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. Author manuscript; available in PMC: 2020 Oct 3.
Published in final edited form as: Mol Cell. 2019 Aug 14;76(1):177–190.e5. doi: 10.1016/j.molcel.2019.06.044

Figure 6. ARF nucleo-cytoplasmic partitioning regulates auxin responsiveness and disruption of ARF condensate formation results in morphological defects.

Figure 6

(A) Photos of 8d-old seedlings from wild-type (Wt; Col-0), two independent UBQ10:YFP-ARF19 (ARF19) lines, and two independent UBQ10:YFP-ARF19K962A (ARF19K) lines. Bar = 1 cm.

(B) Mean root lengths (+SE; n ≥ 15) of 8d-old seedlings.

(C) Mean cotyledon area (+SE; n ≥ 30) of 8d-old seedlings.

(D) Histograms of root hair lengths from 6d-old seedlings.

(E) In cells displaying dampened auxin responsiveness, activating ARF proteins localize to cytoplasmic biomolecular assemblies; protein assembly formation is driven by the PB1 domain and MR IDR. Conversely, ARF proteins localize to the nucleus in actively growing, highly auxin-responsive tissues, such as the root tip. Localization of these transcription factors to the cytoplasm (in cells with low auxin responsiveness) or nucleus (in cells with high auxin responsiveness) may confer cellular competence for auxin response.