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Trichome patterning

Trichome patterning on Arabidopsis rosette leaves serves as a model to study how cells are specified in a regular spacing pattern from initially equivalent cells. The spacing pattern is established by a conserved gene casette consisting of the bHLH proteins GL3 and EGL3, the R2R3MYBs GL1 and AtMYB23 and the WD40 factor TTG1. These three proteins form protein complexes and act as transcriptional regulators promoting the fate of trichome cells. Their action is counteracted  the redundantly acting R3 single repeat MYB proteins TRY and CPC and several additional homologs. The regulatory network formed by these factors can be described in two mechanistically different models, an activator/inhibitor and a depletion model.

The activator-inhibitor model of trichome patterning

The activator/inhibitor scenario explains the establishment of a pattern by a regulatory feedback loop in which the activators activate the inhibitors which in turn repress the activators. The inhibitors can move between cells an mediate the intercellular communication. In the depletion model TTG1 can move between cells and is trapped in trichome cells due to its interaction with GL3. It is thought that both mechanisms work in parallel probably stablizing each other outcome. In our lab we focus on two major questions.

Mutual regulation of protein localization

The various interactions between the proteins also lead to a relocalization of the respective proteins and thereby also a change in their biological activities. One excellent exampl is the interaction GL3 and TTG1 that leads to a recruitment of TTG1 to the nucleus and changes the intercellular movement behaviour. We explore this aspect for the above mentioned core components and additional trichome specific factors.

Analysis of the theoretically postulated positive feed back loop

All theoretical models require a positive feed back loop of the activators that has not been demonstrated yet. This is required because patterning begins with a field of initially equivalent cells and the initial balance has to broken by some kind of non-linear amplification mechanism. We use iterative experimental/theoretical approaches to tackle this question.