The Arabidopsis hypocotyl is a valuable model for studying axial growth phenomena in flowering plants owing to its dramatic cell elongation in the absence of cell division and its sensitivity to environmental cues. When grown in the dark, a hypocotyl rapidly elongates, using the energy reserves in the seed to drive the cotyledons upward into the light. Once light is detected, axial cell growth slows in favor of more radial cell growth due to the action of light receptors and myriad downstream signaling targets. The composition of the cell wall and the spatial organization of polymerous wall materials provide a means to guide cell expansion to produce cell shape. Microtubules, too, are essential for specifying axial cell elongation in plants. Cortical microtubules are organized into patterns that influence cell shape by directing the deposition of new cell wall materials. Drugs that perturb the microtubule cytoskeleton do not block cell growth per se but lead to apparent swelling and distention in growing cells, indicating a block to the mechanisms controlling cellular morphogenesis. Although auxin plays a central role in controlling plant cell growth and morphogenesis, our present understanding of how cell growth (i.e. increase in size) is coordinated with the cytoskeleton to determine hypocotyl cell shape (i.e. cellular morphogenesis) is limited. To examine the requirements for auxin-induced microtubule array patterning, True and Shaw (10.1104/pp.19.00928) used an Arabidopsis double auxin f-box (afb) receptor mutant, afb4-8 afb5-5, that responds to auxin (indole-3-acetic acid) but has a strongly diminished response to the auxin analog, picloram. The authors show that picloram induces immediate changes to microtubule density and later transverse microtubule patterning in wild-type plants but does not cause microtubule array reorganization in the afb4-8 afb5-5 mutant. Additionally, auxin-induced microtubule array reorganization was found to occur in a dominant mutant (axr2-1) for the auxin coreceptor AUXIN RESPONSIVE2 (AXR2). The authors also observed that brassinosteroid application mimicked the auxin response, showing microtubule array effects, and inducing transverse patterning in the axr2-1 mutant. Application of auxin to the brassinosteroid synthesis mutant, diminuto1, induced transverse array patterning but did not produce significant axial growth. Thus, exogenous auxin induces transverse microtubule patterning through the TRANSPORT INHIBITOR 1/AUXIN F-BOX (TIR1/AFB) transcriptional pathway and acts independently of brassinosteroids.