Journal of Biotechnology & Biomaterials
Open Access

Abstract

Bloom�s syndrome (BS) is caused by mutations in the BLM gene encoding the BLM helicase. The BLM protein contains a conserved RecQ helicase domain and unwinds various DNA substrates including replication forks. Cells from BS patients lack the BLM protein show defects in the response to replicative stress and contain a multitude of chromosomal aberrations. A BLM homolog (HIM-6) has been identified in C. elegans based on its close homology to human BLM. Here, we used singlemolecule FRET technology to observe DNA unwinding in real time. Our results show that the HIM-6 repetitively unwound a long forked DNA depending on ATP concentration and resolved flap and D-loop DNA, all of which are intermediates in DNA repair. Also, we found that HIM-6 unwound at most 25 base pairs of duplex DNA in a speed of 28 nucleotides per second before returning. Besides, repetitive unwinding mode of HIM-6 was changed to unidirectional unwinding in the presence of RPA, indicating that its unwinding mode can be modulated by partner proteins in vivo. This study can be used to search proteins which would modulate a HIM-6 unwinding mode on different DNA structures such as Holliday junction and G4-quadruplex.

Biography

Byungchan Ahn is a Professor of Department of Life Science, University of Ulsan, South Korea.