Researchers studying how Drosophila melanogaster macrophages migrate have uncovered new insights about the role of Moesin, a protein integral to the coordination of actin networks within cells.
Actin networks are known for their distinct forms, primarily categorized as either lamellar, which extends flatly at the leading edge, or cortical, which surrounds the cell membrane. Traditionally, these networks were thought to function separately, driving specific modes of cell movement. This study challenges this perspective, demonstrating instead the coexistence and interdependence of both types of actin networks during cellular migration.
The findings stem from research conducted by scientists including B.J. Sánchez-Sánchez and B.M. Stramer, who utilized innovative imaging techniques to track and analyze the dynamic behavior of actin networks as Drosophila macrophages undergo developmental dispersal. The authors noted, “These data reveal hemocyte motility requires both lamellipodial and cortical actin architectures in homeostatic equilibrium.” This suggests the necessity for the two structures to work together to facilitate proper cell movement.
The significance of this work extends beyond Drosophila; as cell migration is fundamental across many biological processes, including embryonic development, immune responses, and wound healing. Understanding how different actin structures work together may help elucidate mechanisms underlying diseases linked to improper cell migration, such as cancer metastasis.
By focusing on Moesin, which is known to regulate cortex actin-membrane crosslinking, the researchers observed how this protein is involved not just at the cell’s leading edge, but also at the rear where it correlates with lamella dynamics. “Moesin association with the actin cortex is regulated by phosphorylation, and its activity is required for normal lamellar actin flow and leading edge dynamics,” explained the authors, emphasizing Moesin's multifaceted regulatory role.
The study utilized live-cell imaging to visualize how the actin network flows from the front of the cell to the rear, providing valuable insights on how the cortical network aids the lamella and vice versa. Using various genetic tools, researchers identified the mutations present when Moesin function was compromised, leading to altered hemocyte morphology and impairments in migratory behavior.
Interestingly, results indicated disruptions to hemocyte development when Moesin was mutated or its function was inhibited, particularly highlighting defects in leading edge dynamics and overall cell movement. The alterations were marked by changes to cell shape, as the once flat lamellar structures became compromised, leading to increased cell body volume and reduced migratory efficiency. The ultimate impacts of this work help paint a broader picture of cellular mechanics and their roles during migration.
This groundbreaking research contributes to our fundamentals of cellular biology by highlighting how proteins like Moesin can integrate and stabilize diverse actin architectures, many of which are pivotal during cellular processes. Moving forward, this research not only opens the door for additional studies on Drosophila model systems, but may also inform therapeutic strategies aimed at improving cell mobility seized by various medical conditions.
With this comprehensive look at the engaging dance between Moesin, lamellar, and cortical actin networks, researchers are well-equipped to explore the impacts of other regulatory proteins, as well as extend this knowledge to other cell types and conditions. The capacity of macrophages to adapt their migration to maintain homeostasis could reflect on the body’s broader physiological responses, linking tissue development and repair to cellular regulation.