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Abstract Detail

Mechanisms of Gene Regulation

Tiwari, Shiv [1], Hagen, Gretchen [1], Guilfoyle, Tom [1].

Nonredundant functions of Aux/IAA proteins.

Aux/IAA proteins are a large family of repressors that regulate auxin response genes in an auxin concentration-dependent manner. Elevated auxin levels in cells trigger the destruction of Aux/IAA repressors, resulting in the derepression/activation of auxin response genes. Most Aux/IAA proteins contain four conserved domains. Domain I functions as an active repression domain with a conserved LxLxL motif. Domain II confers instability to Aux/IAA repressors by functioning as a degron in the ubiquitin proteasome pathway. Domains III and IV facilitate interactions among both Aux/IAA repressors and Auxin Response Factor (ARF) activators. Mutations in Domain I compromise repression, while mutations in Domain II compromise auxin-dependent degradation of the Aux/IAA repressors. Single and even multiple Aux/IAA gene knockouts are phenotypically normal, suggesting a substantial amount of redundancy in the function of Aux/IAA proteins. On the other hand, mutations in Domain II generally result in strong auxin-related phenotypes that vary in character among the different Aux/IAA members. To further assess redundant functions of Aux/IAA proteins, we expressed four different Aux/IAA proteins containing mutations in Domains I and II under control of either their natural promoters or the strong constitutive 35S promoter. We also used the same promoters to express Aux/IAA proteins that had been converted from repressors to activators. Our results indicate that expression of stabilized Aux/IAA proteins causes distinct phenotypes among the four Aux/IAA proteins tested even when their expression is regulated by the same promoter. Why distinct phenotypes result from expression of different stabilized Aux/IAA proteins expressed under identical conditions will be discussed.

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1 - University of Missouri, Biochemistry, 117 Schweitzer Hall, Columbia, MO, 65211, USA

none specified

Presentation Type: ASPB Minisymposium
Session: M17
Location: Waldorf Room/Hilton
Date: Monday, July 9th, 2007
Time: 10:40 AM
Number: M17001
Abstract ID:677

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