FMNL2 associates with Formin2 and Arp2/3 complex for actin assembly, which further regulates spindle migration and INF2/Cofilin-related organelle dynamics during mammalian oocyte maturation.

FMNL1β is phosphorylated on S1086 in a protein kinase C δ (PKCδ)-dependent manner and S1086-phosphorylated FMNL1β acts downstream of PKCδ to regulate centrosome and multivesicular bodies polarization to the immunological synapse and exosome release.

Lymphocyte migration and autoimmunity induction rely on Formin-like 1-mediated actin network remodeling to push the lymphocyte nucleus through restrictive endothelial barriers.

Genomic deletions formed from inter-fork strand annealing associated with a collapsed replication fork are suppressed by the FANCM-related DNA helicase Fml1 in conjunction with its partner proteins Mhf1 and Mhf2.

Ena/VASP proteins act as positive regulators of cell motility and are required for the formation of microspikes, as opposed to filopodia that can arise from distinct molecular mechanisms.

Formins slow elongation of actin filament by either sterically blocking the addition of actin subunits or flattening the helical twist of the filament end.

Proteomic and genetic analysis discovers a new cytoskeletal mechanism of presynaptic short-term plasticity common across neuronal cell types.

Genomic deletions and gene conversions, caused by template switching associated with restarted DNA replication, are detected downstream of a collapsed replication fork and are suppressed by several conserved DNA helicases.

Two modes of actin polymerization, branched and linear, cooperate in B cells to extract antigens from surfaces of presenting cells.

The discovery of a mechanism that causes DNA deletions during non-canonical DNA replication termination is described.