High impact information on BIG

• Double mutants of tir3 with the auxin mutants pin1, pid, and axr1 display severe defects in auxin-dependent growth of the inflorescence [1].
• We have found that two mutants of Arabidopsis-doc1, which displays altered expression of light-regulated genes, and tir3, known for its reduced auxin transport-have similar defects and define mutations in a single gene that we have renamed BIG [1].
• Because the tir3 mutants have a substantial defect in NPA binding, their phenotype provides genetic evidence for a role for the NBP in plant growth and development [2].
• Reduced naphthylphthalamic acid binding in the tir3 mutant of Arabidopsis is associated with a reduction in polar auxin transport and diverse morphological defects [2].
• Biochemical studies indicate that tir3 plants have a reduced number of N-1-naphthylphthalamic (NPA) binding sites, suggesting that the TIR3 gene is required for expression, localization, or stabilization of the NPA binding protein (NBP) [2].

Biological context of BIG

• One of these QTL, LPR1, located in a 2.8 Mb region at the top of chromosome 1, explains 52% of the variance of the PRL [3].

Associations of BIG with chemical compounds

• Expression-profiling experiments indicate that altered expression of multiple light-regulated genes in doc1 mutants can be suppressed by elevated levels of auxin caused by overexpression of an auxin biosynthetic gene, suggesting that normal auxin distribution is required to maintain low-level expression of these genes in the dark [1].
• Treatment of wild-type Arabidopsis seedlings with brefeldin A, a fungal metabolite that blocks auxin transport, phenocopies the root developmental alterations observed in lpr1 mutants in both high and low P conditions, suggesting that BIG participates in vesicular targeting of auxin transporters [4].
• Three independent trp5 mutants defective in the Arabidopsis thaliana AS alpha subunit structural gene ASA1 were identified by selection for resistance to the herbicidal compound 6-methylanthranilate [5].
• In independent genetic screens, for shade-avoidance response and cytokinin sensitivity, we identified two Arabidopsis mutants, attenuated shade avoidance 1 (asa1) and umbrella1 (umb1), which have very similar pleiotropic phenotypes. asa1 and umb1 are allelic to tir3-1, and are caused by mutations in BIG, which is required for normal auxin efflux [6].

References