Cell division is a fundamental event common to most forms of life. In eukaryotes, the mechanisms that regulate it and most of the key factors involved are evolutionarily conserved and are mostly studied for their relevance to cancer research.

Already in 2021, Patrizio Dimitri's group from the Charles Darwin Department of Biology and Biotechnology of Sapienza University of Rome had unveiled a non-canonical function of the SRCAP protein in the control of cell division, independent of its role as an epigenetic regulator of the structure and function of chromatin, i.e. the complex of proteins and nucleic acids that makes up the cellular genome of eukaryotes.

A new study, coordinated by Patrizio Dimitri and Giovanni Messina of the Charles Darwin Department of Biology and Biotechnology of Sapienza University of Rome in collaboration with the Pasteur Institute Italy - Cenci Bolognetti Foundation, investigated the possible non-canonical functions of other chromatin proteins in the control of cell division in human cells and the model organism Drosophila melanogaster.

The results, published in the journal BMC Biology, show that it is not only the SRCAP protein that has a dual function. In fact, dozens of other proteins belonging to the same chromatin remodelling complex that SRCAP and the related p400/Tip60 complex are part of a transfer from the interphase nucleus to the mitotic apparatus to ensure that cell division takes place correctly.

'These proteins,' says Patrizio Dimitri, study coordinator, 'have a 'double life': initially, in the interphase nucleus, they are involved in the epigenetic control of gene expression, and subsequently, during the progression of the cell cycle, they transfer to the centrosomes, spindle and midbody to ensure their function, thus ensuring successful cell division and equal distribution of chromosomes in the two daughter cells. This 'mitotic journey' represents a massive and evolutionarily conserved phenomenon that has never been described before.

The lack of these proteins causes alterations in cell division and chromosome number, leading to genetic instability, a condition that can trigger cancer.

'The hope of our research team,' concludes Giovanni Messina, first author of the study, 'is to delve deeper into the mechanisms underlying a complex scenario in which phenomena such as chromatin remodelling, the cell cycle, tumorigenesis and developmental diseases are interconnected.

References:

Evolutionary conserved relocation of chromatin remodeling complexes to the mitotic apparatus - Giovanni Messina, Yuri Prozzillo, Francesca Delle Monache, Maria Virginia Santopietro, Patrizio Dimitri - BMC Biology (2022) https://doi.org/10.1186/s12915-022-01365-5

Further Information

Patrizio Dimitri
Charles Darwin Department of Biology and Biotechnology
patrizio.dimitri@uniroma1.it

Giovanni Messina
Charles Darwin Department of Biology and Biotechnology
giovanni.messina@uniroma1.it