Cytokinin Receptors are Required for Normal Development of Auxin-transporting Vascular Tissues in the Hypocotyl but not in Adventitious Roots

We describe the wooden leg-3 mutant with weak root apical dominance. wol-3 is a novel allele of the ARABIDOPSIS HISTIDINE KINASE 4 gene that encodes a cytokinin receptor

Takeshi Kuroha; Chiharu Ueguchi; Hitoshi Sakakibara; Shinobu Satoh


Scholarcy highlights

  • In higher plants, the root system is composed of primary, adventitious and lateral components
  • To clarify whether the extensive auxin response in the hypocotyl and the inhibition of lateral root formation in the wol-3 mutant was caused by inhibition of basipetal auxin transport in the hypocotyl, we investigated the basipetal movement of 3H-labeled IAA applied to the top of the hypocotyl
  • Previous studies showed that reduced cytokinin signals inhibit the development of vascular tissues in the hypocotyl, we suggest that this phenotype is caused by an inhibition of auxin transport resulting in the accumulation of auxin in the hypocotyl
  • The ARABIDOPSIS HISTIDINE KINASE 4 gene encodes a cytokinin receptor that is a sensor histidine kinase, and mutants with the wol-3 allele included in this gene exhibit a cytokinin-insensitive phenotype
  • The wol-3 mutation at M436, which is conserved in all cytokinin receptors, suggests that this residue is important for the function of AHK4
  • Auxin transport assay Seedlings were grown on 1.5% purified agar supplemented with
  • Basipetal auxin transport from the hypocotyl to the primary root in the wol-3 mutant was significantly inhibited compared with the wild type. These results suggest that the inhibition of lateral root formation in the wol-3 mutant is not caused by the reduction of cell numbers in the vascular systems of the primary root, but results from the inhibition of auxin transport from the hypocotyl
  • This suggests that the differences in the expression patterns lead to different phenotypes of the vascular tissue in the hypocotyls and adventitious roots of the wol-3 and ahk2 ahk3 ahk4 mutants

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