She was on the right track, as the group found that loss of trypanosomal Centrin2 inhibited Golgi duplication. It was not, however, doing this job from the centrosome, but rather from an odd bi-lobed cytoplasmic structure. One lobe was associated with the cell's only Golgi stack. The second lobe was free during early interphase, but later was associated with the newly forming Golgi stack.
Centrin is phosphorylated by PKA in a cell cycle–regulated manner, which might determine when the new stack is seeded. Alternatively, centrin might help separate duplicated stacks, as algal Centrin is known to be part of an ancient contractile system. Centrin might also control the duplication of the bi-lobed structure itself, an event that occurred after Golgi duplication and led to two bi-lobed structures, each with a single Golgi stack.
“Mammalian centrins,” says He, “form a pericentrosomal haze reminiscent of the Golgi ribbon.” This haze was considered to be insignificant centrosomal overflow, but with the new findings it warrants a closer examination.