Monday, November 4, 2013

Archaea species exhibits accelerated growth and ability to sidestep normal replication process

A recent report in Nature entitled: 'Accelerated growth in the absence of DNA replication origins' describes the work of The University of Nottingham scientists studying the archaea species Haloferax volcanii. Archaea are single celled organisms that are best known for their ability to survive and thrive in some of the worlds harshest environments, such as extreme temperatures and pH's. Haloferax volcanii are able to live in high-salt conditions and the ones used in this study originate from the Dead Sea.

Salt deposit at Dead Sea
Archaea are single-celled, and therefore similar to bacteria, but also have other characteristics that are more similar to eukaryotes, such as humans. Therefore, archaea fall into their own category of classification. The arahaea characteristic that was the focus of this study was the fact that when they copy their DNA prior to cell division they exhibit multiple origins of replication, similar to eukaryotes, where bacteria have a single origin of replication. In humans, if these replication origins are eliminated DNA replication cannot proceed and cells eventually die. When all replication origins were eliminated in a strain of  Haloferax volcanii not only were no growth defects apparent but growth faster than wild type was observed!

The origin-less replication occurred at dispersed sites rather than discrete origins and in order to perform this origin-less replication Haloferax volcanii adapted another cellular function, homologous recombination, to initiate DNA replication. In fact, they found that the recombinase RadA was absolutely essential for replication in the absence of origins.

The unregulated and accelerated growth of the origin-less Haloferax volcanii strain can be compared to cancer cells. It is the hope of the authors of this study that by better understanding the phenomena they observed they may shed light on how cancer cells avoid normal controls and this understanding could lead to new targets to selectively effect cancer cells.