The amount of femorotibial alignment correction through total knee arthroplasty may affect postoperative hindfoot alignment.

Purpose: This study was performed to investigate the relationship between the amount of femorotibial alignment correction and the amount of improvement of hindfoot alignment in total knee arthroplasty (TKA). Methods: A total of 159 knees undergoing TKA in 120 patients were assessed preoperatively and at 2 weeks, 1 month, 3 months and 6 months postoperatively. Standing hindfoot alignment was evaluated using the leg-heel angle (LHA). The amount of change in hindfoot alignment was compared between patients with severe varus knee (Group 1) and those with moderate varus, neutral or valgus knee (Group 2). Results: The mean values of pre- and postoperative hip-knee-ankle (HKA) angle were -14 ± 4° and -1 ± 3° in Group 1 and -7 ± 5° and -1 ± 3° in Group 2, respectively. The differences between pre- and postoperative LHA were significantly larger in Group 1 than in Group 2 at 2 weeks, 1 month and 3 months postoperatively (p = 0.006, 0.001 and 0.03, respectively). At 6 months postoperatively, no differences were observed between the two groups (p = 0.31). Conclusion: The amount of change in hindfoot alignment was larger in Group 1 than in Group 2 at 2 weeks, 1 month and 3 months after TKA, but there was no significant difference between the two groups at 6 months after TKA. Level of Evidence: Prognostic Level II.

Plk1 phosphorylation of CAP-H2 triggers chromosome condensation by condensin II at the early phase of mitosis.

Condensin complexes play crucial roles in chromosome condensation that is a fundamental process to establish the "rod-like" shape of chromosome structure in mitosis. Failure of the chromosome assembly causes chromosome segregation errors and subsequent genomic instability. However, a molecular mechanism that controls condensin function for the chromosomal organization has not been fully understood. Here, we show that the abundance of CAP-H2, one of the condensin II subunits, is fluctuated during the cell cycle in accordance with Plk1 kinase activity. Inhibition of Plk1 leads to Cdc20-mediated degradation of CAP-H2 in mitosis. Plk1 phosphorylation of CAP-H2 at Ser288 is required for the accumulation of CAP-H2 and accurate chromosomal condensation during prophase. These findings suggest that Plk1 phosphorylation regulates condensin II function by modulating CAP-H2 expression levels to facilitate proper mitotic chromosome organization.

The functional role for condensin in the regulation of chromosomal organization during the cell cycle.

In all organisms, the control of cell cycle progression is a fundamental process that is essential for cell growth, development, and survival. Through each cell cycle phase, the regulation of chromatin organization is essential for natural cell proliferation and maintaining cellular homeostasis. During mitosis, the chromatin morphology is dramatically changed to have a "thread-like" shape and the condensed chromosomes are segregated equally into two daughter cells. Disruption of the mitotic chromosome architecture physically impedes chromosomal behaviors, such as chromosome alignment and chromosome segregation; therefore, the proper mitotic chromosome structure is required to maintain chromosomal stability. Accumulating evidence has demonstrated that mitotic chromosome condensation is induced by condensin complexes. Moreover, recent studies have shown that condensin also modulates interphase chromatin and regulates gene expression. This review mainly focuses on the molecular mechanisms that condensin uses to exert its functions during the cell cycle progression. Moreover, we discuss the condensin-mediated chromosomal organization in cancer cells.

Mps1 phosphorylation of condensin II controls chromosome condensation at the onset of mitosis.

During mitosis, genomic DNA is condensed into chromosomes to promote its equal segregation into daughter cells. Chromosome condensation occurs during cell cycle progression from G2 phase to mitosis. Failure of chromosome compaction at prophase leads to subsequent misregulation of chromosomes. However, the molecular mechanism that controls the early phase of mitotic chromosome condensation is largely unknown. Here, we show that Mps1 regulates initial chromosome condensation during mitosis. We identify condensin II as a novel Mps1-associated protein. Mps1 phosphorylates one of the condensin II subunits, CAP-H2, at Ser492 during mitosis, and this phosphorylation event is required for the proper loading of condensin II on chromatin. Depletion of Mps1 inhibits chromosomal targeting of condensin II and accurate chromosome condensation during prophase. These findings demonstrate that Mps1 governs chromosomal organization during the early stage of mitosis to facilitate proper chromosome segregation.