Elucidating the mechanism of organ size control by KLU-dependent intercellular signalling

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Plant organ size is under tight genetic control. Recent studies in model species suggest that the timing of the transition from cell proliferation to cell expansion is a crucial step in regulating final organ size. However, the central question of how this transition is coupled to the attainment of a certain primordium size or cell number is still unanswered. Studies of the Arabidopsis cytochrome P450 KLUH (KLU) have indicated that the organ margins play a crucial role in controlling organ size. The KLU gene is only expressed in a subset of marginal cells in leaves and floral organs, where it appears to contribute to the generation of a mobile growth regulator distinct from the classical phytohormones that promotes cell proliferation throughout the organ. This suggests a simple model of measuring organ size via the concentration of the presumed growth regulator; the growth regulator is progressively diluted as the organ enlarges, until at a certain size its concentration can no longer sustain further proliferation. This proposal combines the complementary strengths of the Lenhard and Napier groups to gain a better understanding of how the KLU-dependent growth regulator controls organ size. Firstly, to test whether this signal is mobile enough for the above dilution model to be feasible, we will determine its mobility by imaging the expression of a specific downstream reporter gene. Secondly, we will test the hypothesis of a metabolic pathway leading to the active growth signal that involves additional, KLU-responsive cytochrome P450 encoding genes. Thirdly, the substrate(s) and product(s) of KLU will be isolated by a metabolomic approach. Fourthly, additional genes required for generating, perceiving and transducing the presumed growth regulator will be isolated by screening for mutants that suppress the transcriptional response to induced KLU activity.

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