but not in condensin I, display hyperclustering of chromocenters, indicating that condensin II has a specific role in suppressing chromocenter clustering. Whilst early studies suggested the possibility that condensins may directly participate in regulating gene expression, some recent studies argue against this hypothesis. Mutants of the fission yeast Schizosaccharomyces pombe were obtained that had a temperature sensitive and/or DNA damage sensitive phenotype. Some of these mutants were defective in the HEAT subunits of condensin indicating that the HEAT subunits are required for DNA repair. Posttranslational modifications Condensin subunits are subjected to various posttranslational modifications in a cell cycle-dependent manner. Among them, the best-studied example is phosphorylation. For instance, Cdk1 (Cyclin-dependent kinase 1) activates condensin I, whereas CK2 (Casein kinase 2) negatively regulate its activity. It has been reported that, in D. melanogaster, the CAP-H2 subunit of condensin II is degraded through the action of SCFSlimb ubiquitin ligase. Relevance to diseases It was demonstrated that MCPH1, one of the proteins responsible for human primary microcephaly, has the ability to negatively regulate condensin II. In mcph1 patient cells, condensin II (but not condensin I) is hyperactivated, leading to premature chromosome condensation in G2 phase (i.e., before entering mitosis). There is no evidence, however, that misregulation of condensin II is directly related to the etiology of mcph1 microcephaly. More recently, it has been reported that hypomorphic mutations in condensin I or II subunits cause microcephaly in humans. In mice, hypomorphic mutations in condensin II subunits cause specific defects in T cell development, leading to T cell lymphoma. It is interesting to note that cell types with specialized cell division modes, such as neural stem cells and T cells, are particularly susceptible to mutations in condensin subunits. Evolutionary implications Prokaryotes have primitive types of condensins, indicating that the evolutionary origin of condensins precede that of histones. The fact that condensins I and II are widely conserved among extant eukaryotic species strongly implicates that the last eukaryotic common ancestor (LECA) had both complexes. It is therefore reasonable to speculate that some species such as fungi have lost condensin II during evolution. Then why do many eukaryotes have two different condensin complexes? As discussed above, the relative contribution of condensins I and II to mitosis varies among different organisms. They play equally important roles in mammalian mitosis, whereas condensin I has a predominant role over condensin II in many other species. In those species, condensin II