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First published online August 2, 2005
doi: 10.1242/10.1242/dev.01952


Development 132, 3577-3585 (2005)
Published by The Company of Biologists 2005


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Surge and destroy: the role of auxin in plant embryogenesis

Pablo D. Jenik and M. Kathryn Barton*

Department of Plant Biology, Carnegie Institution, 260 Panama Street, Stanford, CA 94305, USA



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Fig. 1. Model for auxin transport and action in the plant cell. Auxin is moved into cells through influx carriers encoded by the AUX1 gene. It is expelled from the cell by localized auxin-efflux carriers associated with PIN auxin facilitators. Auxin efflux carriers are asymmetrically targeted through a mechanism that involves the presence/absence of the PINOID kinase. Auxin-efflux carriers cycle to and from the membrane through the endosomal compartment. At some threshold concentration, auxin triggers the activity of the SCFTIR ubiquitin E3 ligase which marks the AUX/IAA transcriptional represssor (IAA) for destruction via the proteosome. The auxin-response factor is then free to act as a transcriptional activator.

 


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Fig. 2. Auxin transport relative to early events in Arabidopsis embryo patterning. (A) An early Arabidopsis embryo, consisting of an apical cell (ac) and a basal cell (bc). Green arrows indicate the direction of auxin transport; stippling indicates regions with high auxin levels. (B) Eight-cell/octant-stage embryo. (Cell numbers used to stage embryos reflect the number of cells in the apical cell lineage.) The apical domain (pink) and central domain (blue) both derive from the apical cell and each consists of four cells. The basal domain (yellow) derives from the basal cell. (C) A 16-cell stage, early globular embryo. (D) In a 32-cell stage globular embryo, auxin transport has shifted direction (green arrows), and auxin now accumulates in the hypophyseal lineage. The hypophyseal lineage is derived from the hypophysis (h) – the suspensor cell closest to the embryo proper. This lineage gives rise to a portion of the root meristem, specifically the quiescent center and the central columella with associated stem cells. (E) A transition stage (transitioning between globular and heart stage) embryo. Auxin transport in the apical domain is directed toward the center of the cotyledon primordia (cot). (F) An early heart-stage embryo, showing the emergence of cotyledons and a cleft where the shoot apical meristem (SAM) will form. Gray indicates regions of vascular development.

 


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Fig. 3. Partitioning of the apical domain into shoot apical meristem and cotyledons. (A) Transition-stage and early heart-stage Arabidopsis embryos showing the direction of auxin transport (arrows) and the partitioning of the embryo into cotyledonary (green) and meristem (orange) domains. (B) Cross section (as shown in A) through the apical domain of a wild-type embryo, showing the region that will develop into the shoot apical meristem (dark orange), the intercotyledonary zones (light orange), the adaxial domain (top) of the cotyledon (dark green) and the abaxial domain (bottom) of the cotyledon (light green). The meristem and intercotyledonary zones have low auxin levels and high CUC levels, whereas the opposite holds for the cotyledon primordia. (C) Cross section of the apical domain from a cup-shaped cuc1 cuc2 cotyledon mutant. No separation is made between the cotyledons and no shoot apical meristem is made in the central region of the embryo. (D) Cross section of the apical domain from a pin pid embryo. These embryos lack the PIN1 auxin transporter. They also lack the PID kinase that appears to be responsible for positioning PIN1 on the apical side of the cell. Lack of high auxin levels in the cotyledon primordia in these embryos would allow CUC accumulation throughout the apical domain, thus preventing cotyledon outgrowth.

 

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© The Company of Biologists Ltd 2005