Poster: Hormones

Abs # 625: PIN1 auxin efflux carrier is mislocalizaed in flavonoid-deficient mutants

Presenter:	Peer, Wendy A, peerw@purdue.edu
Authors	Peer, Wendy A (A)   Bandyopadhyay, Anindita  (A)   Blakeslee, Joshua J (A)   Markham, Srinivas N (A)   Murphy, Angus S (A)
Affiliations:	(A): Purdue University

Based on earlier studies, we hypothesized that aglycone flavonols were active compounds regulating enzyme activity. Previously, we reported that auxin transport was altered in the flavonoid-deficient, chalcone synthase, transparent testa, tt4 mutation, and that flavonoid precursor feeding with naringenin restored both auxin transport and flavonoid localization to wildtype levels. We have also demonstrated that flavonoids are localized in regions of state transition: the cotyledonary node, the root-shoot transition zone, and the distal elongation zone. Here, we report that auxin transport profiles are also altered in mutants of the early genes in the biosynthetic pathway: tt7, a flavone 3'-hydroxlase mutant, accumulating kaempferol; and tt3, a dihydroflavonol reductase mutant, accumulating excess quantities of kaempferol and quercetin. We hypothesized that these differences in auxin transport may be due to altered localization of auxin efflux carriers. Consistent with the altered auxin transport profiles, the localization PIN1 was also altered in tt4, tt7, and tt3 compared to wildtype accumulation patterns. PIN1 localization in tt4 was restored to the wildtype pattern when the precursor naringenin was supplied. However, when alglycone flavonols were supplied to tt4, PIN1 localization was altered. These data suggest that certain flavonol species are required for correct targeting of PIN1 to basal cell membranes and support our hypothesis that alglycone flavonols act as autocrine effectors.