BIG: a calossin-like protein required for polar auxin transport in Arabidopsis

Abstract

Polar auxin transport is crucial for the regulation of auxin action and required for some light-regulated responses during plant development. 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. BIG is very similar to the Drosophila gene Calossin/Pushover, a member of a gene family also present in Caenorhabditis elegans and human genomes. The protein encoded by BIG is extraordinary in size, 560 kD, and contains several putative Zn-finger domains. 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. Double mutants of tir3 with the auxin mutants pin1, pid, and axr1 display severe defects in auxin-dependent growth of the inflorescence. Chemical inhibitors of auxin transport change the intracellular localization of the auxin efflux carrier PIN1 in doc1/tir3 mutants, supporting the idea that BIG is required for normal auxin efflux.

Master and servant: Regulation of auxin transporters by FKBPs and cyclophilins

“…Higher NPA concentrations are thought to block protein trafficking [105,118,119] and could affect auxin transports by interfering with their cycling at the plasma membrane. NPA indeed interferes with PIN1 trafficking after disruption by the lactone antibiotic, brefeldin A [105], as well as in the tir3 mutant lacking the scaffolding protein, BIG [119].…”

“…Higher NPA concentrations are thought to block protein trafficking [105,118,119] and could affect auxin transports by interfering with their cycling at the plasma membrane. NPA indeed interferes with PIN1 trafficking after disruption by the lactone antibiotic, brefeldin A [105], as well as in the tir3 mutant lacking the scaffolding protein, BIG [119]. It was also shown in an earlier study that the number of NPA-binding sites and polar auxin transport are reduced in the tir3/big mutant [109], collectively supporting a connection between NPA binding to the cytoskeleton, PIN trafficking, and auxin transport.…”

Strigolactone Acts Downstream of Auxin to Regulate Bud Outgrowth in Pea and Arabidopsis

“…In particular, the exact role of auxin content and transport in the regulation of bud outgrowth has been questioned Dun et al, 2006;Ferguson and Beveridge, 2009). Indeed, big and bud1 mutants in Arabidopsis have reduced auxin transport and enhanced branching (Gil et al, 2001;Dai et al, 2006), in contrast to Arabidopsis SMS mutants, which have increased auxin transport and enhanced branching (Bennett et al, 2006). Additionally, depletion of auxin content is not always sufficient to induce bud outgrowth Ferguson and Beveridge, 2009).…”

The BUD2 mutation affects plant architecture through altering cytokinin and auxin responses in Arabidopsis

“…In many plant species, axillary buds become dormant due to the inhibiting effects of the primary shoot apex on the outgrowth of AMs, a phenomenon known as 'apical dominance'. Auxin was first regarded as a direct regulator in this process [14], a notion strengthened thereafter by physiological studies on decapitated shoot apices [15][16][17], and by analyzing auxin biosynthesis, transport and signaling [18][19][20][21][22][23][24][25][26][27][28][29] in plants. However, when radiolabelled auxin was applied to a decapitated stump, the outgrowth of axillary buds was inhibited even though radiolabelled auxin was not found to accumulate in axillary buds, suggesting an indirect suppression effect of auxin on the AM outgrowth [28,30] and the presence of second messengers.…”