DNA double strand break repair in Escherichia coli perturbs cell division and chromosome dynamics.

To prevent the transmission of damaged genomic material between generations, cells require a system for accommodating DNA repair within their cell cycles. We have previously shown that Escherichia coli cells subject to a single, repairable site-specific DNA double-strand break (DSB) per DNA replication cycle reach a new average cell length, with a negligible effect on population growth rate. We show here that this new cell size distribution is caused by a DSB repair-dependent delay in completion of cell division.

RecBCD coordinates repair of two ends at a DNA double-strand break, preventing aberrant chromosome amplification.

DNA double-strand break (DSB) repair is critical for cell survival. A diverse range of organisms from bacteria to humans rely on homologous recombination for accurate DSB repair. This requires both coordinate action of the two ends of a DSB and stringent control of the resultant DNA replication to prevent unwarranted DNA amplification and aneuploidy.

Profiling antibiotic resistance and electrotransformation potential of Ensifer adhaerens OV14; a non-Agrobacterium species capable of efficient rates of plant transformation.

Ensifer adhaerens OV14 underpins the successful crop transformation protocol termed Ensifer-mediated transformation but issues exist in regard to addressing the pleomorphic tendency of the bacterium in suboptimal conditions, identifying the optimal parameters for electrotransformation and defining the strain's antibiotic profile. Here, modifications made to growth medium composition addressed the pleomorphic trait of E. adhaerens OV14, delivering uniform E.

Repair on the go: E. coli maintains a high proliferation rate while repairing a chronic DNA double-strand break.

DNA damage checkpoints exist to promote cell survival and the faithful inheritance of genetic information. It is thought that one function of such checkpoints is to ensure that cell division does not occur before DNA damage is repaired. However, in unicellular organisms, rapid cell multiplication confers a powerful selective advantage, leading to a dilemma.

Histone deacetylase complex1 expression level titrates plant growth and abscisic acid sensitivity in Arabidopsis.

Histone deacetylation regulates gene expression during plant stress responses and is therefore an interesting target for epigenetic manipulation of stress sensitivity in plants. Unfortunately, overexpression of the core enzymes (histone deacetylases [HDACs]) has either been ineffective or has caused pleiotropic morphological abnormalities. In yeast and mammals, HDACs operate within multiprotein complexes.

WITHDRAWN: Symmetries and Asymmetries Associated with Non-Random Segregation of Sister DNA Strands in Escherichia coli.

The Publisher regrets that this article is an accidental duplication of an article that has already been published, http://dx.doi.org/10.

Symmetries and asymmetries associated with non-random segregation of sister DNA strands in Escherichia coli.

The successful inheritance of genetic information across generations is a complex process requiring replication of the genome and its faithful segregation into two daughter cells. At each replication cycle there is a risk that new DNA strands incorporate genetic changes caused by miscopying of parental information. By contrast the parental strands retain the original information.

Non-random segregation of sister chromosomes in Escherichia coli.

It has long been known that the 5' to 3' polarity of DNA synthesis results in both a leading and lagging strand at all replication forks. Until now, however, there has been no evidence that leading or lagging strands are spatially organized in any way within a cell. Here we show that chromosome segregation in Escherichia coli is not random but is driven in a manner that results in the leading and lagging strands being addressed to particular cellular destinations.

SbcCD regulation and localization in Escherichia coli.

The SbcCD complex and its homologues play important roles in DNA repair and in the maintenance of genome stability. In Escherichia coli, the in vitro functions of SbcCD have been well characterized, but its exact cellular role remains elusive. This work investigates the regulation of the sbcDC operon and the cellular localization of the SbcC and SbcD proteins.