Abstract

Roots detect water potential gradients in the soil and orient toward moister areas, a response known as hydrotropism that aids drought avoidance. Although auxin is crucial in tropism, its polar transport is not essential for hydrotropism in Arabidopsis. Moreover, antiauxin treatments in Arabidopsis produced inconsistent outcomes: some studies indicated auxin action was necessary while others did not. In this study, we examined auxin's physiological role in hydrotropism. We found that inhibiting auxin biosynthesis or transport intensified hydrotropic bending not only in wild-type, but also in hydrotropism defective mutants, namely miz1-1 and miz2 plants. Given that miz1-1 and miz2 exhibited compromised hydrotropism even under clinorotated conditions, we infer that auxin biosynthesis and transport directly suppress hydrotropism. Additionally, tir1-10, afb1-3, and afb2-3 displayed augmented hydrotropism. We observed a significant delay in hydrotropic bending in arf7-1arf19-1, suggesting that ARF7 and ARF19 amplify hydrotropism in its early stages. To discern the functional ties of ARF7/19 with MIZ1 and MIZ2, we studied the hydrotropic phenotypes of arf7-1arf19-1miz1-1 and arf7-1arf19-1miz2. Both triple mutants had diminished early-stage hydrotropism yet showed partial but significant recovery in the later stages. Given MIZ1's role in reducing auxin levels and MIZ2's essentiality for MIZ1 functionality, we conclude that auxin inhibits hydrotropism downstream of MIZ1 in later stages to refine root bending. Furthermore, it is posited that gene expression driven by ARF7 and ARF19 is pivotal for early-stage root hydrotropism.

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