SMC protein RecN drives RecA filament translocation for in vivo homology search.

While the molecular repertoire of the homologous recombination pathways is well studied, the search mechanism that enables recombination between distant homologous regions is poorly understood. Earlier work suggests that the recombinase RecA, an essential component for homology search, forms an elongated filament, nucleating at the break site. How this RecA structure carries out long-distance search remains unclear.

A CTP-dependent gating mechanism enables ParB spreading on DNA.

Proper chromosome segregation is essential in all living organisms. The ParA-ParB- system is widely employed for chromosome segregation in bacteria. Previously, we showed that ParB requires cytidine triphosphate to escape the nucleation site and spread by sliding to the neighboring DNA (Jalal et al.

Asymmetric chromosome segregation and cell division in DNA damage-induced bacterial filaments.

Faithful propagation of life requires coordination of DNA replication and segregation with cell growth and division. In bacteria, this results in cell size homeostasis and periodicity in replication and division. The situation is perturbed under stress such as DNA damage, which induces filamentation as cell cycle progression is blocked to allow for repair.

Live-Cell Fluorescence Imaging of RecN in Caulobacter crescentus Under DNA Damage.

Structural maintenance of chromosomes (SMC) proteins play a central role in the organization, segregation and maintenance of chromosomes across domains of life. In bacteria, an SMC-family protein, RecN, has been implicated to have important functions in DNA damage repair. Recent studies have suggested that RecN is required to increase chromosome cohesion in response to DNA damage and may also stimulate specific events during recombination-based repair.