Increased auxin efflux in the IAA-overproducing sur1 mutant of Arabidopsis thaliana: A mechanism for reducing auxin levels?
1999 (English)In: Physiologia Plantarum: An International Journal for Plant Biology, ISSN 0031-9317, E-ISSN 1399-3054, Vol. 107, no 1, 120-127 p.Article in journal (Refereed) PublishedText
With the aim of investigating the mechanisms that maintain auxin homeostasis in plants, we have monitored the net uptake and metabolism of exogenously supplied indole-3-acetic acid (IAA) and naphthalene-1-acetic acid (NAA) in seedlings of wild type and the IAA-overproducing mutant sur1 of Arabidopsis thaliana. Tritiated IAA and NAA entered the seedling tissues within minutes and were mostly accumulated as metabolites, probably amino acid and sugar conjugates, The mutant seedlings were marked by a strong increase of [H-3]IAA metabolism and a reduction of the accumulation levels of both free [H-3]IAA and [H-3]NAA. The same characteristics were observed in wild-type seedlings grown on 5 mu M picloram. We measured [H-3]NAA uptake in the presence of high concentrations of unlabeled NAA or the auxin efflux carrier inhibitor naphthylphthalamic acid (NPA). This abolished the difference in free [H-3]NAA accumulation between the mutant or picloram-treated seedlings and wild-type seedlings. These data indicated that active auxin efflux carriers were present in Arabidopsis seedling tissues. Picloram-treated seedlings and seedlings of the IAA-overproducing mutant sur1 displayed increased auxin efflux carrier activity as well as elevated conjugation of IAA. There is previous evidence to suggest that conjugation is a means to remove excess IAA in plant cells. Here, we discuss the possibility of efflux constituting an additional mechanism for regulating free IAA levels in the face of an excess auxin supply.
Place, publisher, year, edition, pages
1999. Vol. 107, no 1, 120-127 p.
IdentifiersURN: urn:nbn:se:umu:diva-114195DOI: 10.1034/j.1399-3054.1999.100116.xOAI: oai:DiVA.org:umu-114195DiVA: diva2:914099
Times Cited: 10 102016-03-232016-01-152016-03-23