During plant growth, dividing cells in meristems must coordinate transitions from division to expansion and differentiation, thus generating three distinct developmental zones: the meristem, elongation zone and differentiation zone 1 . Simultaneously, plants display tropisms, rapid adjustments of their direction of growth to adapt to environmental conditions. It is unclear how stable zonation is maintained during transient adjustments in growth direction. In Arabidopsis roots, many aspects of zonation are controlled by the phytohormone auxin and auxin-induced PLETHORA (PLT) transcription factors, both of which display a graded distribution with a maximum near the root tip 2-12 . In addition, auxin is also pivotal for tropic responses 13,14 . Here, using an iterative experimental and computational approach, we show how an interplay between auxin and PLTs controls zonation and gravitropism. We find that the PLT gradient is not a direct, proportionate readout of the auxin gradient. Rather, prolonged high auxin levels generate a narrow PLT transcription domain from which a gradient of PLT protein is subsequently generated through slow growth dilution and cell-to-cell movement. The resulting PLT levels define the location of developmental zones. In addition to slowly promoting PLT transcription, auxin also rapidly influences division, expansion and differentiation rates. We demonstrate how this specific regulatory design in which auxin cooperates with PLTs through different mechanisms and on Reprints and permissions information is available at www.nature.com/reprints.

SummaryBackground-Regeneration, a remarkable example of developmental plasticity displayed by both plants and animals, involves successive developmental events driven in response to environmental cues. Despite decades of study on the ability of the plant tissues to regenerate complete fertile shoot system after inductive cues, the mechanisms by which cells acquire pluripotency and subsequently regenerate complete organs remain unknown.

Dynamically polarized membrane proteins define different cell boundaries and have an important role in intercellular communication-a vital feature of multicellular development. Efflux carriers for the signalling molecule auxin from the PIN family 1 are landmarks of cell polarity in plants and have a crucial involvement in auxin distribution-dependent development including embryo patterning, organogenesis and tropisms 2-7 . Polar PIN localization determines the direction of intercellular auxin flow 8 , yet the mechanisms generating PIN polarity remain unclear. Here we identify an endocytosisdependent mechanism of PIN polarity generation and analyse its developmental implications. Realtime PIN tracking showed that after synthesis, PINs are initially delivered to the plasma membrane in a non-polar manner and their polarity is established by subsequent endocytic recycling. Interference with PIN endocytosis either by auxin or by manipulation of the Arabidopsis Rab5 GTPase pathway prevents PIN polarization. Failure of PIN polarization transiently alters asymmetric auxin distribution during embryogenesis and increases the local auxin response in apical embryo regions. This results in ectopic expression of auxin pathway-associated root-forming master regulators in embryonic leaves and promotes homeotic transformation of leaves to roots. Our results indicate a two-step mechanism for the generation of PIN polar localization and the essential role of endocytosis in this process. It also highlights the link between endocytosis-dependent polarity of individual cells and auxin distribution-dependent cell fate establishment for multicellular patterning.The plant signalling molecule auxin acts as a versatile trigger in many aspects of plant development and mediates different cellular responses on the basis of its graded distribution between cells. Establishment and maintenance of these auxin gradients requires local auxin biosynthesis 9,10 and directional cell-to-cell transport that depends on PIN auxin transporters 11 . PINs have a polar plasma membrane localization that determines the direction of intercellular auxin flow 8 . Thus, the mechanisms underlying PIN polarity belong to centralCorrespondence and requests for materials should be addressed to P.D. (E-mail: P.B.Dhonukshe@uu.nl) or J.F. (E-mail: jiri.friml@psb.ugent.be). * These authors contributed equally to this work.Supplementary Information is linked to the online version of the paper at www.nature.com/nature.Reprints and permissions information is available at www.nature.com/reprints. are important components of polar PIN localization. However, it remains unresolved how PIN polarity is initially generated. In mammalian epithelia, segregation of membrane proteins into apical and basolateral plasma membrane domains is mainly achieved by polar exocytosis of newly synthesized proteins, or by non-polar exocytosis followed by endocytosis and polarized recycling 19 . Here we demonstrate an endocytosis-dependent mechanism for PIN polarity generation, and its import...

Author for correspondence (r.offringa@biology.leidenuniv.nl)The authors informed us of problems related to Fig. 3C and Fig. 7D in Development 137, 3245-3255. Both issues were noted by an investigation by the Technical Committee of Utrecht University (UTC) into this publication. Based on the findings provided (detailed below), the journal has decided that the major conclusions of the paper are not affected and that retraction is not required, but that a correction should be provided with an explanation of the circumstances. This course of action complies with our policy on correction of issues in the scientific record, which states: "Should an error appear in a published article that affects scientific meaning or author credibility but does not affect the overall results and conclusions of the paper, our policy is to publish a Correction".For Fig. 3C, the UTC concluded that it was the result of "cut-and-paste", which is "not indicated by a solid line, nor is it mentioned in the figure legend, as prescribed by journal policy". Fig. 3C presents results of in vitro phosphorylation of the different PIN2 hydrophilic loop (PIN2 HL) versions by the kinases PID, WAG1 and WAG2. The results were more or less similar for the three kinases ( Fig. 3 revised version), and in order to reduce the figure size, it was decided that it would be sufficient to show the full data for the PINOID kinase, and to focus on the phosphorylation results for the wild-type version and the loss-of-phosphorylation version of the PIN2 HL for the WAG1 and WAG2 kinases. This involved splicing, and although the splicing is clearly visible in the original Fig. 3C, the appropriate presentation according to the standards of the journal would have been to leave space between the spliced parts. As demonstrated by the comparison between the revised Fig. 3 (below) and the original Fig. 3C, the spliced version represents part of the original data. In the revised version of Fig. 3 the full data set is shown and a more detailed description of the results is provided in the revised figure legend text.With respect to Fig. 7D, the UTC noted that "it is not possible that random background noises, taken from two images, are identical. The most likely explanation is that the same green panel was used for the left and middle panel of Fig. 7D". The original data were not available to the UTC, and this anomaly could not be resolved. Development also appointed its own independent expert to analyse the images, who concluded that "the two images are almost identical (except for the region purporting to show photoconversion) and it is highly unlikely that these could represent different time points. The analysis suggests that one of these images appears to have been generated by manipulating the other." For this reason the authors and editors have seriously considered retraction of Development 137, 3245-3255. However, the thorough analysis by the UTC and the Development editors identified no other abnormalities in the data. The authors and editors therefore feel that remov...

SummaryGrass flowers are highly derived compared to their eudicot counterparts. To delineate OsMADS1 functions in rice floret organ development we have examined its evolution and the consequences of its knockdown or overexpression. Molecular phylogeny suggests the co-evolution of OsMADS1 with grass family diversification. OsMADS1 knockdown perturbs the differentiation of specific cell types in the lemma and palea, creating glume-like features, with severe derangements in lemma differentiation. Conversely, ectopic OsMADS1 expression suffices to direct lemma-like differentiation in the glume. Strikingly, in many OsMADS1 knockdown florets glume-like organs occupy all the inner whorls. Such effects in the second and third whorl are unexplained, as wild-type florets do not express OsMADS1 in these primordia and because transcripts for rice B and C organ-identity genes are unaffected by OsMADS1 knockdown. Through a screen for OsMADS1 targets we identify a flower-specific Nt-gh3 type gene, OsMGH3, as a downstream gene. The delayed transcription activation of OsMGH3 by dexamethasone-inducible OsMADS1 suggests indirect activation. The OsMGH3 floret expression profile suggests a novel role for OsMADS1 as an early-acting regulator of second and third whorl organ fate. We thus demonstrate the differential contribution of OsMADS1 for lemma versus palea development and provide evidence for its regulatory function in patterning inner whorl organs.