Related Experiment Video
Updated: Aug 14, 2026

Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols
Published on: June 6, 2017
Suppression of p160ROCK bypasses cell cycle arrest after Aurora-A/STK15 depletion
1Cold Spring Harbor Laboratory, 1 Bungtown Road, Cold Spring Harbor, NY 11724, USA.
Abstract:
Alterations in the expression and activity of the centrosomal kinase, Aurora-A/serine/threonine kinase 15 (STK15), affect genomic stability, disrupt the fidelity of centrosome duplication, and induce cellular transformation. Here, we provide evidence that p160ROCK, a Rho-associate serine/threonine kinase, associates with Aurora-A in a protein complex with other STK15-associated factors. Suppression of Aurora-A by small interfering RNA in HeLa cells blocks the ability of centrosomes to organize normal mitotic spindles, induces G(2)/M cell cycle arrest, and promotes accumulation of tetraploid cells. In many cases, one outcome of such abnormalities is apoptosis. Introduction of a second genetic lesion, suppression of p160ROCK by RNA interference, can rescue abnormal mitotic spindle formation, release the G(2)/M cell cycle arrest, and alleviate apoptosis, leading to a greater accumulation of aneuploid cells. These results suggest that Aurora-A and p160ROCK act in a common genetic pathway that promotes and monitors progression through G(2)/M.
Insights
Aurora-A and p160ROCK kinases are involved in cell cycle progression. Suppressing Aurora-A causes cell cycle arrest and apoptosis, while also suppressing p160ROCK rescues these effects, suggesting a common pathway.
Area of Science:
- Cell Biology
- Molecular Biology
- Genetics
Background:
- Aurora-A (serine/threonine kinase 15) is a centrosomal kinase crucial for genomic stability and cell cycle regulation.
- Aberrant Aurora-A expression and activity are linked to genomic instability, centrosome duplication errors, and cellular transformation.
- Rho-associated kinase (ROCK) pathways are implicated in various cellular processes, including cell division.
Purpose of the Study:
- To investigate the interaction between Aurora-A and p160ROCK.
- To elucidate the roles of Aurora-A and p160ROCK in regulating the G2/M cell cycle transition and mitotic spindle formation.
- To determine if Aurora-A and p160ROCK function within a common genetic pathway.
Main Methods:
- Small interfering RNA (siRNA) and RNA interference (RNAi) were used to suppress Aurora-A and p160ROCK expression in HeLa cells.
- Protein complex formation was assessed.
- Mitotic spindle organization, cell cycle progression (G2/M arrest), ploidy (tetraploid and aneuploid cell accumulation), and apoptosis were analyzed.
Main Results:
- p160ROCK was found to associate with Aurora-A in a protein complex.
- Suppression of Aurora-A led to defective mitotic spindle formation, G2/M cell cycle arrest, tetraploid cell accumulation, and apoptosis.
- Simultaneous suppression of p160ROCK rescued abnormal spindle formation, released G2/M arrest, alleviated apoptosis, and increased aneuploid cell accumulation.
Conclusions:
- Aurora-A and p160ROCK function in a shared genetic pathway that governs G2/M phase progression.
- This pathway appears to monitor and promote cell cycle progression through mitosis.
- The interplay between Aurora-A and p160ROCK is critical for maintaining genomic integrity and preventing aberrant cell division.
More Related Videos
Related Concept Videos
Negative Regulator Molecules
DNA Damage can Stall the Cell Cycle
Inhibition of Cdk Activity
Abnormal Proliferation
Anaphase Promoting Complex
DNA Damage Can Stall the Cell Cycle

