Cohesins coordinate gene transcriptions of related function within Saccharomyces cerevisiae.

Cohesion factors pair together sister chromatids from early S-phase until anaphase onset. Numerous findings also establish an additional role in transcription. In humans, mutations in cohesion factors result in developmental abnormalities such as Cornelia de Lange, Roberts Syndrome/SC-Phocomelia, Rothman-Thompson Syndrome and others.

Positional analyses of BRCA1-dependent expression in Saccharomyces cerevisiae.

Mutations in BRCA1 account for a significant proportion of hereditary breast and ovarian cancers, but analysis of BRCA1 function is complicated by pleiotropic effects and binding partners (Pol II holoenzyme and transcription factors, chromatin remodelers, recombination complexes and E3 ligases). In vertebrate cells, efforts to elucidate BRCA1 transcriptional effects have focused on specific genes or restricted portions of the genome-limiting analyses of BRCA1 effects on adjoining DNA sequences and along chromosome lengths. Here, we use microarray analyses on the genetically tractable yeast cell system to elucidate BRCA1-dependent genomewide positional effects on both gene induction and repression.

Fork it over: the cohesion establishment factor Ctf7p and DNA replication.

To produce viable progeny, cells must identify the products of chromosome replication as sister chromatids, pair them together and then maintain this cohesion until chromosome segregation. It is well established that cohesin ring-like structures maintain sister chromatid cohesion, but the molecular mechanism by which only sisters become paired (termed establishment) is highly controversial. One of the first establishment models posited in the literature suggested that cohesin complexes associated with each sister become tethered together through an active process that is intimately coupled to progression of the DNA replication fork.