Figure 6.

Working models to explain the photochrome A-induced enhancement of phototropin-dependent phototropism in wild-type Arabidopsis seedlings and the recover of response in nph4 mutants lacking the auxin response factor ARF7.

From studies of the nph4/arf7 mutants it appears that phyA-dependent increases in the phototropic response of etiolated hypocotyls occur because of a partial activation of a second ARF (Stowe-Evans et al., 2001). Two obvious models can be developed. Both models assume that when multiple ARFs are expressed in the same cell any one ARF can specifically regulate the expression of auxin-responsive genes involved in a distinct biological phenomenon because of differences in the auxin sensitivities of the different ARFs (Liscum and Reed, 2001). First (A) phyA activation could lead to changes in auxin transport and/or metabolism leading to increases in auxin concentration on the side away from light (red block), above that induced by phot1 activation alone (blue block). Whereas the auxin concentration induced by phot1 action alone would result only in the activation of NPH4/ARF7, the auxin concentration established under both phot1 and phyA activating conditions would lead to the activation of both NPH4/ARF7 and ARFy. Alternatively (B) phyA action could lead to changes in the auxin sensitivity of ARFy. Note shift of ARFy response curve (red line) to lower auxin concentration range as compared to panel A. These models are not mutually exclusive, but each can account for the increase in phototropic response of wild-type seedlings, as well as the partial recovery of response in the nph4/arf7 null mutants.