Disease relevance of Alanap Plus

• Transcripts up-regulated in the AZ following deblading/decapitation or treatment with naphthylphthalamic acid were isolated from plants pretreated with 1-methylcyclopropene before deblading to help select against ethylene-induced genes [1].
• Changes in GH3:gusA expression were monitored after the inoculation of Rhizobium leguminosarum biovar trifolii, non-host rhizobia, lipo-chitin oligosaccharides (LCOs), chitin oligosaccharides, a synthetic auxin transport inhibitor (naphthylphthalamic acid; NPA), auxin, the ENOD40-1 peptide or different flavonoids [2].
• The toxicity of Dyanap, a mixture of DNBP and alanap, was lower than that of DNBP; there was no apparent synergism between DNBP and alanap in the mixture [3].

High impact information on Alanap Plus

• The results indicate that these two MDR-like genes of Arabidopsis encode 1-naphthylphthalamic acid binding proteins that are required for normal auxin distribution and auxin-mediated development [4].
• Reduced naphthylphthalamic acid binding in the tir3 mutant of Arabidopsis is associated with a reduction in polar auxin transport and diverse morphological defects [5].
• Together, these experiments indicate that NPA binding activity is peripherally associated with the plasma membrane and interacts with the cytoskeleton in vitro [6].
• NPA binding activity partitioned into the detergent-insoluble cytoskeletal pellet obtained from both zucchini and maize membranes and was released from these pellets by KI treatment [6].
• Treatment of this pellet with KI released NPA binding activity, actin, and alpha-tubulin [6].

Chemical compound and disease context of Alanap Plus

• Transcript expression was then examined in leaf and stem AZs over the period they became ethylene competent following indole-3-acetic acid (IAA) depletion either by leaf deblading, treatment with the IAA transport inhibitor naphthylphthalamic acid, or cutting the stem above a node (decapitation) [1].

Biological context of Alanap Plus

• This study uses a novel technique of transiently applying a polar auxin transport inhibitor, N-1-naphthylphthalamic acid (NPA), to developing Arabidopsis flowers to further characterize the role of auxin in organogenesis [7].
• Using low concentrations of 1-N-naphthylphthalamic acid that leave cell division and axiality of division unaltered, we observe that the frequencies of files with even and uneven cell numbers are equalized [8].
• Additionally, a protein that binds auxin transport inhibitors, the naphthylphthalamic acid binding protein, which has been previously suggested to associate with the actin cytoskeleton, was eluted in a single peak from the F-actin column [9].
• Non-transformed control seedlings could be induced to display this phenotype after treatment with inhibitors of auxin translocation such as 2,3,5-triiodobenzoic acid or N-1-naphthylphthalamic acid [10].
• In Arabidopsis, colocalization of NPA amidase and aminopeptidase (AP) activities, inhibition of auxin transport by artificial beta-naphthylamide substrates, and saturable displacement of NPA by the AP inhibitor bestatin suggest that PM APs may be involved in both low-affinity NPA binding and hydrolysis [11].

Anatomical context of Alanap Plus

• N-1-Naphthylphthalamic acid (NPA) binding activity is released into the supernatant when plasma membranes are subjected to high-salt treatment, indicating that this activity is peripherally associated with the membrane [6].

Associations of Alanap Plus with other chemical compounds

• Extraction of plasma membrane vesicles with Triton X-100 resulted in retention of NPA binding activity in the detergent-insoluble cytoskeletal pellet [6].
• In contrast, specific binding sites for [3H]-NPA were found on dopamine cell bodies and the terminals of strio-nigral fibres [12].

Gene context of Alanap Plus

• PM proteins were purified by gel permeation, anion exchange, and NPA affinity chromatography monitored for tyrosine-AP activity [11].
• Also, petiole treatment of Arabidopsis with 1-N-naphthylphthalamic acid similarly inhibited leaf growth of both wild-type plants and ethylene-insensitive ein4 mutants [13].
• The auxin-inducible homeobox gene Oshox1 of rice (Oryza sativa) is a positive regulator of procambial cell fate commitment, and its overexpression reduces the sensitivity of polar auxin transport (PAT) to the PAT inhibitor 1-N-naphthylphthalamic acid (NPA) [14].
• Local application of the auxin-transport inhibitor naphthylphthalamic acid (NPA) at the root-shoot junction decreased the number and density of lateral roots and reduced the free indoleacetic acid (IAA) levels in the root and [3H]IAA transport into the root [15].

Analytical, diagnostic and therapeutic context of Alanap Plus

• We therefore tested the patterns obtained after treatment with 1-N-naphthylphthalamic acid, an inhibitor of auxin efflux carriers [8].
• We report the purification and molecular cloning of NPA-binding PM APs and associated proteins from Arabidopsis [11].

References