Proteins involved in CTR duplication, maturation or separation as well as effectors of the mitotic clock itself can be substrates of these enzymes. The role of the giant protein AKAP450, which interacts with several partners of intracellular signalling pathways, is particularly studied. Our results suggest that this pool, which cannot be easily quantified, is probably low. In a collaborative program with physicists from Curie Institute, a study of the isolated CTR using physical approaches has been undertaken. It involves atomic force microscopy, X rays microscopy, and the measurement of elastic properties of the centrosomal matrix.
Solid tumors are genetically unstable.
Whereas unstability can be observed at the nucleotide level in few cases and is due to defects in DNA repair, in most cases, instability is observed at the chromosomal level, with gain or loss of entire chromosomes. In both cases, unstability appears early in the tumor progression. Genes which could promote, when altered, chromosomal unstability are acting either on mechanisms up stream mitosis, such as chromosome condensation, interchromatid cohesion, structure and functions of kinetochores, CTR reproduction or MTs dynamics, or on checkpoint mechanisms ensuring the normal progression od the cell division cycle. Abnormal numbers of CTRs, likely due to defects in the control of CTR reproduction, are often observed in tumor cells. It is important to understand the molecular basis of chromosomal unstability in tumors linked to CTR reproduction defects.