Retrotransposition of a bacterial group II intron

Benoit Cousineau, Stacey Lawrence, Dorie Smith and Marlene Belfort ()
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Benoit Cousineau: Molecular Genetics Program, Wadsworth Center, and School of Public Health, State University of New York at Albany
Stacey Lawrence: Molecular Genetics Program, Wadsworth Center, and School of Public Health, State University of New York at Albany
Dorie Smith: Molecular Genetics Program, Wadsworth Center, and School of Public Health, State University of New York at Albany
Marlene Belfort: Molecular Genetics Program, Wadsworth Center, and School of Public Health, State University of New York at Albany

Nature, 2000, vol. 404, issue 6781, 1018-1021

Abstract: Abstract Self-splicing group II introns may be the evolutionary progenitors of eukaryotic spliceosomal introns1,2,3,4,5,6,7, but the route by which they invade new chromosomal sites is unknown. To address the mechanism by which group II introns are disseminated, we have studied the bacterial Ll.LtrB intron from Lactococcus lactis8. The protein product of this intron, LtrA, possesses maturase, reverse transcriptase and endonuclease enzymatic activities9,10,11. Together with the intron, LtrA forms a ribonucleoprotein (RNP) complex which mediates a process known as retrohoming11. In retrohoming, the intron reverse splices into a cognate intronless DNA site. Integration of a DNA copy of the intron is recombinase independent but requires all three activities of LtrA11. Here we report the first experimental demonstration of a group II intron invading ectopic chromosomal sites, which occurs by a distinct retrotransposition mechanism. This retrotransposition process is endonuclease-independent and recombinase-dependent, and is likely to involve reverse splicing of the intron RNA into cellular RNA targets. These retrotranspositions suggest a mechanism by which splicesomal introns may have become widely dispersed.

Date: 2000
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DOI: 10.1038/35010029

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