Identification of Endogenous Plant Compounds Regulating Auxin Transport in Roots - ISRR 2018 10th Symposium for the International Society of Root Research

Siamsa Doyle ¹ Adeline Rigal ¹ Peter Grones ¹ Michal Karady ¹ Deepak K Barange ^1,2 Mateusz Majda ¹ Aleš Pěnčik ¹ Michael Karampelias ³ Marta Zwiewka ⁴ Fredrik Almqvist ² Ondřej Novák ¹ Karin Ljung ¹ Stéphanie Robert ¹

¹Umeå Plant Science Centre, Department of Forest Genetics and Plant Physiology, Swedish University of Agricultural Sciences (SLU), Umeå, Sweden
²Department of Chemistry, Umeå University, Umeå, Sweden
³Department of Plant Systems Biology, Vlaams Instituut voor Biotechnologie (VIB), and Department of Plant Biotechnology and Bioinformatics, Ghent University, Gent, Belgium
⁴Central European Institute of Technology (CEITEC), Masaryk University, Brno, Czech Republic

Controlled gradients of the phytohormone auxin are essential for plant development and auxin transport via polar plasma membrane-localized PIN-FORMED (PIN) proteins is important for auxin gradient establishment (Vanneste and Friml, 2009). Using a chemical biology approach, we aim to dissect the endomembrane trafficking pathways that control PIN polarity. We isolated the synthetic compound Endosidin 8 (ES8), which disrupts polarity of selective PINs in Arabidopsis root cells, leading to short, agravitropic roots (Doyle et al., 2015). Interestingly, this compound is a structural analogue of anthranilic acid (AA), which is a precursor of the main auxin precursor tryptophan (Ljung K, 2013). We showed that AA itself also affects PIN polarity in roots in a similar way to ES8. However, while AA fully rescues the root length and gravitropism defects of the anthranilate synthase-deficient double mutant wei2-1 wei7-1 (Stepanova et al., 2005), ES8 selectively recovers the root gravitropic defect, without rescuing root length. In contrast to AA itself, ES8 does not influence tryptophan levels, suggesting that it does not modulate tryptophan-dependent auxin biosynthesis. Furthermore, at lower concentration, AA treatment significantly recovers wei2-1 wei7-1 root gravitropism without affecting root length or IAA concentration within the plant tissues. We hypothesize that in the mutant, AA-induced rescue of root length is due entirely to recovery of IAA biosynthesis while AA-induced rescue of root gravitropism is partially due to recovery of PIN polarity regulation. Taken together, our results suggest a previously unknown role for AA in the regulation of auxin transport via control of PIN trafficking, independent of its function in auxin biosynthesis.

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Stepanova AN et al. (2005) Plant Cell 17:2230-42.