| pubmed-article:11573012 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11573012 | lifeskim:mentions | umls-concept:C0033684 | lld:lifeskim |
| pubmed-article:11573012 | lifeskim:mentions | umls-concept:C0699900 | lld:lifeskim |
| pubmed-article:11573012 | lifeskim:mentions | umls-concept:C0243125 | lld:lifeskim |
| pubmed-article:11573012 | lifeskim:mentions | umls-concept:C1521828 | lld:lifeskim |
| pubmed-article:11573012 | lifeskim:mentions | umls-concept:C0004409 | lld:lifeskim |
| pubmed-article:11573012 | pubmed:issue | 20 | lld:pubmed |
| pubmed-article:11573012 | pubmed:dateCreated | 2001-9-26 | lld:pubmed |
| pubmed-article:11573012 | pubmed:abstractText | Aux/IAA gene family members were first identified by their rapid transcriptional increase in response to auxin. Auxin/indole-3-acetic acid protein (Aux/IAA) luciferase (LUC) fusions expressed in Arabidopsis under control of a non-auxin-responsive promoter were used to monitor the effect of auxin on protein abundance independent of transcriptional regulation by auxin. After 2 hr in the presence of 1 microM exogenous dichlorophenoxyacetic acid (2,4D), a synthetic auxin, the levels of pea IAA6 (PSIAA6) and Arabidopsis IAA1 LUC activity were 35% and 67%, respectively, of mock-treated genetically identical seedlings, whereas the activity of LUC alone from equivalently treated seedlings remained unaltered. The steady-state level of an Aux/IAA fusion protein lacking domain II, one of the conserved domains found in all Aux/IAA proteins, was not reduced in the presence of auxin. Higher levels of exogenous auxin were required to affect the steady-state level of the PSIAA6LUC fusion with a point mutation in domain II. A 13-aa consensus sequence from domain II fused to LUC created an auxin-responsive fusion protein. The change in steady-state levels in response to auxin is extremely rapid, with a decrease in LUC activity detectable by 2 min after auxin application. Direct half-life measurements show that the decrease caused by exogenous auxin is due to the decrease in fusion protein half-life. These results suggest that auxin rapidly modulates the degradation rate of Aux/IAA proteins, with higher levels of auxin increasing the proteolytic rate of Aux/IAA family members. | lld:pubmed |
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| pubmed-article:11573012 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:11573012 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:11573012 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11573012 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:11573012 | pubmed:issn | 0027-8424 | lld:pubmed |
| pubmed-article:11573012 | pubmed:author | pubmed-author:CallisJJ | lld:pubmed |
| pubmed-article:11573012 | pubmed:author | pubmed-author:ZenserNN | lld:pubmed |
| pubmed-article:11573012 | pubmed:author | pubmed-author:EllsmoreAA | lld:pubmed |
| pubmed-article:11573012 | pubmed:author | pubmed-author:LeasureCC | lld:pubmed |
| pubmed-article:11573012 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11573012 | pubmed:day | 25 | lld:pubmed |
| pubmed-article:11573012 | pubmed:volume | 98 | lld:pubmed |
| pubmed-article:11573012 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11573012 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11573012 | pubmed:pagination | 11795-800 | lld:pubmed |
| pubmed-article:11573012 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:11573012 | pubmed:year | 2001 | lld:pubmed |
| pubmed-article:11573012 | pubmed:articleTitle | Auxin modulates the degradation rate of Aux/IAA proteins. | lld:pubmed |
| pubmed-article:11573012 | pubmed:affiliation | Section of Molecular and Cellular Biology, Graduate Group in Plant Biology, University of California, 1 Shields Avenue, Davis, CA 95616, USA. | lld:pubmed |
| pubmed-article:11573012 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11573012 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:11573012 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
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