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Summary Indole acetic acid (IAA/auxin) profoundly affects wood formation but the molecular mechanism of auxin action in this process remains poorly understood. We have cloned cDNAs for eight members of the Aux/IAA gene family from hybrid aspen (Populus tremula L. × Populus tremuloides Michx.) that encode potential mediators of the auxin signal transduction pathway. These genes designated as PttIAA1-PttIAA8 are auxin inducible but differ in their requirement of de novo protein synthesis for auxin induction. The auxin induction of the PttIAA genes is also developmentally controlled as evidenced by the loss of their auxin inducibility during leaf maturation. The PttIAA genes are differentially expressed in the cell types of a developmental gradient comprising the wood-forming tissues. Interestingly, the expression of the PttIAA genes is downregulated during transition of the active cambium into dormancy, a process in which meristematic cells of the cambium lose their sensitivity to auxin. Auxin-regulated developmental reprogramming of wood formation during the induction of tension wood is accompanied by changes in the expression of PttIAA genes. The distinct tissue-specific expression patterns of the auxin inducible PttIAA genes in the cambial region together with the change in expression during dormancy transition and tension wood formation suggest a role for these genes in mediating cambial responses to auxin and xylem development. [ABSTRACT FROM AUTHOR]

SummaryLateral root development is a post-embryonic organogenesis event that gives rise to most of the underground parts of higher plants. Auxin promotes lateral root formation, but the molecular mechanisms involved are still unknown. We have isolated a novel Arabidopsis mutant, solitary-root (slr ), which has reduced sensitivity to auxin. This dominant slr-1 mutant completely lacks lateral roots, and this phenotype cannot be rescued by the application of exogenous auxin. Analysis with cell-cycle and cell-differentiation markers revealed that the slr-1 mutation blocks cell divisions of pericycle cells in lateral root initiation. The slr-1 mutant is also defective in root hair formation and in the gravitropic responses of its roots and hypocotyls. Map-based positional cloning and isolation of an intragenic suppressor mutant revealed that SLR encodes IAA14, a member of the Aux/IAA protein family. Green fluorescent protein-tagged mutant IAA14 protein was localized in the nucleus, and the gain-of-function slr-1/iaa14 mutation decreased auxin-inducible BA -GUS gene expression in the root, suggesting that SLR/IAA14 acts as a transcriptional repressor. These observations indicate that SLR/IAA14 is a key regulator in auxin-regulated growth and development, particularly in lateral root formation. [ABSTRACT FROM AUTHOR]

Summary Aux/IAA proteins are short-lived transcriptional regulators involved in auxin signaling. Using Aux/IAA luciferase (LUC) fusion proteins expressed in Arabidopsis thaliana , we previously showed that rapid degradation of these proteins requires conserved Aux/IAA domain II and that exogenous auxin accelerates their degradation. To further examine auxin-mediated increases in proteolysis, the degradation of two other LUC fusion proteins, a non-cleavable ubiquitin LUC fusion (UB1–72::LUC) and SAUR15::LUC was determined in vivo in seedlings. Their half-lives were 20 ± 4 and 104 ± 10 min, respectively. SAUR15::LUC half-life was not affected by pre-incubation with 2,4-D. Auxin did not have an equivalent effect on UB(1–72)::LUC steady-state levels as compared to PsIAA6:LUC. LUC fused to an Aux/IAA domain II degraded more rapidly following auxin application, demonstrating that this region is sufficient for auxin-mediated acceleration of proteolysis. Hormonal cross-talk at the level of Aux/IAA proteolysis was examined. 1-aminocyclopropane-1-carboxylic acid (ACC), benzyladenine (BA), abscisic acid (ABA), and brassinolide (BL) did not affect the degradation rate of IAA1::LUC, and gibberellic acid (GA3 ) and salicylic acid (SA) did not specifically affect the steady-state levels of Aux/IAA::LUC proteins. An Aux/IAA::LUC transgene was crossed into the auxin resistant-1 (axr1–12 ) background. In axr1–12 , the half-life of PsIAA6(1–73)::LUC increased 4.5-fold, but proteolysis still accelerated in response to exogenous auxin. These data suggest that auxin is the only phytohormone that accelerates Aux/IAA proteolysis, and that this acceleration is specific for Aux/IAA proteins. In addition, AXR1 plays an important role in rapid basal proteolysis of Aux/IAA proteins, but is not required for auxin-mediated acceleration of their degradation. [ABSTRACT FROM AUTHOR]