Figure 6. Speculative model of LOTR1 function.

The following model for LOTR1 function is simply one scenario that can plausibly integrate the data on LOTR1’s predicted activity, expression, subcellular localization, as well as phenotypes by loss-of-function and dominant-interference by misexpression. Wild-type: LOTR1 is a predicted protease (scissors), experimentally determined to be expressed in the stele and to localize in the cell wall. We speculate that LOTR1 cleaves a cortex-derived substrate (grey, dark-red coffee bean, inactive), activating it in the stele (red half-bean, active). This substrate then inhibits ectopic CASP-domain formation (green) at the stele-facing endodermal surface by unknown means. lotr1 mutant: Absence of LOTR1 would not allow activation of the ectopic CASP-domain inhibitor in the endodermal, stele-facing apoplast, leading to the observed formation of ectopic, stable CASP-domain predominantly at the stele-facing side of the endodermal surface. LOTR1 cortex mis-expression: This model explains the observation that cortical mis-expression of LOTR1 dominantly interferes with wild-type LOTR1 action, if it would precociously cleave and activate the LOTR1 substrate, not allowing it to reach the stele to be activated by wild-type LOTR1. This would lead to the observed, similar phenotype than the lotr1 knock-out.