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Bipolar localization of the group II intron Ll.LtrB is maintained in Escherichia coli deficient in nucleoid condensation, chromosome partitioning and DNA replication
Author(s) -
Beauregard Arthur,
Chalamcharla Venkata R.,
Piazza Carol Lyn,
Belfort Marlene,
Coros Colin J.
Publication year - 2006
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/j.1365-2958.2006.05419.x
Subject(s) - biology , intron , nucleoid , group ii intron , genetics , origin of replication , chromosome segregation , chromosome , rna , microbiology and biotechnology , gene , escherichia coli , dna replication , rna splicing
Summary Group II introns are mobile genetic elements that invade their cognate intron‐minus alleles via an RNA intermediate, in a process known as retrohoming. They can also retrotranspose to ectopic sites at low frequency. In Escherichia coli , retrotransposition of the lactococcal group II intron, Ll.LtrB, occurs preferentially within the Ori and Ter macrodomains of the E. coli chromosome. These macrodomains migrate towards the poles of the cell, where the intron‐encoded protein, LtrA, localizes. Here we investigate whether alteration of nucleoid condensation, chromosome partitioning and replication affect retrotransposition frequencies, as well as bipolar localization of the Ll.LtrB intron integration and LtrA distribution in E. coli . We thus examined these properties in the absence of the nucleoid‐associated proteins H‐NS, StpA and MukB, in variants of partitioning functions including the centromere‐like sequence migS and the actin homologue MreB, as well as in the replication mutants Δ oriC , seqA , tus and topoIV ts . Although there were some dramatic fluctuations in retrotransposition levels in these hosts, bipolar localization of integration events was maintained. LtrA was consistently found in nucleoid‐free regions, with its localization to the cellular poles being largely preserved in these hosts. Together, these results suggest that bipolar localization of group II intron retrotransposition results from the residence of the intron‐encoded protein at the poles of the cell.