Journal
CURRENT BIOLOGY
Volume 24, Issue 3, Pages 287-292Publisher
CELL PRESS
DOI: 10.1016/j.cub.2013.11.050
Keywords
-
Categories
Funding
- National Institutes of Health [GM086466]
- Harvard College PRISE Program
- Harvard College Herchel Smith Research Program
Ask authors/readers for more resources
SMC condensin complexes play a central role in organizing and compacting chromosomes in all domains of life [1, 2]. In the bacterium Bacillus subtilis, cells lacking SMC are viable only during slow growth and display decondensed chromosomes, suggesting that SMC complexes function throughout the genome [3, 4]. Here, we show that rapid inactivation of SMC or its partner protein ScpB during fast growth leads to a failure to resolve newly replicated origins and a complete block to chromosome segregation. Importantly, the loss of origin segregation is not due to an inability to unlink precatenated sister chromosomes by Topoisomerase IV. In support of the idea that ParB-mediated recruitment of SMC complexes to the origin is important for their segregation, cells with reduced levels of SMC that lack ParB are severely impaired in origin resolution. Finally, we demonstrate that origin segregation is a task shared by the condensin complex and the parABS partitioning system. We propose that origin-localized SMC constrains adjacent DNA segments along their lengths, drawing replicated origins in on themselves and away from each other. This SMC-mediated lengthwise condensation, bolstered by the parABS system, drives origin segregation.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available