The segregation of genetic material between newly formed daughter cells during cell division is a highly dynamic, intricately orchestrated cellular process. The sheer size of eukaryotic genomes poses a fundamental problem that must be overcome to ensure proper transmission of genetic
material to daughter cells. After DNA replication, a typical human skin cell contains more than twelve feet of DNA, housed within a space measuring less than a millimeter across. Beyond simply
containing this mass of DNA, cells must achieve a dramatic reorganization of their chromosomes during mitosis in order for them to be evenly divided between daughter cells. Mitotic chromosome condensation, the process by which chromosomes resolve into discrete bodies prior to nuclear division, must be faithfully carried out to ensure that each pair of sister-chromatids, the identical
copies of each chromosome formed during DNA replication, disjoins during nuclear division. If chromosomes fail to condense during early mitosis, tangles between sister-chromatids can lead to breaks in the DNA or an outright failed segregation of sister-chromatids. Previous research has shown that topoisomerase II and the condensin complexes (condensin I and condensin II) are essential for mitotic chromosome segregation. However, a significant body of recent work suggests
that there are more components to the chromosome condensation machinery than previously thought. In this work, I identify several novel proteins that could play a role in mitotic chromosome condensation. The identification of these proteins opens up new avenues of study, potentially providing the missing link between the physical phenomenon of mitotic chromosome condensation
and our incomplete picture of the process on the protein level. With the future verification, of these proteins as essential players in mitotic chromosome condensation, we will hopefully be poised to take further steps to understand this fundamental cellular process.