Mobile genetic elements (MGEs) are a type of genetic materials can move around within a genome, or they can also be transferred from one species or replicon to another. MGEs are found in all organisms. In the human, approximately 50% of the genome is thought to be MGEs[1]. MGEs play a distinct role in evolution. Gene duplication events can also happen through the mechanism of MGEs. MGEs can also cause mutations in protein coding regions, which alters the protein functions. In addition, they can also rearrange genes in the host genome. One of the examples of MGEs in evolutionary context is that virulence factors and antibiotic resistance genes of MGEs can be transported to share them with neighboring bacteria. Newly acquired genes though this mechanism can increase fitness by gaining new or additional functions. On the other hand, MGEs can also decrease fitness by introducing disease-causing alleles or mutations.[2]
Types of mobile genetic elements:
edit- Transposons (also called transposable elements) are DNA sequences that can move locations within a genome, which includes retrotransposons and DNA transposons.
- Retrotransposons are the most widespread class of transposons in mammals [3]. An RNA transcript of MGEs is copied by reverse transcriptase. Then, the DNA sequence can be inserted back to a random location of the genome[4].
- DNA transposons are a DNA segment that can move to a new location by a “cut-and-paste” strategy.
- Plasmids of bacteria are a transferable genetic element through bacterial conjugation. This is a mechanism of horizontal gene transfer that bacteria can share virulence factors and antibiotic resistance genes.
- Bacteriophage elements, like Mu, which integrates randomly into the genome by transduction[5]
Group I and II introns is a product from self-splicing in the host transcripts, and they act as ribozymes that can invade tRNA, rRNA, and protein coding genes in bacteria[6]
Research examples
edit- CRISPR-Cas systems in bacteria and archaea are a form of adaptive immune system to protect against deadly consequences from MGEs. Using comparative genomic and phylogenetic analysis, researchers found that CRISPR-Cas variants are associated with distinct types of MGEs such as transposable elements. In addition, CRISPR-Cas controls transposable elements for their propagation[7].
- MGEs such as plasmids by a horizontal transmission are generally beneficial to an organism. The ability of transferring plasmids (sharing) is important in an evolutionary perspective. Tazzyman and Bonhoeffer found that fixation (receiving) of the transferred plasmids in a new organism is just as important as the ability to transfer them[8]. Beneficial rare and transferrable plasmids have a higher fixation probability. Whereas, deleterious transferable genetic elements have a lower fixation probability to avoid lethality to the host organisms.
- Transposition by transposable elements is mutagenic. Thus, organisms have evolved to repress the transposition events, and failure to repress the events causes cancers in somatic cells. Cecco et al. found that during early age transcription of retrotransposable elements are minimal in mice, but in advanced age the transcription level increases [9]. Interestingly, this age-dependent expression level of transposable elements is reduced by calorie restriction diet.
Diseases
editThe consequence of mobile genetic elements can alter the transcriptional patterns, which frequently leads to genetic disorders such as immune disorders, breast cancer, multiple sclerosis, and amyotrophic lateral sclerosis[1]. In humans, stress can lead to transactional activation of MGEs such as endogenous retrovirus, and this activation has been linked to neuro-degeneration[10].
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| | This is a user sandbox of Ynam1. You can use it for testing or practicing edits. This is not the sandbox where you should draft your assigned article for a dashboard.wikiedu.org course. To find the right sandbox for your assignment, visit your Dashboard course page and follow the Sandbox Draft link for your assigned article in the My Articles section. |
- ^ a b Mu, X.; Ahmad, S.; Hur, S. Endogenous Retroelements and the Host Innate Immune Sensors. pp. 47–69. doi:10.1016/bs.ai.2016.07.001.
- ^ Singh, Parmit Kumar; Bourque, Guillaume; Craig, Nancy L.; Dubnau, Josh T.; Feschotte, Cédric; Flasch, Diane A.; Gunderson, Kevin L.; Malik, Harmit Singh; Moran, John V. (2014-11-18). "Mobile genetic elements and genome evolution 2014". Mobile DNA. 5: 26. doi:10.1186/1759-8753-5-26. ISSN 1759-8753.
{{cite journal}}: CS1 maint: unflagged free DOI (link) - ^ Richardson, Sandra R.; Garcia-Perez, José Luis; Doucet, Aurélien J.; Kopera, Huira C.; Moldovan, John B.; Moran, John V. (2015-03-05). "The Influence of LINE-1 and SINE Retrotransposons on Mammalian Genomes". Microbiology Spectrum. 3 (2). doi:10.1128/microbiolspec.mdna3-0061-2014. ISSN 2165-0497.
- ^ Hsu, Ellen; Lewis, Susanna M. The Origin of V(D)J Diversification. pp. 133–149. doi:10.1016/b978-0-12-397933-9.00009-6.
- ^ Rankin, D. J.; Rocha, E. P. C.; Brown, S. P. (January 2011). "What traits are carried on mobile genetic elements, and why?". Heredity. 106 (1): 1–10. doi:10.1038/hdy.2010.24. ISSN 0018-067X.
- ^ Hausner, Georg; Hafez, Mohamed; Edgell, David R. (2014-03-10). "Bacterial group I introns: mobile RNA catalysts". Mobile DNA. 5: 8. doi:10.1186/1759-8753-5-8. ISSN 1759-8753.
{{cite journal}}: CS1 maint: unflagged free DOI (link) - ^ Peters, Joseph E.; Makarova, Kira S.; Shmakov, Sergey; Koonin, Eugene V. (2017-08-29). "Recruitment of CRISPR-Cas systems by Tn7-like transposons". Proceedings of the National Academy of Sciences. 114 (35): E7358–E7366. doi:10.1073/pnas.1709035114. ISSN 0027-8424. PMID 28811374.
- ^ Tazzyman, Samuel J.; Bonhoeffer, Sebastian (December 2013). "Fixation probability of mobile genetic elements such as plasmids". Theoretical Population Biology. 90: 49–55. doi:10.1016/j.tpb.2013.09.012. ISSN 1096-0325. PMID 24080312.
- ^ De Cecco, Marco; Criscione, Steven W.; Peterson, Abigail L.; Neretti, Nicola; Sedivy, John M.; Kreiling, Jill A. (December 2013). "Transposable elements become active and mobile in the genomes of aging mammalian somatic tissues". Aging. 5 (12): 867–883. doi:10.18632/aging.100621. ISSN 1945-4589. PMC 3883704. PMID 24323947.
{{cite journal}}: CS1 maint: PMC format (link) - ^ Antony, Joseph M; Marle, Guido van; Opii, Wycliffe; Butterfield, D Allan; Mallet, François; Yong, Voon Wee; Wallace, John L; Deacon, Robert M; Warren, Kenneth (2004-09-26). "Human endogenous retrovirus glycoprotein–mediated induction of redox reactants causes oligodendrocyte death and demyelination". Nature Neuroscience. 7 (10): 1088–1095. doi:10.1038/nn1319. ISSN 1546-1726.