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American Society of Plant Biologists
Arabidopsis Research Heats Up in Seville
a Instituto de Biología Molecular y Celular de Plantas Consejo Superior de Investigaciones Científicas Universitat Politècnica de València València, Spain dalabadi{at}ibmcp.upv.es Seville, Spain, was the setting of the 13th International Conference on Arabidopsis Research from June 28 to July 2, 2002. This fascinating city, with its spectacular gardens, beautiful Mudéjar royal palaces, and Gothic cathedral, provided an excellent backdrop for the conference, and the staff and facilities at the Seville Conference and Exhibition Center handled the 900-plus conferees with commendable smoothness and efficiency. Complete abstracts of the meeting can be found at http://www.arabidopsis2002.com/. We report here on some of our favorite presentations, with apologies to those whose work could not be cited as a result of space limitations.
The Arabidopsis Functional Genomics Network is a 10-year program launched in November 2001 with support from the Deutsche Forschungsgemeinschaf. There are currently 11 contributing members and three associated groups. The coordinator of the network is Lutz Nover. The focus of the initiative is the functional analysis of multiprotein families, including analysis of all members of a given multiprotein family with respect to their expression and function during the Arabidopsis life cycle. Abstracts of the projects and additional information are available at http://www.uni-frankfurt.de/fb15/botanik/mcb/AFGN/AFGNHome.html.
Functional Analysis of MLO Proteins
SCF Ubiquitin Ligase Complexes Related to EID1
The U.S. National Science Foundation 2010 Project is an ambitious funding program designed to determine the functions of 25,000 genes in Arabidopsis by the year 2010. More than $50 million was awarded in 2001 for 29 different projects for a period of 2 to 4 years each. A complete list of awardees and project abstracts can be found at http://www.nsf.gov/search97cgi/vtopic.
Arabidopsis Haplotype Map
Seed Development
P450 Genes
Transcriptional Profiling of Plant Defense Responses
Functional Analysis of Ubiquitin Protein Ligase Families
A Knockout for Every Gene
Chris Helliwell (Commonwealth Scientific and Industrial Research Organization [CSIRO] Plant Industry, Canberra, Australia) described another large-scale reverse genetics project (a collaboration with Peter Waterhouse and colleagues at CSIRO) with potential for creating gene family knockouts using gene silencing. Waterhouse and colleagues (Smith et al., 2000  ) demonstrated the efficacy of gene silencing in plants using inverted-repeat transgene constructs that encode a hairpin RNA structure. The most important applications are likely to be silencing of multiple members of gene families, especially if the family members are closely related (and therefore likely functionally redundant), and also knocking out of specific gene functions in ecotypes or mutants that are not being used in large-scale gene knockout projects. Helliwell and colleagues demonstrated that conserved sequences from the PhyC or PhyD genes also silenced PhyB, but nonconserved sequences did not. Furthermore, effective silencing of two different genes could be achieved by the introduction of a single construct containing sequences corresponding to both genes.
Caroline Dean (John Innes Centre, Norwich, UK) and Candice Sheldon (CSIRO Plant Industry) presented recent work regarding how vernalization and the autonomous pathway regulate flowering time. Vernalized seeds have a "mitotic memory" of vernalization. Separation between the timing and the effect of vernalization, and the lack of transmission to progeny, suggest an epigenetic basis of this phenomenon. FLC encodes a repressor of flowering that is central to the vernalization response. Early-flowering Arabidopsis accessions exhibit low expression of FLC and show no response to vernalization, whereas late-flowering accessions have high expression of FLC and are late flowering in the absence of vernalization but become early flowering and have reduced FLC expression after vernalization. Sheldon presented results from FLC:GUS fusion constructs that showed that different regions of FLC are required for the two components of the vernalization response: initial repression and maintenance of repression. Both promoter and intragenic regions are required for the initial repression, and sequences within intron I are likely to be important for maintenance. Furthermore, the gene adjacent to FLC also is repressed by vernalization, indicating that this repression affects a wider region, rather than just the FLC gene, providing support for the idea that a modification of chromatin structure occurs.
Dean elaborated on the activity of two other genes, VRN1 and VRN2, which are required for the stable repression of FLC after vernalization. VRN2 encodes a polycomb group protein (Gendall et al., 2001 Yoo-Sun Noh (University of Wisconsin, Madison) spoke about the molecular cloning and characterization of ef57, an early-flowering suppressor mutant of the late-flowering fri phenotype. The gene encodes a SWI2/SNF2-like chromatin remodeling factor that regulates FLC function. Noh and colleagues proposed that EF57 may act as an integrator of the pathways that regulate FLC-dependent floral transition. Takashi Araki (Kyoto University, Japan) focused on downstream events in floral induction pathways and presented work on the FD gene, which acts specifically downstream of the floral inducer FT. The fd mutation suppresses the early-flowering phenotype of plants expressing 35S::FT but not that caused by the expression of 35S::LFY or 35S::SOC1. FD encodes a basic domain/Leu zipper (bZIP) transcription factor that is able to interact with FT in yeast, suggesting that this interaction is important for FT function. Phil Wigge (Salk Institute, La Jolla, CA) seeks to understand why two very closely related proteins such as FT and TFL1 have antagonistic roles in the promotion of flowering. Wigge reported on the finding of a bZIP transcription factor that is very similar to FD and, like FD, is able to interact with both FT and TFL1. The group proposes that the bZIP protein may recruit FT or TFL1 to specific target promoters and that a third, yet unidentified factor would give transcriptional activation ability to the FT complex.
In recent years, Xing-Wang Deng and colleagues (Yale University, New Haven, CT) have been unmasking molecular components of a central signaling pathway involved in the light control of photomorphogenesis, defined by many of the COP/DET/FUS loci. As summarized by Deng, COP1 represents the rate-limiting component of this pathway, possibly acting as part of an E3 ubiquitin ligase that targets positive regulators of photomorphogenesis, such as HY5 and HYH, for degradation in the absence of light (Holm et al., 2002 ). In this process, the COP9 signalosome may replace the lid of the 26S proteosome and act in concert with COP1 to repress photomorphogenesis in the dark. The involvement of ubiquitination and the proteosome in this pathway is supported further by the finding that COP10 encodes an E2 variant ubiquitin-conjugating enzyme (Suzuki et al., 2002) that could work as a heterodimer with a canonical E2 enzyme and that links COP1 and the COP9 complex both functionally and physically.
Virtudes Mira-Rodado (working with Klaus Harter, University of Freiburg) reported on the functional interaction of Arabidopsis Response Regulator4 (ARR4) with the N terminus of PHYB (Sweere et al., 2001 Karen Kaczorowsky (University of California, Berkeley) is involved in the search for mutants hyposensitive to red light. Among a battery of new alleles of known genes, two alleles of a previously unidentified gene involved in red light signaling were found. Mutant plants had longer hypocotyls under red and far-red light. Positional cloning revealed that the lesion af-fected a pseudo-response regulator, APRR7, which belongs to a small family of circadian clock–regulated pseudo-response regulators that includes the clock gene TOC1. Members of this family lack the Asp residue involved in a phosphorelay characteristic of response regulators. Interestingly, Paloma Más (Scripps Research Institute, La Jolla, CA) reported that plants lacking TOC1 function show defects in deetiolation under white, red, and far-red light, whereas no phenotype was observed under blue light and in darkness. This finding reveals a new and unexpected role for TOC1 as an element acting downstream of PHYB and PHYA in the control of morphogenic responses. These plants also helped to define the role of TOC1 in the molecular clock mechanism, revealing that it is essential for clock function under red light and in darkness, whereas other clock components may compensate partially for its loss under blue light. The ZTL/ADO1 family of proteins may act at the interface between light signaling and the core of the clock. Jose Jarillo (Instituto Nacional de Investigaciones Agrarias, Madrid, Spain) reported on the pheno-typic analysis of plants deficient in each of the three family members, showing enhanced red light sensitivity for hypocotyl growth inhibition and later flowering time compared with any of the single mutants. How the clock defines the phase of output genes, such as the evening-phased gene CAT3, was addressed by Rob McClung (Dartmouth College, Hanover, NH). McClung's group showed in vivo that a change of 1 bp in the evening element present in the CAT3 promoter to the related CCA1 binding site associated with a morning phase is enough to switch the phase of expression from dusk to dawn.
The plastid proteome contains up to 3500 proteins, and  500 of these are membrane proteins. Klaas J. van Wijk (Department of Plant Biology, Cornell University, Ithaca, NY) reported on his work in collaboration with Gunnar von Heijne (Department of Biochemistry and Biophysics, Stockholm University, Sweden) aimed at defining Arabidopsis plastid subproteomes and characterizing a number of plastid-localized processes. The group is using two-dimensional gels, mass matrix-assisted laser desorption ionization time-of-flight mass spectrometry, and nanoelectrospray tandem mass spectrometry on chloroplast proteins obtained from different subcellular fractions. They quantitatively separated the hydrophilic thylakoid proteome into three subproteomes: the soluble thylakoid lumenal proteome, the peripheral thyla-koid proteome, and a tightly membrane-anchored peripheral proteome (Peltier et al., 2002). They also identified a chloroplast-localized 350-kD Clp core protease complex likely to be involved in subcellular protein housekeeping and the regulation of plastid gene expression (Peltier et al., 2001). Knockout mutants in different Clp genes are being used for proteomics studies aimed at determining the effect of Clp gene disruption on Clp complex composition. The experimental proteome data will be used to train neural network subcellular protein localization predictors to screen the Arabidopsis genome for the complete plastid proteome.
Role of NPR1 in Systemic Acquired Resistance Systemic acquired resistance (SAR) is a secondary defense response that can be induced after infection by an avirulent pathogen. Xinnian Dong presented data on the Arabidopsis NPR1 protein, an essential signaling component of SAR. Molecular genetic characterization showed that the nuclear localization of NPR1 and phosphatase activity is required for PR1 induction. Using a dominant-negative 3' fragment of the transcriptional activator TGA2 and a chimera reporter system, they found that NPR1 interacts in vivo with TGA2 and regulates the binding affinity of TGA2 to DNA (Fan and Dong, 2002 ). Therefore, NPR1 regulation of SAR-related gene expression may occur through interaction with transcription factors.
Salicylate (SA) and jasmonate (JA) play an important role in differentially regulating induced plant defenses against pathogens and insects (Kunkel and Brooks, 2002
RAR1 Function
QTLs Associated with Freezing Tolerance
New Salt and Osmotic Stress Mutants
Abed Chaudhury (CSIRO Plant Industry) discussed epigenetic processes during seed development. In fis mutants (comprising fis1/mea, fis2, and fis3/fie), the endosperm forms without fertilization, and after fertilization, the embryo is arrested and endosperm tissue overproliferates. FIS1/MEA encodes a polycomb group protein similar to Drosophila Enhancer of Zeste, and FIS3/FIE encodes a protein similar to Drosophila Extra Sex Combs, a WD-40 group protein. FIS2 encodes a zinc finger protein that shows homology with Drosophila SU(Z)12 and to the Arabidopsis proteins EMF2 and VRN2. Expression of a FIS2:GUS fusion protein showed that expression starts in the two haploid central nuclei that form the central cell. Experimental crosses showed that fis2 and fis1 homozygous mutants could be rescued by hypomethylation in the pollen donor even without paternal FIS function (i.e., a fis1 or fis2 homozygous female mutant pollinated by pollen from homozygous fis1 or fis2 mutants hypomethylated by antisense inhibition of the DNA methyltransferase gene) (Luo et al., 2000 ). Chaudhury hypothesized that FIS1 and FIS2 encode repressors of endosperm transcription, and hypomethylated pollen brings about repression of the genes that were derepressed as a result of the fis mutation. Using a number of maternal endosperm-specific markers and pollination by hypomethylated pollen, Chaudhury showed evidence of the repression of maternal gene expression by the hypomethylated paternal genome. Claudia Köhler (Universität Zürich, Switzerland) applied a genomic approach to identify target genes of MEA. She reported on the identification of the type 1 MADS box gene PHERES (PHE; initially called TOM1) as a potential target. It is strongly upregulated in both mea and fie mutants, and inhibition of PHE expression directed by the MEA promoter partially rescues the mea phenotype. These results indicate that the mea and fie phenotypes are attributable, at least in part, to high levels of expression of PHE. Jiri Friml (University of Tübingen, Germany) presented recent work on the implication of auxin in early embryogenesis. The mp and bdl mutants lack some basal pattern elements as a result of a defect during specification of the hypophysis. MP and BDL encode ARF5 and IAA12 auxin response regulators, respectively. It is proposed that auxin releases MP from the inhibition caused by BDL and thus allows MP to modify gene expression, leading to root meristem specification in a non-cell-autonomous manner. This process also may involve PIN auxin transporter regulators, which are important to establish an auxin gradient during embryogenesis.
Auxin, SCFTIR1, and Aux/IAA Proteins Auxin response in Arabidopsis is dependent on the SCFTIR1 ubiquitin ligase (E3) complex (Gray et al., 1999 ). Auxin response factors (ARFs) and Aux/IAAs are both large families of transcription factors that regulate the expression of auxin-inducible genes. Stefan Kepinski, working with Ottoline Leyser (Department of Biology, University of York, UK), and in collaboration with Mark Estelle (Institute for Cellular and Molecular Biology, University of Texas, Austin), reported on an elegant analysis demonstrating that the degradation of the AUX/IAA proteins AXR2 and AXR3 is regulated by auxin via the SCFTIR1 complex (Gray et al., 2001). Importantly, auxin accelerates the degradation of Aux/IAAs by promoting their interaction with SCFTIR1. The authors are currently trying to understand how changes in Aux/IAA levels affect the transcription of auxin-regulated genes.
JA Signaling
Two-Component Systems in Cytokinin and Ethylene Signaling Continuing with two-component systems, Uta Sweere (University of Freiburg) proposed a second ethylene signaling pathway downstream of ETR1 that includes AHP2 and ARR2. AHP2 is proposed to act as a pivotal element in the integration of several signals.
Brassinosteroid Signaling
Plant cell walls are complex composites of polysaccharides, proteins, and phenolic compounds. Very little is known about the processes involved in the biosynthesis, transport, and assembly of cell wall polymers. Fourier transform infrared (FTIR) microspectroscopy can be used to dis-tinguish mutants with altered cell walls from the wild type. Herman Höfte (Laboratoire de Biologie Cellulaire, Institut National de la Recherche Agronomique, Versailles, France) is using this technique to isolate mutants with defects in cellulose or pectin synthesis as well as mutants with alterations in the cortical cytoskeleton. By hierarchical clustering of FTIR data, his group was able to identify alleles of the same locus even in the absence of other observable phenotypic changes. Höfte described the isolation and characterization of KOBITO1, which encodes a novel plasma membrane protein necessary for normal cellulose synthesis during cell expansion (Pagant et al., 2002 ), and QUASIMODO1, which encodes a putative membrane-bound glycosyltransferase required for normal pectin synthesis and cell adhesion in Arabidopsis (Bouton et al., 2002).
One of most striking features of plant growth and development is the precise regulation of cell volume increase. Keiko Sugimoto, working with Maureen McCann (Department of Cell and Developmental Biology, John Innes Centre), conducted a screen to search for Arabidopsis mutants with reduced hypocotyl elongation and identified two mutants, hypocotyl6 (hyp6) and hypocotyl7 (hyp7), that are defective in cell expansion in different tissues of mature plants. HYP7 encodes the nucleus-localizing protein RHL1 (Schneider et al., 1998 ). FTIR microspectroscopy indicated that the cell walls of the mutants have normal levels of cellulose, but they are altered in pectin composition and the alignment of microfibrils is disrupted from the wild-type transverse array. These observations suggest that cellulose alignment is not necessary for organ strength but that this and other cell wall changes may affect the elasticity of the organ.
We thank all of the authors who agreed to contribute unpublished data to this report.
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