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First published online 17 August 2005
doi: 10.1242/dev.01969
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1 Lehrstuhl für Genetik, Technische Universität München,
Wissenschaftszentrum Weihenstephan, Am Hochanger 8, 85350 Freising,
Germany
2 Bayerische Landesanstalt für Landwirtschaft, Institut für
Pflanzenbau und -züchtung, IPZ 1b, Am Gereuth 2, 85354 Freising,
Germany
3 Institut für Pathologie, GSF-Forschungszentrum für Umwelt und
Gesundheit GmbH, 85764 Neuherberg, Germany
Author for correspondence (e-mail:
ramon.torres{at}wzw.tum.de)
Accepted 5 July 2005
During Arabidopsis embryo development, cotyledon primordia are generated at transition stage from precursor cells that are not derived from the embryonic shoot apical meristem (SAM). To date, it is not known which genes specifically instruct these precursor cells to elaborate cotyledons, nor is the role of auxin in cotyledon development clear. In laterne mutants, the cotyledons are precisely deleted, yet the hypocotyl and root are unaffected. The laterne phenotype is caused by a combination of two mutations: one in the PINOID (PID) gene and another mutation in a novel locus designated ENHANCER OF PINOID (ENP). The expression domains of shoot apex organising genes such as SHOOT MERISTEMLESS (STM) extend along the entire apical region of laterne embryos. However, analysis of pid enp stm triple mutants shows that ectopic activity of STM does not appear to cause cotyledon obliteration. This is exclusively caused by enp in concert with pid. In pinoid embryos, reversal of polarity of the PIN1 auxin transport facilitator in the apex is only occasional, explaining irregular auxin maxima in the cotyledon tips. By contrast, polarity of PIN1:GFP is completely reversed to basal position in the epidermal layer of the laterne embryo. Consequently auxin, which is believed to be essential for organ formation, fails to accumulate in the apex. This strongly suggests that ENP specifically regulates cotyledon development through control of PIN1 polarity in concert with PID.
Key words: laterne, PINOID, ENHANCER OF PINOID, Embryo, Arabidopsis, Pattern formation, Auxin, PIN1, Organogenesis, Cotyledons
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