Strigolactone-Regulated Hypocotyl Elongation Is Dependent on Cryptochrome and Phytochrome Signaling Pathways in Arabidopsis

We demonstrate that strigolactone inhibition of hypocotyl elongation is dependent on cryptochrome and phytochrome signaling pathways

Kun-Peng Jia; Qian Luo; Sheng-Bo He; Xue-Dan Lu; Hong-Quan Yang


Scholarcy highlights

  • Strigolactones were originally isolated from plant root exudates acting as seed germination stimulants of root parasitic plants such as Striga and Orobanche species
  • First we identified two null mutants of MAX2 gene, and we measured the hypocotyl length of wild-type and the two max2 mutant seedlings treated with various concentrations of GR24 in darkness and white light
  • When treated with low concentrations of GR24, hypocotyl elongation of WT seedlings grown in WL rather than darkness was inhibited by GR24 in a dosage-dependent manner, with an inhibition percentage of 45% at 10 μM GR24, whereas the max2-3 and max2-4 mutants showed almost no response to GR24 in WL or in darkness
  • When the GR24 concentration was further increased to 50 μM, hypocotyl elongation in the WT, max2-3, and max2-4 was reduced in both WL and darkness
  • We demonstrate that MAX2-mediated strigolactone signaling inhibits hypocotyl elongation and is dependent on light and both cryptochrome and phytochrome photoreceptors based on two lines of evidence: first, low concentrations of GR24 inhibited hypocotyl elongation in WL but not in darkness; second, under monochromatic blue, red, and far-red light, GR24 exerted strong inhibitory effects on hypocotyl elongation of WT seedlings, but showed significantly reduced inhibitory effects on the cry1 cry2, phyB, and phyA mutants
  • Our results strongly indicate that cryptochromes and phytochromes are required for strigolactone inhibition of hypocotyl elongation
  • According to our results, HY5 is a downstream factor of strigolactone signaling in regulating seedling growth including hypocotyl elongation, and the synergistic effects observed for MAX2 and HY5 can be explained by our model, in which, other than HY5, there may exist phytochromeinteracting factors-regulated components that act downstream from MAX2, and HY5 is regulated by CONSTITUTIVE PHOTOMORPHOGENIC1 other than MAX2

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