![]() | Figure 1 A bleb blocks mating with a cell lacking Kex2. |
A complex of membrane fusion proteins is deployed by an influenza virus as it invades its host cell. But the comparable machinery of most eukaryotic cells that fuse has not been identified. Several years ago, the group identified one protein crucial for the process by studying yeast mating, in which two fungal cells stick together, dissolve their cell walls at the point of contact, and join their membranes. Yeast missing the protein Prm1 snuggle up to one another but often can't unite, the researchers found.
But mating succeeds in about half of the cells lacking Prm1, suggesting that fusion requires other proteins. To tease out these collaborators, the researchers have now screened yeast mutants for cells that are even worse at combining. The screen fingered the protein Kex2.
During mating, cells lacking both Kex2 and Prm1 display different defects than cells missing only Prm1. The cell walls of Kex2-deficient yeast often sport blebs, or blisters, and some cells contain blank areas of cytoplasm devoid of organelles that the researchers dubbed “enormous, barren bubbles.” These unique features suggest that Kex2 orchestrates a different part of the fusion pathway than does Prm1.
How loss of Kex2 blocks cell unification remains uncertain. Unlike Prm1, Kex2 is not embedded in the plasma membrane. Its home is the Golgi apparatus, where it trims proteins destined for other parts of the cell. The researchers speculate that Kex2 spurs cell fusion by aiding in the maturation of another protein that passes through the Golgi apparatus. They are now hunting for this Kex2-modified molecule.