title: The gene ENHANCER OF PINOID controls cotyledon development in the Arabidopsis embryo.
abstract: 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.
authors.affiliation: Lehrstuhl für Genetik, Technische Universität München, Wissenschaftszentrum Weihenstephan, Am Hochanger 8, 85350 Freising, Germany.
authors.forename: Birgit S
authors.initials: BS
authors.lastname: Treml
authors.forename: Sabine
authors.initials: S
authors.lastname: Winderl
authors.forename: Roman
authors.initials: R
authors.lastname: Radykewicz
authors.forename: Markus
authors.initials: M
authors.lastname: Herz
authors.forename: Günther
authors.initials: G
authors.lastname: Schweizer
authors.forename: Peter
authors.initials: P
authors.lastname: Hutzler
authors.forename: Erich
authors.initials: E
authors.lastname: Glawischnig
authors.forename: Ramón A Torres
authors.initials: RA
authors.lastname: Ruiz
mesh_terms: D017360:Arabidopsis / Q000196:embryology*; D029681:Arabidopsis Proteins / Q000235:genetics* / Q000378:metabolism*; D002874:Chromosome Mapping; D018548:Cotyledon / Q000196:embryology*; D017931:DNA Primers; D018507:Gene Expression Regulation, Developmental; D018506:Gene Expression Regulation, Plant; D049452:Green Fluorescent Proteins; D018398:Homeodomain Proteins / Q000235:genetics; D017403:In Situ Hybridization; D007210:Indoleacetic Acids / Q000378:metabolism*; D009154:Mutation / Q000235:genetics; D010641:Phenotype; D017346:Protein Serine-Threonine Kinases / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction
chemical_list: D029681:Arabidopsis Proteins; D017931:DNA Primers; C508612:Enhancer of Pinoid protein, Arabidopsis; D018398:Homeodomain Proteins; D007210:Indoleacetic Acids; C097496:STM protein, Arabidopsis; D049452:Green Fluorescent Proteins; C405165:PINOID protein, Arabidopsis; D017346:Protein Serine-Threonine Kinases