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The accurate distribution of chromosomes to daughter cells is on of the most fundamental requirements of cell division. However, errors are frequently made during the attachment process, resulting in cells with an abnormal number of chromosomes, which is called aneuploidy. Aneuploidy results in developmental defects in humans and is also a classical hallmark of cancer. In the Campbell lab, we aim to determine the mechanisms that cells use to prevent the formation of aneuploidy as well as the downstream repercussions of the failure of such mechanisms.
We use a combination of cell biology, genetics, and molecular biology techniques to perform mechanistic studies of fundamental processes related to chromosome segregation, primarily in the budding yeast model system. In addition, we conduct long-term adaptation experiments to determine how the structure of the genome changes to cope with elevated instability. We have also developed methods for the engineering of aneuploid karyotypes to determine the identity of genes responsible for aneuploid phenotypes.
Chris Campbell received his PhD in biochemistry and cell biology from the University of California San Francisco. He then conducted a postdoctoral fellowship at the University of California San Diego before forming his own group at the Max Perutz Labs in 2015.
We recently adapted yeast to extremely high rates of chromosome missegregation and found that they develop complex karyotypes with multiple aneuploid chromosomes per strain. By analyzing the patterns in the adapted karyotypes, we found that certain chromosomes were never found to be aneuploid at the same time, suggesting that certain types of aneuploidy are incompatible with each other. We then directly tested this theory by engineering different combinations of aneuploid chromosomes and found that the correlation between two aneuploid chromosomes in adapted strains correlates with their fitness when combined de novo. We call these genetic interaction between aneuploid chromosomes chromosomal copy number interactions (CCNIs) and are currently working to determine their underlying basis.
The chromosomal passenger complex (CPC) has many substrates at the outer kinetochore, which it phosphorylate to disrupt the connections between the chromosomes and the microtubules of the mitotic spindle. We have recently determined which of the domains in the CPC are required to specifically target it to these outer kinetochore substrates. We are now working to determine exactly how these domains promote proximity to the kinetochore.
Aurora B activity is promoted by cooperation between discrete localization sites in budding yeast.
Marsoner, Theodor; Yedavalli, Poornima; Masnovo, Chiara; Fink, Sarah; Schmitzer, Katrin; Campbell, Christopher S
Genetic interactions between specific chromosome copy number alterations dictate complex aneuploidy patterns.
Ravichandran, Madhwesh C; Fink, Sarah; Clarke, Matthew N; Hofer, Franziska Christina; Campbell, Christopher S
An engineered minimal chromosomal passenger complex reveals a role for INCENP/Sli15 spindle association in chromosome biorientation.
Fink, Sarah; Turnbull, Kira; Desai, Arshad; Campbell, Christopher S
Tension sensing by Aurora B kinase is independent of survivin-based centromere localization.
Campbell, Christopher S; Desai, Arshad
Christopher Campbell is part of the SFB "Meiosis"
The Campbell Group is supported through the "Vienna Research Groups for Young Investigators" program.
The Campbell group participates in in the special Doctoral Program 'Chromosome Dynamics' reviewed and funded by the Austrian Research Fund FWF.