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Shoot phototropism enables plants to position their photosynthetic organs in favorable light conditions and thus benefits growth and metabolism in land plants. To understand the evolution of this response, we established an experimental system to study phototropism in gametophores of the moss Physcomitrella patens. The phototropic response of gametophores occurs slowly; a clear response takes place more than 24 hours after the onset of unilateral light irradiation, likely due to the slow growth rate of gametophores. We also found that red and far-red light can induce phototropism, with blue light being less effective. These results suggest that plants used a broad range of light wavelengths as phototropic signals during the early evolution of land plants.

Inflorescences of a dominant mutant of Arabidopsis Aux/IAA7, axr2, showed negative phototropism with a similar fluence response curve to the positive phototropism of wild-type stems. Application of a synthetic auxin, NAA, and an inhibitor of polar auxin transport, NPA, increased and decreased respectively the magnitude of the phototropic response in the wild type, while in axr2 application of NAA reduced the negative phototropic response and NPA had no effect. Decapitation of the apex induced a small negative phototropism in wild-type stems, and had no effect in axr2 plants. Inflorescences of the double mutants of auxin transporters, pgp1 pgp19, showed no phototropic response, while decapitation resulted in a negative phototropic response. These results suggest that negative phototropism can occur when the level of auxin or of auxin signaling is reduced to a minimal level, and that in plant axial organs the default phototropic response to unilateral blue light may be negative. Expression of axr2 protein by an endodermis-specific promoter resulted in agravitropism of inflorescences in a similar way to that of axr2, but phototropism was normal, confirming that the endodermis does not play a critical role in phototropism.

We isolated a new recessive allele at the AUXIN RESISTANT6/CULLIN1 (AXR6/CUL1) locus, axr6-101, from an EMS-mutagenized population of Arabidopsis thaliana, the Landsberg erecta ecotype. axr6-101 is auxin resistant and semi-dwarf similar to the other recessive axr6 mutants. The axr6-101 phenotype is caused by the E716K substitution of the CUL1 protein, which is likely to affect its ability to bind to the C-terminal RING domain of RING-box 1 (RBX1). The previously reported allele of AXR6, cul1-7, is caused by a substitution at T510 that binds to the N-terminal β-strand of RBX1. Although cul1-7 shows temperature-sensitive phenotype, the axr6-101 phenotype is largely unaffected by temperature. axr6-101 may provide an important genetic resource for study of the structure-function relationship of the CUL1 protein.

Arabidopsis has Aux/IAA proteins that lack domain II which is a binding site for the TIR1 auxin receptor. These proteins have been shown to be more stable than the canonical Aux/IAA proteins. We investigated the phenotypes of overexpression lines of domain II-less Aux/IAA proteins, IAA20 and IAA30, by the use of 35S promoter. The transgenic lines showed many aberrant phenotypes in auxin physiology. The most conspicuous phenotype was collapse of the root apical meristem as occurred in plt1 plt2 double mutants. Because IAA20 and IAA30 were early auxin-inducible and were expressed in the root apical meristem, they may have a physiological role in maintaining the stem cell niche of root, by keeping the activity of MP/ARF5 and NPH4/ARF7 at an acceptable level. On the other hand, domain-II less Aux/IAA proteins are not present in balck cottonwood tree or grapevine, suggesting wide diversification of Aux/IAA proteins in higher plants.

In the auxin signal transduction, two protein families, Aux/IAAs and auxin response factors, play a crucial role just downstream of auxin F-box receptors. Distinct and overlapping phenotypes of the dominant Aux/IAA mutants suggest some functional differentiation of the Aux/IAA genes in auxin signaling. Taking advantage of unique phenotypes of the msg2/iaa19 mutants, we carried out promoter-exchange experiments, where cDNA of the msg2, axr2/iaa7 or slr/iaa14 gene was driven by the MSG2 or AXR2 promoter. The cDNAs were translationally fused to the green fluorescent protein gene to measure levels of expressed protein. Results showed that many abnormal phenotypes of the dominant Aux/IAA mutants were governed by their promoter activity, but some were dependent on their gene products. The latter result highlights the possible importance of Aux/IAA protein level controled by auxin F-box receptors.