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First published online November 21, 2008; 10.1105/tpc.108.061713 The Plant Cell 20:3038-3049 (2008) © 2008 American Society of Plant Biologists Maternal Control of Male-Gamete Delivery in Arabidopsis Involves a Putative GPI-Anchored Protein Encoded by the LORELEI Gene[W]
a Department of Plant Biology, University of California, Davis, California 95616 6 Address correspondence to sundar{at}ucdavis.edu.
In Angiosperms, the male gametes are delivered to the female gametes through the maternal reproductive tissue by the pollen tube. Upon arrival, the pollen tube releases the two sperm cells, permitting double fertilization to take place. Although the critical role of the female gametophyte in pollen tube reception has been demonstrated, the underlying mechanisms remain poorly understood. Here, we describe lorelei, an Arabidopsis thaliana mutant impaired in sperm cell release, reminiscent of the feronia/sirène mutant. Pollen tubes reaching lorelei embryo sacs frequently do not rupture but continue to grow in the embryo sac. Furthermore, lorelei embryo sacs continue to attract additional pollen tubes after arrival of the initial pollen tube. The LORELEI gene is expressed in the synergid cells prior to fertilization and encodes a small plant-specific putative glucosylphosphatidylinositol-anchored protein (GAP). These results provide support for the concept of signaling mechanisms at the synergid cell membrane by which the female gametophyte recognizes the arrival of a compatible pollen tube and promotes sperm release. Although GAPs have previously been shown to play critical roles in initiation of fertilization in mammals, flowering plants appear to have independently evolved reproductive mechanisms that use the unique features of these proteins within a similar biological context.
In plants, the gametes are not directly generated as products of meiosis, but result from division and differentiation of the multicellular haploid gametophytes. In angiosperms, the gametophytes are the pollen and the embryo sac, producing the male and female gametes, respectively. Furthermore, the male gametes are nonmobile and are instead carried, after germination of the pollen grain on the female stigma, by the pollen tube. The pollen tube emanates from the pollen grain and finds its way in the female tissues, ultimately delivering two sperm cells to the embryo sac, at the mycropylar end. The canonical mature embryo sac, as in Arabidopsis thaliana, is composed of seven cells: the egg cell and the central cell, which will receive the two sperm cells, two synergids at the micropylar end, and three antipodal cells at the chalazal end. The proper delivery of the male gametes relies on a series of signals from the embryo sac. Through laser ablation experiments in Torenia fournieri, Higashiyama et al. (2001)  showed that the synergid is the direct source of attractant for the pollen tube, while recent work in maize (Zea mays) has shown that the egg cell may also play a role in this guidance (Dresselhaus, 2006). Furthermore, work by Chen et al. (2007) has shown an involvement of the central cell in the guidance of the pollen tube in Arabidopsis. Upon arrival at the embryo sac, the pollen tube releases the sperm cells for the double fertilization to proceed. Furthermore, the embryo sac loses its ability to attract pollen tubes after fertilization is initiated.
Recently, the identification in Arabidopsis of the receptor-like kinase FERONIA has shed some light on potential signaling mechanisms responsible for these processes. In feronia and sirène mutants, the pollen tube can reach the embryo sac, but instead of arresting and delivering the two sperm cells, the pollen tube does not arrest and continues to grow and invades the embryo sac (Huck et al., 2003
The lorelei Mutation Causes an Invasive Pollen Tube Phenotype and Failure of Fertilization To obtain more data on the role of the embryo sac in pollen tube guidance, we performed a genetic screen to isolate mutants deficient in pollen tube reception and pollen tube arrest typical of the sirène class represented by the two alleles srn and fer. Plants from a population of Columbia (Col) wild-type seeds irradiated by gamma rays were used as pollen donors to fertilize wild-type ovules. We did not obtain male gametophytic mutants defective for fertilization among 2000 lines. However, we isolated mutant lines that showed >25% of seeds arrested at early stages after self-fertilization. The line GM474 showed a phenotype similar to srn and fer. Ovules from self-fertilized lre-1/+ plants showed failure of pollen tube arrest with further curling or invasive growth of the pollen tube in the embryo sac (Figure 1B). We tentatively named the mutation carried by GM474 lorelei-1 (lre-1) in reference to the mermaid names used for this class of phenotype. Genetic mapping based on 2108 plants determined that the mutation lre-1 location is within an interval between the BACs F14M19 and F10M23.
In parallel, we previously described a Ds element insertion collection in Arabidopsis for gametophytic mutants (Pagnussat et al., 2005 ). One of these mutants, called une17 (for unfertilized embryo sac 17), displayed a segregation ratio of the kanamycin resistance, carried by the Ds element, of 1.09:1, clearly indicative of a gametophytic defect. Furthermore, it proved impossible to recover a plant homozygous for the Ds element. Reciprocal crosses with the wild type as an ovule or pollen donor showed a mainly female lethality (0.12:1 and 0.84:1, respectively) and reduced genetic transmission from the female but not from the male gametes (Table 1).
Differential interference contrast (DIC) observation of cleared heterozygous siliques after pollination showed that 28.6% of the embryo sacs displayed a failure of pollen tube arrest and sperm discharge. Instead, these embryo sacs contained an invasive pollen tube, either curling at the micropylar end (Figure 1H) or entering in the central cell region and then turning back toward the micropyle (Figure 1G). Because of its similarity to the previously identified lorelei mutation, which mapped to the same chromosomal region (see below), this mutant was renamed lorelei-2 (lre-2).
Crosses between ovules from lre/+ plants and wild-type pollen produced siliques in which approximately one-quarter of the embryo sacs were aborted and had invasive pollen tube growth (Table 2). By contrast, there was very limited ovule abortion in crosses between wild-type ovules and pollen from lre/+ plants. The proportion of aborted ovules with invasive pollen tube growth between lre/+ siliques pollinated with wild-type pollen and self-pollinated lre/+ siliques showed little variation. However,  10% of the seeds aborted in self-pollinated lre/+ plants as a result of early embryo and endosperm arrest between the 2- to 8-cell stage in the embryo. Although the Ds element insertion primarily affected the embryo sac function, there was also some reduced transmission of the transposon through the lre-2 pollen, but we did not detect a reduced transmission through lre-1 pollen (Table 1), indicating that the pollen defect might be allele specific. In conclusion, the mutations lre-1 and lre-2 primarily affect the capacity of the embryo sac to be fertilized, and the phenotype exhibits a moderate penetrance.
To confirm the observations made with DIC on cleared ovules, the phenotypes were rescored using samples stained with aniline blue. This method allow for easy visualization of the pollen tube (Figures 1A to 1C, Table 3). In both lre deletions, the proportion of embryo sacs showing an invasion by a pollen tube was similar to the one observed with DIC. We were also able to score the number of pollen tubes reaching a single ovule using aniline blue staining. Table 4 shows that embryo sacs in lre-/+ can attract supernumerary pollen tubes, as >20% of the ovules had two or more pollen tubes reaching them (Figure 1F). Overall, the defects observed in lre/+ siliques are quite similar to those described in the feronia/sirène (Huck et al., 2003 ; Rotman et al., 2003) and amc mutants (Boisson-Dernier et al., 2008), with an overgrowth of the pollen tube in the embryo sac and attraction of supernumerary pollen tubes. However, the penetrance of the lre-1 and lre-2 mutations is lower than what was observed in feronia/sirène. While ovules from fer/+ siliques showed invasion by the pollen tube almost 50% of the time, the percentage of occurrence in lre-2 is lower at 25%. These observations, in addition to the possible transmission of lre through the female suggest that the defect is not as drastic in lre-2 compared with fer and srn, which are not transmitted through the female gametes (Huck et al., 2003; Rotman et al., 2003). A direct comparison with amc is not possible because while lre-2 and fer are independent of the male gametophyte, the amc phenotype appears only if both the pollen and the embryo sac carry the mutation, and amc embryo sacs are able to receive wild-type pollen normally (Boisson-Dernier et al., 2008).
To examine whether the invasive pollen tube phenotype observed in lre/+ siliques arose from defective embryo sac development, analysis using DIC of the developing embryo sacs was performed. No defects could be observed during embryo sac development, and the mature, unpollinated embryo sacs appeared uniformly normal in lre/+ siliques. Furthermore, ovules from lre-1/+ plants expressed the β-glucuronidase reporters for the genes MEA and FIS2 the same those from the wild type. Similarly, lre-2/+ correctly expressed the β-glucuronidase genes associated with the embryo sac marker lines ET119 and ET2634 (Gross-Hardt et al., 2007 ) in specific cell types in the embryo sac, the egg cell, and the synergids (data not shown). Similar experiments performed on feronia also failed to show defects during the embryo sac development (Huck et al., 2003).
Molecular Characterization of lre-1 and lre-2
To confirm that the phenotype observed in lre-2/+ siliques was indeed caused by this deletion, we transformed lre-2/+ plants with a binary vector, JatY53G03, containing a section of the chromosome IV, including the genes from At4g26350 to At4g26530 (Figure 2A). The resulting T2 plants were screened for complementation of the Ds transmission frequency using the Kanr/Kans ratio. Several independent transformants displaying an increase in Kanr/Kans were recovered (Table 5). The line lre-2/+;JatY53G03-1/+ was further characterized for pollen tube invasion in the embryo sac as well as the Barr/Bars ratio, indicative of the complementing construct that confers resistance to Basta. As shown in Tables 6 and 7, the invasive pollen tube phenotype was entirely rescued in the progeny of the T2 plants 1.2 of the complementing line, corresponding to the complementing construct in a homozygous state, as indicated by the complete Basta resistance in this family.
This complementation experiment indicated that the locus responsible for the lorelei phenotype was located between At4g26350 and At4g26530. To identify the specific gene, all of the 19 annotated genes present on JatY53G03 were independently cloned in binary vectors and transformed in lre-2/+ plants. The F2 progeny from those transformants were screened for their Kanr/Kans ratio. However, we noted that one of the genes contained in the original deletion, and also on the complementing BAC JatY53G03, was At4g26500, which has been identified as embryo lethal (Xu and Møller, 2006 ). Therefore, the expected ratio after rescue in the case of a single copy of the complementing construct containing a single gene would be 2:1 at best. Of the 17 constructs tested, only one construct, pC450 (Figure 2A), resulted in a significant increase of Kanr/Kans ratio, as shown in Table 8.
Identification of Additional lorelei Alleles The vector pC450 contained 10 kb of Arabidopsis genomic DNA surrounding At4g26450. Several T-DNA insertion lines were available in this region, and five of them were investigated further (Figure 2B). Three of those lines did not display any invasive pollen tube phenotype (SALK_007165, SALK_059671, and SALK_135772). However, the lines SALK_040289 and SAIL_8_C08 presented the same invasion of the embryo sac by the pollen tube as the lre mutants (Figures 1D and 1E) and were renamed lre-3 and lre-4, respectively. Observations made on siliques from lre-3/+ and lre-4/+ showed a similar penetrance of the invasive pollen tube phenotype in those lines (Table 9).
A homozygous line for lre-3 was recovered and analyzed. The occurrence of the lorelei phenotype in the homozygote was double what was observed in the lre-3 heterozygote, as expected from twice the number of mutant embryo sacs in the homozygote (Table 9). Importantly, the homozygous knockout plants were healthy and had no other visible phenotypes, suggesting that the LRE gene functions specifically in fertilization. While the lre-3 homozygous line displayed a strong increase in invasive pollen tube frequency, half of the mutant embryo sacs are able to receive the pollen tube normally. It could therefore be hypothesized that the function of LRE in the signaling pathway is partially redundant and/or is, to some extent, dispensable (see below).
Isolation of the LORELEI Gene When the work to identify the LORELEI gene was performed, the gene At4g26466 was not annotated. In silico analysis of the region lead to the discovery of another gene at the At4g26450 locus, which was identified as LORELEI and appears under the number At4g26466 in the AGI V8 annotation (see Supplemental Results online). To confirm that At4g26466 was indeed LORELEI, a construct covering the sequences between the exon 5 of At4g26450 and the stop codon of At4g26460 was transformed in lre-3 homozygotes and able to rescue the phenotype (Table 10). Furthermore, a cDNA matching the sequence of the predicted At4g26466 was recovered through RT-PCR (see Supplemental Results online).
LORELEI Is Expressed in the Synergid Cells of the Embryo Sac Preliminary studies showed that LORELEI was expressed at a low level throughout the plants, including in floral organs (see Supplemental Results online). To determine the pattern of localization of LORELEI mRNA, we performed in situ hybridization in longitudinal sections of wild-type ovules, using a digoxygenin-labeled probe of 181 bp corresponding to a small portion of the 3rd exon in At4g26466. We find that LORELEI expression occurs in differentiated ovules that contain cellularized female gametophytes prior to pollination. Specifically, LORELEI mRNA was localized in the egg apparatus, predominantly in both synergids prior to degeneration (Figure 3A). Sporadically, a weak signal was detected in the cytoplasm of the egg cell (Figure 3A); however, no mRNA was localized in the central cell and the antipodals either before or after pollination. After pollination, abundant mRNA was found localized in synergids at the micropylar pole of the female gametophyte (Figures 3B and 3C). Although this signal could reflect a higher concentration of mRNA confined to a restricted portion of cytoplasm in degenerating synergids, it could also be the result of an increase in LORELEI expression following pollination. Developing ovules undergoing megasporogenesis or megagametogenesis did not show LORELEI mRNA localization at any developmental stage, indicating that LORELEI is active only in the fully differentiated cells of the egg apparatus.
LORELEI Encodes a Conserved, Plant-Specific, GPI Anchor Protein Sequence comparison of the predicted protein showed strong similarity with a small family of GAPs with three known members in Arabidopsis and more in other plants, including rice (Oryza sativa), maize, and Physcomitrella patens. Using BLAST (Altschul et al., 1990 ) with the LORELEI sequence against the Medicago truncatula and Populus trichocarpa genome allowed the identification of partial sequences of three putative orthologs in Medicago and one in Populus. Performing the same type of analysis as used for LORELEI (see above and Supplemental Results online), it was possible to reconstruct four full ORFs sharing similar gene structures between themselves and with LORELEI. The newly identified ORFs have been named Mt LORELEI-related 1, 2, 3, and Pt LORELEI-related1 for the Medicago and poplar sequences, respectively.
No significant similarities were found with animal or yeast proteins. Further in silico analysis of the LORELEI sequence using SignalP (Nielsen et al., 1997
A ClustalW alignment (Larkin et al., 2007 ) is shown on Figure 4B, displaying a central conserved domain. The domain does not show any similarity with previously described protein domains and appears specific to the LORELEI protein family. Within the domain, several amino acids are conserved in all sequences, such as a series of Cys residues (C62, C72, C73, C81, C117, and C126) as well as several hydrophobic residues (M98, F99, F113, and L124). However, the significance of those conserved residues is unclear. Outside of the central domain, little conservation is observed, particularly in the N-terminal signal peptide and the C-terminal GPI anchor signal. Out of the three identified LRE paralogs, At5g56170 is the closest, with 58% identity and 76% similarity. The two remaining (At4g28280 and At2g20700) show more differences, with 55 and 46% identity and 71 and 65% similarity, respectively. However, At4g28280 and At2g20700 are highly similar to each other, showing 83% identity. Both At2g20700 and At4g28280 have been found to be expressed strongly in the mature pollen tube in an earlier study, while At5g56170 was not detected in the same experiment (Lalanne et al., 2004).
To address the intracellular localization of the LRE protein, a green fluorescent protein (GFP) fusion was engineered between the signal peptide and the rest of LRE. First, a modified GFP protein was created with the N-terminal signal peptide of LRE. This modified GFP was fused to the central domain and the GPI anchor domain of LRE to generate an N-signal peptide-GFP-LRE-C fusion (Figure 5A).
Unfortunately, efforts to obtain GFP fluorescence in a transient expression experiment by particle bombardment in intact onion cells were not successful with this fusion, although strong expression was obtained with a 35S-GFP control plasmid (data not shown). This suggested the possibility that the fusion protein might be unstable or that it was quenching the GFP fluorescence. Another possible reason for the failure to detect GFP fluorescence in intact tissues might be that localization of the fusion protein on the outer leaflet of the plasma membrane, predicted for a GPI anchor protein, results in exposure of GFP to unfavorable conditions in the extracellular environment, such as low pH, as noted by others (Nadeau and Sack, 2002
GAPs are eukaryotic proteins known to function in cell–cell signaling, and are anchored at their C termini to the extracellular surface of the plasma membrane of the cell though the GPI moiety (Muñiz and Riezman, 2002 ). The GPI anchor is synthesized in the endoplasmic reticulum membrane in a multistep process, and the processed protein is ultimately trafficked to the cell surface, where it is believed to be tethered to lipid rafts (Orlean and Menon, 2007). GAPs can be released from their anchor into the extracellular medium; this release can be catalyzed by phospholipase C or by ACE (reviewed in Sharom and Lehto, 2002; Mayor, 2005). Only a few genes encoding GAPs have been characterized in terms of function in Arabidopsis. The gene COBRA is required for polarized cell expansion in the root (Schindelman et al., 2001), and the gene NDR-1 is involved in signal transduction during disease resistance (Coppinger et al., 2004). A classical arabinogalactan protein containing a GPI anchor has been shown to be involved in the initiation of female gametogenesis in Arabidopsis and has been proposed to be involved in intercellular signaling between sporophytic and gametophytic cells (Acosta-Garcia and Vielle-Calzada, 2004). In addition, three Arabidopsis mutants affecting biosynthesis of the GPI anchor have also been described. Mutations in two Arabidopsis genes, SETH1 and SETH2, encoding Arabidopsis homologs of two subunits of the enzymatic complex responsible for the first step of the GPI synthesis, have been shown to be male sterile, preventing pollen germination and pollen tube growth. The peanut1 mutant, which is defective for another enzyme of the GPI synthesis pathway, is seedling lethal and causes severe morphological defects in the embryo (Gillmor et al., 2005). However, the lack of GPI synthesis did not affect the fertility of the embryo sac in the above mutants. It is plausible that maternally produced enzymes are carried over during the development of the female gametophyte and can synthesize sufficient GPI for LRE function, as illustrated by mutations in many essential biosynthetic genes that result in embryo arrest rather than in gametophytic defects (Tzafrir et al., 2004).
The function of LRE appears specific to the process of fertilization because lre mutant homozygous plants are otherwise normal with no observable growth or developmental defects, consistent with the observed expression pattern of LRE with the highest expression in the synergids within the ovule. In mammals, GAPs appear to be critical for fertilization, as mouse eggs lacking GAPs on their surface, generated by conditional knockout of GPI synthesis, are unable to fuse with the sperm (Alfieri et al., 2003
While the specific role of LRE in the communication between the pollen tube and the embryo sac remains to be elucidated, the known properties of GAPs suggest some models for future studies. LRE might act in the signaling pathway informing the embryo sac of the arrival of a pollen tube, acting in concert with the FER receptor kinase, for example, by modifying the lipid microenvironment (van Meer, 2002
Genetic Screen and Mapping The line GM 474 (Col-0 accession background) was obtained from the genetic screen of  -ray mutagenized Arabidopsis thaliana seeds previously described (Guitton et al., 2004) and was crossed with wild-type Ler to generate F1 plants heterozygous for polymorphic markers between Col and Ler. The F1 mutant plants were allowed to self to generate F2 mapping populations. A mapping population of 2108 F2 plants from the GM474 line was analyzed. Markers for mapping were designed using the polymorphisms of the Cereon (www.arabidopsis.org/Cereon/index/html) online database.
Plant Transformation and Selection Seeds were surface-sterilized and plated onto medium (half-strength Murashige and Skoog salts, 1% sucrose, and 0.9% agar, pH 5.7) supplemented with 50 mg/L kanamycin (for lre-2/+), 50 mg/L kanamycin and 6 mg/L gluphosinate (for lre-2/+ transformed with JatY53G03), 50 mg/L kanamycin and 15 mg/L hygromycin (for lre-2/+ transformed with pC450), or 15 mg/L hygromycin (for lre-3/- and lre-4/+ transformed with pC450). After 2 d at 4°C, the plates were transferred to a Percival growth chamber (Percival Scientific) with a 16-h-light/8-h-dark cycle at 22°C. Antibiotic resistance was scored after 2 weeks. Plants were then transferred on soil and grown under the condition described above with 60% humidity. For crosses, flowers of the ovule donor were emasculated and manually pollinated 48 h later.
Cleared Whole-Mount Ovule
Aniline Blue Staining of Pollen Tubes
In Situ Hybridization
GFP-LORELEI Localization
Arabidopsis Genomic DNA Extraction
T-DNA Lines
Molecular Analysis of the une17 Line and T-DNA Lines The SALK lines flanking sequences were checked using the Lba1 primer (5'-TGGTTCACGTAGTGGGCCATCG-3') with the following gene-specific primers: 5'-CCTGAAAACGTCTCAGGGAGCTA-3' for SALK_007165, 5'-AATTGTTGCCGGAGCCAGAT-3' for SALK_059671, 5'-TCATTATTGCACTATCGACCTTAGGC-3' for SALK_135772, and 5'-TGGTTGGAAACAGAATGTGAAGTGA-3' for SALK_040289. For the line SAIL_8_C08, the following primers were used to amplify the left border flanking sequence: 5'-TTCATAACCAATCTCGATACAC-3' and 5'-TGCTGCAACCGCTGTTTTTG-3'. The right border sequence of SALK_040289 was amplified using 5'-AACGGCTTGTCCCGCGTCAT-3' and 5'-TGGCTCTTTCAATTTCCTTTGATTG-3'. Both the left border and right border flanking sequences of SALK_040289 were purified and sequenced.
Plasmids A 2.6-kb fragment containing the sequence of LORELEI along with 1.4 kb of promoter and 0.45 kb of terminator sequences was amplified with the following primers 5'-ATATATGTCGACAATTGTTGCCGGAGCCAGAT-3' and 5'-ATATATGTCGACCCGTGTGCTCTGTCTGCATT-3'. This fragment was cloned in pCAMBIA 1300 with SalI to create pCLRE.
To generate the GFP-LORELEI fusion, the LORELEI sequence, minus the first 69 bp corresponding to the N-terminal signal peptide was amplified by PCR. A HindIII and an 8x Ala linker was added to the 5' with the primer, and an EcoRI site was added after the STOP codon at the 3' with the primers. The primers used are 5'-ATATATAAGCTTGCGGCTGCCGCGGCAGCGGCAGCCTCGGATGGTGTGTTTGAAT-3' and 5'-ATATATGAATTCTCAAGTCAACACTAACAAAG-3'. EGFP was modified through PCR. The sequence corresponding to the N-terminal signal peptide was added in three successive rounds of PCR as well as an Asp-718 restriction site at the 5' end. A HindIII site was added at the 3' end. The primers used for the 5' end elongation were 5'-ATATATTCTCTCTCCTCTTCAAGTTCCATAATGAGTAAAGGAGAAGAACT-3', 5'-ATATATCTTCTTTCTGATGGCACTGTTGGTATCTCTCTCCTCTTCAAGTTC-3', and 5'-ATATATGGTACCATGGAGCTGATATTATTATTCTTCTTTCTGATGGCACTGT-3', successively. The 3' primer was 5'- ATATATAAGCTTTTTGTATAGTTCATCCATGC-3'. The EGFP fragment and the LORELEI fragment were combined in a vector containing a 35S promoter and a NOS terminator described by Griffith et al. (2007)
Accession Numbers
Supplemental Data
We thank Ueli Grossniklaus for generously providing cell-specific marker lines used in this study, Quy Ngo for many helpful suggestions, and Thomas Berleth for discussions. This work was supported by National Science Foundation Grants 2010 0313501 and IOS-0745167 to V.S. and USDA/CSREES/NRICGP Grant 2005-35304-16031 to B.L. Research in the J.-P.V.-C. lab is supported by CONCyTEG, UC-MEXUS, and HHMI. A.C. was supported by an EMBO Long-Term Fellowship.
1 Current address: Department of Cell Systems Biology, University of Toronto, 25 Willcocks St., Toronto, ON M5S 3B2, Canada. 
2 Current address: Unité Mixte de Recherche, Interactions Plante Micro-organisme et Santé Végétale, Centre National de la Recherche Scientifique/Institut National de la Recherche Agronomique/Unice, 400 Route des Chappes, Sophia Antipolis, F-06903 France.
3 Current address: Department of Molecular Neurogenetics, McGill University/Montréal Neurological Institute, 3801 Rue University, Montreal, Quebec H3A 2B4, Canada.
4 Current address: European Commission, Research Directorate General, Research Infrastructures (Unit B3) Office SDME 1/133, B-1049 Brussels, Belgium.
5 Current address: Temasek Life Sciences Laboratory, 1 Research link, National University of Singapore, Singapore 117604. The author responsible for distribution of materials integral to the findings presented in this article in accordance with the policy described in the Instructions for Authors (www.plantcell.org) is: Venkatesan Sundaresan (sundar{at}ucdavis.edu).
[W] Online version contains Web-only data. www.plantcell.org/cgi/doi/10.1105/tpc.108.061713 Received June 27, 2008; Revision received October 1, 2008. accepted November 4, 2008.
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