XXXX and phytochrome B control shade-avoidance responses in @entity958 via partially independent hormonal cascades.

@entity14980 @entity958 @entity14979 @entity16656 @entity16606 @entity72701 @entity72700
Plants respond to a reduction in the red/far-red ratio (R:FR) of light, caused by the proximity of other plants, by initiating morphological changes that improve light capture. In @entity958 , this response (shade avoidance syndrome, SAS) is controlled by phytochromes (particularly phyB), and is dependent on the @entity72700 pathway of auxin biosynthesis. However, when grown in real canopies, we found that phyB mutants and mutants deficient in TAAI ( @entity72700 ) still display robust SAS responses to increased planting density and leaf shading. The SAS morphology (leaf hyponasty and reduced lamina/petiole ratio) could be phenocopied by exposing plants to blue light attenuation. These responses to blue light attenuation required the UV-A/blue light photoreceptor @entity16606 . Moreover, they were mediated through mechanisms that showed only limited overlap with the pathways recruited by phyB inactivation. In particular, pathways for polar auxin transport, auxin biosynthesis and gibberellin signaling that are involved in SAS responses to low R:FR were not required for the SAS responses to blue light depletion. By contrast, the @entity16656 response appeared to be required for the full expression of the SAS phenotype under low blue light. The phyB and @entity16606 inactivation pathways appeared to converge in their requirement for the basic/helix-loop-helix (bHLH) transcription factors @entity72701 ( @entity14979 and @entity14980 ) to elicit the SAS phenotype. Our results suggest that blue light is an important control of SAS responses, and that @entity14979 and @entity14980 are critical hubs for a diverse array of signaling routes that control plant architecture in canopies.
