Cortical branched actin determines cell cycle progression.

Cell cycle regulation is tightly linked to cytoskeletal dynamics. Prior research has shown that actin networks influence cell motility and signaling. However, the role of branched actin in controlling cell cycle phases remains unclear. This gap motivated the investigation into how cortical actin structures regulate cell cycle progression. No prior work had resolved the connection between actin branching and G1 phase duration. It was already known that Arp2/3 complexes regulate actin polymerization. Yet, the specific contribution of ARPC1B-containing complexes to cell cycle control had not been established. This uncertainty drove the exploration of ARPC1B's role in mammary epithelial cells. The study aimed to clarify how branched actin structures influence cell cycle progression.

The study aimed to determine how cortical branched actin regulates cell cycle progression in mammary epithelial cells. The researchers focused on ARPC1B-containing Arp2/3 complexes and their role in generating branched actin networks. They sought to understand how these networks are monitored by type I coronins. The study also examined the RAC1/WAVE/ARPIN pathway's role in regulating these structures. The researchers wanted to link actin dynamics to cell migration and G1 phase duration. They explored whether cortical actin integrates growth factor and mechanotransduction signals. The goal was to uncover how these signals influence S-phase entry. The findings could provide insights into cancer progression and therapeutic strategies.

The researchers used mammary epithelial cells to study cortical actin structures. They employed genetic and pharmacological tools to manipulate Arp2/3 complexes. Live-cell imaging tracked lamellipodial protrusions and migration patterns. Immunostaining and biochemical assays identified ARPC1B and coronin interactions. The team used RNA interference to knock down specific subunits of Arp2/3 complexes. They measured cell cycle phase durations using time-lapse microscopy. Growth factor signaling and substratum rigidity were tested for their effects on actin networks. The study also included tumor cell lines to compare actin dependence in normal and cancerous cells.

Cortical branched actin networks depend on ARPC1B-containing Arp2/3 complexes. These networks are specifically monitored by type I coronins. The RAC1/WAVE/ARPIN pathway regulates ARPC1B-dependent actin structures. Lamellipodial protrusions are driven by these actin networks. The G1 phase duration scales with migration persistence in single cells. Cortical actin integrates growth factor and mechanotransduction signals. S-phase entry is determined by these actin structures. Tumor cells often lose this dependence on cortical branched actin.

The study shows that cortical branched actin structures control cell cycle progression. ARPC1B-containing Arp2/3 complexes are essential for these networks. Type I coronins monitor these structures to regulate the cell cycle. The RAC1/WAVE/ARPIN pathway controls actin network dynamics. Migration persistence correlates with G1 phase duration. Actin structures integrate soluble and mechanical signals to determine S-phase entry. Tumor cells often bypass this regulation. Arp2/3 specificity may offer diagnostic and therapeutic opportunities in cancer.