Extended Data Fig. 4: ABP1 and TMKs in vasculature formation and regeneration.
From: ABP1–TMK auxin perception for global phosphorylation and auxin canalization
a, GUS staining revealed specific upregulation of TMK1::GUS, TMK3::GUS and TMK4::GUS expression around the wound 2 or 4 days after wounding (daw). Representative micrographs from 2 experiments (n = 8 for each). Scale bar, 100 µm. b, GUS staining revealed specific upregulation of ABP1::GUS but not LRR4::GUS expression around the wound. ABP1::GFP-ABP1 confirmed the GUS staining. Representative micrographs from 2 experiments (n = 8 for each). Scale bar, 100 µm. c, Quantification of vasculature regeneration in wounded Arabidopsis stems in abp1-c1 and abp1-TD1 mutants as well as corresponding complemented lines (comp-c1 and comp-TD1) confirms that the vasculature regeneration defects are due to disruption of the ABP1 locus. Total number of samples for each observation, n = 20. d, Exogenous IAA application (green oval shape) on stems triggered the formation of a channel (visualized by toluidine blue (TBO); indicated by white arrow) from this local source to the existing vascular tissue in WT but not abp1-TD1 mutant 6 days after application (daa). Scale bar, 100 µm. e, Quantification of de novo vasculature formation from local auxin source (as visualized by TBO) 4 days after application (4 daa) in abp1-c1 and abp1-TD1 mutants as well as corresponding complemented lines (comp-c1 and comp-TD1) confirms that the vasculature regeneration defects are due to the ABP1 locus disruption. Total number of samples for each observation, n = 20. f, Quantification of de novo vasculature formation from local auxin source (as visualized by TBO) in tmk mutants. tmk4 shows stronger defects followed by tmk3 and tmk1 whereas tmk2 has almost normal vasculature formation. Total number of samples for each observation n = 20.
