Other researchers have also suggested that actin dynamics play a role in membrane scission. These experiments focused on the internalization steps at PM, but this actin-induced scission may also apply to EEs. SNX4 has been shown to be a candidate factor driving membrane tubulation in the EE-to-RE pathway, and may contribute to membrane tubulation and scission together with actin dynamics. Another study also reported that myosin VI and its interacting protein lemur tyrosine kinase 2 siRNAs led to swollen, enlarged EEs and reduced EHD3- containing tubule formation. These results suggest that actin motor threo Ifenprodil hemitartrate proteins also participate in the EE-to-RE pathway. Indeed, at the trans-Golgi network, GOLPH3 bridges phosphatidylinositol and actomyosin to promote efficient tubulation and vesicle formation. We propose that actin filaments contribute to efficient fission by cooperating with factors driving membrane tubulation, such as SNX4. Actin polymerization has been shown to be involved in homotypic fusion of endosomes as well as yeast vacuoles. In Dictyostelium, inhibition of actin polymerization induced LEs to form clusters and blocked endosomal transport and movement, suggesting that the actin coat surrounding LEs prevents endosomes from clustering, docking, and fusing with each other. On the other hand, fusion between phagosomes and LEs and between LEs themselves is affected by the inhibition of actin polymerization in vitro, indicating that the actin filaments assembled on LEs or phagosomes may facilitate endosomal fusion. These findings suggest that the actin filaments may regulate endosomal fusion at several distinct steps during intracellular transport. We demonstrated that EEs fused with each other forming enlarged EEs after inhibition of actin dynamics. On the other hand, induction of actin-polymerization by LatB washout induced dissociation of EEs and translocation of each vacuolar domain. Furthermore, we observed that the dissociation of EEs by actin polymerization was independent of microtubules. Thus, actin filaments may provide a track for actin-based motor proteins to prevent aggregation or homotypic fusion. As the actindependent movement was limited among endosomes, the observation of endosomal movement under SB 334867 nocodazole treatment would be difficult. Phagocytosis of pathogens initiates the innate immune response. Macrophages rely heavily on phagocytosis and subsequent degradation of microbes to help clear the invading pathogens.