipient bacterium already carries a wild-type copy of the gene. MGEs are typically present in more than one copy per host bacterium, and as a consequence, genetic dominance favors the fixation of dominant mutations over recessive ones. In this study, we uncovered the central role of genetic dominance shaping genetic cargo in MGEs, using antibiotic resistance as a model system. However, the rules governing the repertoire of traits encoded on MGEs remain unclear. Mobile genetic elements (MGEs), such as plasmids, promote bacterial evolution through horizontal gene transfer (HGT).
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