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Decoding the Molecular Network that Drives Hypocotyl Elongation

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Auxin and brassinosteroid (BR) promote cell expansion through interdependent and synergistic pathways (reviewed in Hardtke et al., 2007). Although the biosynthetic pathways that produce these phytohormones have been characterized and the downstream response factors that trigger cell expansion are known (Oh et al., 2014), the transcriptional network that brings about localized changes in auxin and BR levels in response to endogenous developmental signals is unclear. The TEOSINTE BRANCHED 1, CYCLOIDEA, PROLIFERATING CELL FACTOR (TCP) family of miR319-targeted transcription factors influence multiple developmental processes in plants and can have a striking effect on plant architecture. For instance, a founding member of this family, Zea mays TEOSINTE BRANCHED 1, represses the growth of axillary organs and has been implicated in the domestication of maize (Doebley et al., 1997). Emerging evidence suggests that TCP proteins modulate hormone synthesis, transport, and signal transduction (reviewed in Nicolas and Cubas, 2016). Thus, the recent finding that cell expansion is enhanced in the hypocotyls of Arabidopsis seedlings expressing a hyper-activated form of TCP4 (Sarvepalli and Nath, 2011) suggests that TCP4 stimulates cell expansion in developing hypocotyls by regulating auxin and BR biosynthesis or signaling.

Now, Challa et al. (2016) investigated this possibility using a series of single and higher order mutants and transgenic lines that produce various levels of TCP4 transcript. The jaw-D mutant (which has reduced expression of TCP2, 3, 4, 10, and 24) had the shortest hypocotyls, whereas the Pro35S:mTCP4:GR line (which expresses a miR319-resistant form of TCP4 upon induction with dexamethasone) had the longest hypocotyls, when grown under inductive conditions. RT-qPCR analysis revealed that the extent of hypocotyl elongation was directly proportional to the abundance of TCP4 transcript, confirming that TCP4 promotes hypocotyl elongation.

The authors then evaluated if TCP4- dependent hypocotyl elongation is mediated by phytohormones. Growth assays in which transgenic seedlings were treated with various concentrations of epi-brassinolide (a bioactive BR), picloram (a synthetic auxin anolog), and propiconazole (an inhibitor of BR biosynthesis) indicated that TCP4 function during hypocotyl elongation depends on auxin and BR responses. In agreement with this, transcriptome analysis of jaw-D ProTCP4:mTCP4:GR seedlings revealed that the expression of numerous genes involved in auxin and BR responses changed soon after TCP4 induction. Interestingly, the transcript level of YUCCA5 (YUC5), which encodes an enzyme involved in auxin biosynthesis, exhibited a ~2.5-fold increase within 1 h of TCP4 induction. Further analysis suggested that TCP4 strongly and specifically binds to the YUC5 locus and hence that YUC5 is a direct target of TCP4. In addition, an analysis of transgenic seedlings harboring both the ProTCP4:mTCP4:GR construct and the auxin-response marker ProDR5:GUS in the jaw-D background indicated that TCP4 induces the auxin response in planta.

Next, the authors crossed the jaw-D ProTCP4:mTCP4:GR line with a range of mutants defective in auxin or BR responses and monitored the effect of TCP4 induction on hypocotyl elongation. These experiments revealed that TCP4-dependent hypocotyl elongation relies both on auxin-mediated activation of AUXIN RESPONSE FACTOR 6/8 (ARF 6/8) and on BR-mediated activation of BRASSINAZOLE-RESISTANT 1 (BZR1), further linking TCP4 function to auxin and BR signaling.

This work establishes a link between TCP4 and auxin and BR signaling and expands existing models of the molecular network driving hypocotyl elongation (see figure).

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