Their model was the shoot apical meristem (SAM). The SAM has a central zone (CZ) of stem cells plus various surrounding cells that make the transcription factor WUSCHEL. Although WUSCHEL creates a signal that promotes stem cell identity back in the CZ, it also induces these stem cells to produce CLAVATA3 (CLV3), an extracellular ligand that keeps WUSCHEL repressed centrally. This forces the inducing ring to keep its distance from the induced stem cells.
Reddy and Meyerowitz turned on an RNAi-inducing transcript that knocked down CLV3. As others have found, the end result was more WUSCHEL activity, and thus more promotion of stem cell identity and an expanded CZ and SAM. Unfortunately, says Reddy, any such terminal phenotype is the sum of changes in multiple interacting components of a network. The function of individual genes, he suggests, is best understood via a transient perturbation that allows changes in cell identities and cell division to be observed as the phenotype develops.
To see this kind of dynamics, the pair used GFP-labeled cell markers and transient induction of the CLV3 RNAi. Soon after this treatment the CZ expanded, via the dedifferentiation or respecification of surrounding cells. Only later was there an increase in the division rate of cells more distant from the stem cell area, but still within the SAM.
The separable effects point to a complicated system of signaling. WUSCHEL is no doubt part of the answer, but real-time analysis of a few more genes will probably be necessary to understand fully how plants keep a group of stem cells at a buffered and consistent size.