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General Information/ Relationship Between IS and Eukaryotic TE

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Relationship Between IS and Eukaryotic TE

In spite of their obvious similarities, there is often poor transfer of knowledge between studies of prokaryotic and of eukaryotic TE. This artificial barrier is reflected in their nomenclature systems: Prokaryotic TE are named following the basic logic of bacterial genetics built on the initial Demerec rules[1]; Eukaryotic TE, on the other hand, have more colorful names in keeping with the culture of nomenclature used in eukaryotic genetics. To a certain extent, this camouflages the diversity and relationships between members of the eukaryotic TE superfamilies and their prokaryotic cousins.

It is important to appreciate that the basic chemistry of transposition is identical for both prokaryotic and eukaryotic elements[2][3][4][5][6][7]. Moreover, many eukaryotic DNA transposons have similar sizes and organization to those of prokaryotic IS and, since most do not carry additional “passenger” genes, they are not transposons in the prokaryotic sense and should strictly be considered as eukaryotic IS. The major differences lie in how Tpase expression and activity is regulated[8]. One important difference is that most eukaryotic transposons are “insulated” by constraints of the nucleus (which physically separate the transposition process from that of Tpase expression) while those of prokaryotes are not since prokaryotic transcription and translation are coupled. In addition, eukaryotic transposons are subject to a hierarchy of regulation via small RNAs[9][10][11][12]. In prokaryotes, it is possible that CRISPRs may impose some control at this level but, although it has been demonstrated that CRISPRs are active against mobile genetic elements and may regulate some endogenous gene expression [see [13]], these are limited to plasmids and phage and to our knowledge have not yet been demonstrated to act on intracellular Mobile Genetic Element such as IS and transposons.

In spite of these differences, a significant number of eukaryotic DNA TE are related to prokaryotic IS (Table Characteristics of IS families; Table MGE transposases examined by secondary structure prediction programs), and moreover, eukaryotic TE including passenger genes are now being identified [see e.g. [14]]. This reinforces the view that the borders between different types of TE are “fuzzier” than previously recognized.

Bibliography

  1. ↑ Demerec et al.. A proposal for a uniform nomenclature in bacterial genetics. Genetics. 1966. 54. pp. 61-76. doi: 10.1093/genetics/54.1.61. PMID: 5961488.
  2. ↑ Dyda et al.. Crystal structure of the catalytic domain of HIV-1 integrase: similarity to other polynucleotidyl transferases. Science (New York, N.Y.). 1994. 266. pp. 1981-6. doi: 10.1126/science.7801124. PMID: 7801124.
  3. ↑ Hickman et al.. Integrating prokaryotes and eukaryotes: DNA transposases in light of structure. Critical reviews in biochemistry and molecular biology. 2010. 45. pp. 50-69. doi: 10.3109/10409230903505596. PMID: 20067338.
  4. ↑ Hickman & Dyda. Mechanisms of DNA Transposition. Microbiology spectrum. 2015. 3. pp. MDNA3-0034-2014. doi: 10.1128/microbiolspec.MDNA3-0034-2014. PMID: 26104718.
  5. ↑ Rice et al.. Retroviral integrases and their cousins. Current opinion in structural biology. 1996. 6. pp. 76-83. doi: 10.1016/s0959-440x(96)80098-4. PMID: 8696976.
  6. ↑ Montaño & Rice. Moving DNA around: DNA transposition and retroviral integration. Current opinion in structural biology. 2011. 21. pp. 370-8. doi: 10.1016/j.sbi.2011.03.004. PMID: 21439812.
  7. ↑ Rice & Baker. Comparative architecture of transposase and integrase complexes. Nature structural biology. 2001. 8. pp. 302-7. doi: 10.1038/86166. PMID: 11774877.
  8. ↑ Nagy & Chandler. Regulation of transposition in bacteria. Research in microbiology. 2004. 155. pp. 387-98. doi: 10.1016/j.resmic.2004.01.008. PMID: 15207871.
  9. ↑ Fedoroff. Presidential address. Transposable elements, epigenetics, and genome evolution. Science (New York, N.Y.). 2012. 338. pp. 758-67. doi: 10.1126/science.338.6108.758. PMID: 23145453.
  10. ↑ Dumesic & Madhani. Recognizing the enemy within: licensing RNA-guided genome defense. Trends in biochemical sciences. 2014. 39. pp. 25-34. doi: 10.1016/j.tibs.2013.10.003. PMID: 24280023.
  11. ↑ Russell & LaMarre. Transposons and the PIWI pathway: genome defense in gametes and embryos. Reproduction (Cambridge, England). 2018. 156. pp. R111-R124. doi: 10.1530/REP-18-0218. PMID: 30304932.
  12. ↑ Saito & Siomi. Small RNA-mediated quiescence of transposable elements in animals. Developmental cell. 2010. 19. pp. 687-97. doi: 10.1016/j.devcel.2010.10.011. PMID: 21074719.
  13. ↑ Bikard & Marraffini. Control of gene expression by CRISPR-Cas systems. F1000prime reports. 2013. 5. pp. 47. doi: 10.12703/P5-47. PMID: 24273648.
  14. ↑ Bao & Jurka. Homologues of bacterial TnpB_IS605 are widespread in diverse eukaryotic transposable elements. Mobile DNA. 2013. 4. pp. 12. doi: 10.1186/1759-8753-4-12. PMID: 23548000.

How to Cite?

TnPedia Team. (2025). TnPedia: General Information on Prokaryotic Elements. Zenodo. https://doi.org/10.5281/zenodo.15548171

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