Gotta and Meraldi groups uncovered a cell-type dependent lever to slow down cell division
More than 40’000 new cases of cancer are reported each year in Switzerland. In most cancers, initially normal cells multiply in an uncontrolled way, proliferate and transform into cancer cells. Unfortunately, anti-cancer treatments often cannot stop the division and proliferation of these cells due to resistance mechanisms that allow some cell sub-populations to survive.
A single missing protein, a cascade of effects
In their work published in The Journal of Cell Biology, the groups of Prof. Monica Gotta and Prof. Patrick Meraldi have highlighted how the assembly of the mitotic spindle, the machinery that separates the chromosomes into the 2 daughter cells during cell division, is regulated in two-cell embryos of the nematode Caenorhabditis elegans. When the microtubule depolymerase KLP-7 is missing, formation of the mitotic spindle is slowed down specifically in the cell that will give origin to the somatic tissues but not in the cell from which the germline originates.
Depletion of the protein klp-7 (left picture) slows down centrosome (in white) separation in the anterior cell of the C. elegans embryo from which the somatic tissues orginates in comparison to the posterior cell from which the germline originates (right image). © unige
Understanding cell-type dependent responses
This study highlights how the C. elegans two-cell embryo can serve as model for situations, where the same perturbation can impair cell division in one cell type, while leaving another cell unharmed, as it is observed in human cancer tissues.
Posted by: Véronique Rosset
October 31, 2019