Disease relevance of SHY2

• We concluded that the short-hypocotyl phenotype of transgenic tobacco plants was due to hypersensitivity to blue, UV-A, and green light, resulting from over-expression of the photoreceptor [1].

High impact information on SHY2

• When expressed from the SHY2 promoter, both shy2-2 and bdl inhibited cell elongation and auxin-induced gene expression in the seedling hypocotyl [2].
• We identified a short hypocotyl mutant under red and blue light, hypersensitive to red and blue 1 (hrb1) [3].
• The short hypocotyl phenotypes were completely reversed by the provision of an exogenous supply of sucrose [4].
• Like certain other auxin-response mutants, ibr5 has a long root and a short hypocotyl when grown in the light [5].
• Arabidopsis SHY2/IAA3 inhibits auxin-regulated gene expression [6].

Biological context of SHY2

• The phenotypes suggest that SHY2/IAA3 may activate some auxin responses and repress others [7].
• Metabolic labeling and immunoprecipitation studies with affinity-purified antibodies to IAA3 demonstrate increased in vivo steady-state levels of mutant IAA3 in shy2-2 plants and phosphorylation of the SHY2-2 protein in vivo [8].
• Gain-of-function and loss-of-function shy2 mutations affect auxin-dependent root growth, lateral root formation, and timing of gravitropism, indicating that SHY2/IAA3 regulates multiple auxin responses in roots [7].
• The short hypocotyl of seedlings underexpressing CDC2b was a result of inhibition of cell elongation rather than a reduction in cell number, whereas in cotyledons, inhibition of CDC2b expression resulted in large, open cotyledons with amyloplasts rather than etioplasts [9].

Associations of SHY2 with chemical compounds

• The chemical juglone (5-hydroxy-1,4-naphthoquinone) inhibited the interaction, suggesting that peptidyl-prolyl isomerization may mediate auxin-induced SHY2/IAA3 protein turnover [10].
• Turanose-treated seedlings are characterized by a very short primary root and a short hypocotyl showing the production of adventitious roots [11].

Regulatory relationships of SHY2

• We used the exaggerated short hypocotyl phenotype induced by oat phytochrome A overexpression in transgenic Arabidopsis to monitor the biological activity of mutant phytochrome A derivatives [12].

Other interactions of SHY2

• AXR3 and SHY2 interact to regulate root hair development [13].
• Gain-of-function mutations in SHY2/IAA3 cause enlarged cotyledons, short hypocotyls, and altered auxin-regulated root development [6].
• The data obtained suggest that SHY1 and SHY2 represent a novel class of components involved in the photomorphogenic pathways of Arabidopsis [14].
• A new GH3-related gene, designated DFL2, causes a short hypocotyl phenotype when overexpressed under red and blue light and a long hypocotyl when antisensed under red light conditions [15].
• Transgenic Arabidopsis plants that overexpress COP1b show a de-etiolated phenotype in the dark, with a short hypocotyl, open and developed cotyledons [16].

Analytical, diagnostic and therapeutic context of SHY2

• Recent molecular cloning revealed that the SHY2 gene is identical to the IAA3 gene, a member of the primary auxin-response genes designated the Aux/IAA gene family [17].

References