Light profoundly influences plant development through photoreceptor molecules and their attendant signal transduction pathways. For example, as a seedling pushes up through the soil or leaf litter, it is guided toward the surface by light signals that penetrate the substrate. Guidance of growth by directional light cues (phototropism) is mediated principally by the phototropin 1 (phot1) blue light receptor (1). Once the shoot apex emerges into an appropriately lit environment, elongation of the stem slows, the apical hook decurves, the cotyledons unfold and turn green, and development switches to a program that emphasizes photosynthesis. The cryptochrome blue light receptors (2) and the phytochrome red/far-red receptors are the principal mediators of these effects. This MOVIE shows how mutation of the cryptochrome 1 (cry1) photoreceptor affects the control of hypocotyl elongation by light in Arabidopsis seedlings. Our research in this field orginally focused on some very early ionic and electrical changes related to the process by which blue light affects hypocotyl cell expansion. Subsequent studeis used mutants to specify roles for specific photoreceptors. DNA microarrays were used to survey changes in gene expression. Recent studies have shown connections between the photocontrol of hypocotyl elongation and the transport of auxin by ABCB transporters. The following model is a summary of what our work has added to the understanding of how blue light suppresses elongation of the Arabidopsis hypocotyl during seedling photomorphogenesis.


The National Science Foundation funds this work.



Blue light action model


Notes on the model. The phototropin 1 (phot1) blue-light receptor and the NPH3 protein with which it interacts are both required for phototropism. However, the initial phase of hypocotyl growth inhibition triggered by phot1 does not require NPH3 (3). The transient rise in cytoplasmic calcium concentration trigged by blue light acting through phot1 is not causally related to phototropism but is to the first phase of growth inhibition (4). The cry1, cry2, and phytochrome A (phyA) photoreceptors are each equally necessary for the activation of anion channels at the plasma membrane of hypocotyl cells within seconds, and the phase of growth inhibition that follows approximately 30 minutes later (3). The similar behavior of mutants lacking these receptors in this time period is consistent with them working together as a complex, what we refer to as the 'cry-phy-pie' (5) The anion channels activated by blue light (6) are also calcium sensitive (7), providing a means for interaction between the phot1 and cry1 signaling pathways. Ultimately, these signal transducing steps cause a decrease in the rate of hypocotyl (stem) cell expansion (8). Changes in gibberellin and auxin, two growth regulating hormones, appear to be the proximate causes of the cell expansion changes (9). Counteracting these growth-suppressing processes is a light-dependent process that "pushes" growth. The ultimate rate of hypocotyl elongation is the resultant of these two opposing influences (10). The phyB photoreceptor appears to contribute to this push (11). Not included in the model is the recent finding that auxin transport mediated by the ABCB19 protein may be a component of a cry1-dependent "push" that counteracts cry1-mediated inhibition (12).