The rosettes are striking, but it has taken a long time for them to be identified. “I also spent a lot of time not seeing them,” says Zallen. “It was making movies that made the difference—then you see they are directional. Now when I read papers I see them all the time.”
In a previous model for elongation, called neighbor exchange, single-cell junctions running vertically were proposed to contract to a point, and then expand back out again horizontally. “These behaviors are happening, but we think they are only part of the story,” says Zallen. “The starting order they require is not there.”
But how to define “order”? Initially, says Zallen, “I didn't have a vocabulary to describe it.” But with her physicist father she used quantitation methods familiar to those who study soap bubbles. Paradoxically, they found that disorder at the cellular level increased even as the tissue got closer to its elongated, more globally ordered state.
The increased disorder appears to be from rosette formation. Patterning genes drive actin then myosin accumulation at anterioposterior cell borders, and actomyosin tugging parallel to the membrane probably helps form the rosettes.
When tracked for 25 minutes of so-called germband extension, 87% of cells are transiently incorporated into one or more rosettes. This amount of rearrangement, together with neighbor exchange, can account for most of the elongation seen. The mechanism for rosette resolution is unclear; clues should come from isolating components that lie downstream of patterning genes.