Biomedical subjects

Camilla Sjögren

Publications and source records attributed to Camilla Sjögren.

3 recordsLinked to original sources

PubMed2006

Chromosomal association of the Smc5/6 complex reveals that it functions in differently regulated pathways.

The SMC protein complexes safeguard genomic integrity through their functions in chromosome segregation and repair. The chromosomal localization of the budding yeast Smc5/6 complex determined here reveals that the complex works specifically on the duplicated genome in differently regulated pathways. The first controls the association to centromeres and chromosome arms in unchallenged cells, the second regulates the association to DNA breaks, and the third directs the complex to the chromosome arm that harbors the ribosomal DNA arrays. The chromosomal interaction pattern predicts a function that becomes more important with increasing chromosome length and that the complex's role in unchallenged cells is independent of DNA damage. Additionally, localization of Smc6 to collapsed replication forks indicates an involvement in their rescue. Altogether this shows that the complex maintains genomic integrity in multiple ways, and evidence is presented that the Smc5/6 complex is needed during replication to prevent the accumulation of branched chromosome structures.

Cell Cycle Proteins↗

PubMed2005

DNA damage-induced cohesion.

The protein complex Cohesin, forming protein-links that hold sister chromatids together, is at the heart of chromatid cohesion. Cohesion is important both for correct chromosome segregation and double-strand break (DSB) repair, making Cohesin central for the maintenance of genome stability. Until now, establishment of Cohesin links between chromatids has been shown to occur during DNA replication only. Recently it was however observed that in cells arrested in G2/M, DSB induction not only elicits chromosomal recruitment of Cohesin, but also formation of chromatid cohesion. The establishment of cohesion outside the period of replication opens a new field of investigation. Here we present results further supporting the formation of sister chromatid cohesion in response to DNA damage, and propose a model of how damage-induced cohesion could contribute to the linkage of chromatids during normal cell cycle progression.

Cell Cycle↗

PubMed2004

Postreplicative recruitment of cohesin to double-strand breaks is required for DNA repair.

Chromosome stability depends on accurate chromosome segregation and efficient DNA double-strand break (DSB) repair. Sister chromatid cohesion, established during S phase by the protein complex cohesin, is central to both processes. In the absence of cohesion, chromosomes missegregate and G2-phase DSB repair fails. Here, we demonstrate that G2-phase repair also requires the presence of cohesin at the damage site. Cohesin components are shown to be recruited to extended chromosome regions surrounding DNA breaks induced during G2. We find that in the absence of functional cohesin-loading proteins (Scc2/Scc4), the accumulation of cohesin at DSBs is abolished and repair is defective, even though sister chromatids are connected by S phase generated cohesion. Evidence is also provided that DSB induction elicits establishment of sister chromatid cohesion in G2, implicating that damage-recruited cohesin facilitates DNA repair by tethering chromatids.

Cell Cycle Proteins↗