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First published online August 23, 2002; 10.1105/tpc.002873 American Society of Plant Biologists KOBITO1 Encodes a Novel Plasma Membrane Protein Necessary for Normal Synthesis of Cellulose during Cell Expansion in Arabidopsis
a Laboratoire de Biologie Cellulaire, Institut National de la Recherche Agronomique, Route de Saint-Cyr, 78026 Versailles Cedex, France 1 To whom correspondence should be addressed. E-mail hofte{at}versailles.inra.fr; fax 33-1-30-83-30-99
The cell wall is the major limiting factor for plant growth. Wall extension is thought to result from the loosening of its structure. However, it is not known how this is coordinated with wall synthesis. We have identified two novel allelic cellulose-deficient dwarf mutants, kobito1-1 and kobito1-2 (kob1-1 and kob1-2). The cellulose deficiency was confirmed by the direct observation of microfibrils in most recent wall layers of elongating root cells. In contrast to the wild type, which showed transversely oriented parallel microfibrils, kob1 microfibrils were randomized and occluded by a layer of pectic material. No such changes were observed in another dwarf mutant, pom1, suggesting that the cellulose defect in kob1 is not an indirect result of the reduced cell elongation. Interestingly, in the meristematic zone of kob1 roots, microfibrils appeared unaltered compared with the wild type, suggesting a role for KOB1 preferentially in rapidly elongating cells. KOB1 was cloned and encodes a novel, highly conserved, plant-specific protein that is plasma membrane bound, as shown with a green fluorescent protein–KOB1 fusion protein. KOB1 mRNA was present in all organs investigated, and its overexpression did not cause visible phenotypic changes. KOB1 may be part of the cellulose synthesis machinery in elongating cells, or it may play a role in the coordination between cell elongation and cellulose synthesis.
A major question in plant biology is how cells expand despite the presence of the cell wall. Cell walls are sufficiently rigid to resist the high osmotic pressure of the protoplast and sufficiently plastic to allow cells to grow. The measurement of turgor pressure in expanding cells has shown that, in general, cells grow as a result of the loosening of the wall rather than an increase in turgor (Cosgrove, 1993  ). In vitro studies have shown that expansins are involved in cell wall plasticity (McQueen-Mason et al., 1992). These small cell wall proteins are suspected to promote the slippage between cellulose and xyloglucan chains by breaking the hydrogen bonds that hold these polymers together (McQueen-Mason et al., 1992).
Other cell wall enzymes also may contribute to growth by hydrolyzing, grafting, or modifying xyloglucans or pectins. These wall modifications may lead in turn to changes in the pore size or viscosity of the wall matrix. In most models of growth based on experiments with isolated cell walls, cell wall synthesis is ignored and considered not to play a critical role. This view is further supported by observations that chemical inhibition of cellulose synthesis does not necessarily lead to growth inhibition (Brummell and Hall, 1985
In addition to its role in cell elongation, cellulose synthesis also is crucial for cell plate formation in dividing cells and secondary wall formation after cessation of growth. This is demonstrated clearly by the abnormal cell plate formation in dividing cells in the presence of 2,6-dichlorobenzonitrile (DCB), an inhibitor of cellulose synthesis (Wells et al., 1994
The synthesis of cellulose remains a poorly understood process. The site of synthesis is a plasma membrane–bound hexameric protein complex referred to as "terminal complex" or "rosette" (Mueller and Brown, 1980
Another protein essential for normal cellulose synthesis is KOR, a membrane-bound endo-
By contrast, genetic evidence shows that CESA isoforms are specialized in terms of function. Indeed, strong mutant alleles of rsw1 and prc1 mutated in CESA1 and CESA6, respectively, show cell expansion defects but are not affected in cytokinesis (Fagard et al., 2000 The functional specialization of CESAs for cellulose synthesis may simply reflect the different constraints that are imposed on the cellulose synthesis machinery during cytokinesis, cell elongation, or differentiation. This may relate to differences in carbon metabolism, the size of the microfibrils, the orientation of the microfibrils, or the stability or intracellular localization of the cellulose synthase complex. Against this background, the identification of novel mutants affected specifically in the synthesis of cellulose during particular cellular stages may be highly informative. Here, we describe a new locus, KOBITO1 (KOB1), that was identified by mutations that cause a defect in the synthesis of cellulose during the elongation phase of the cell. By contrast, in dividing cells and in secondary thickenings of xylem vessels of the mutants, microfibrils appeared unaffected. KOB1 encodes a novel plasma membrane–anchored protein. Possible roles for KOB1 in the synthesis of cellulose during cell elongation are discussed.
Kob1 Phenotype A screen for mutants showing reduced growth anisotropy in the dark-grown hypocotyl led to the identification of kob1-1 and kob1-2. The mutants were isolated from a T-DNA–mutagenized population in the accession Wassilewskija (Ws) and an ethyl methanesulfonate–mutagenized population in Columbia (Col0), respectively. Both mutations are recessive, monogenic, and nuclear, and complementation tests showed that they are allelic (data not shown). Hypocotyls of the mutant grown in the dark for 7 days were five times shorter than those of the wild type (Figure 1E) and showed a reduced apical hook compared with wild-type seedlings. When grown in the light, kob1 hypocotyls and roots were shorter than those of the wild type (Figure 1F). Mature greenhouse-grown plants homozygous for kob1 showed a strong dwarf phenotype: inflorescence stems were short with small internodes, and floral organs presented a miniature morphology (Figures 1A to 1D).
Mutant plants were sterile. Root hairs showed normal length and morphology, indicating that kob1 mutations do not affect tip-growing cells (data not shown). This was confirmed by the absence of a segregation bias for kob1 alleles (data not shown), which suggests that pollen tube growth also was unaffected in the mutant. The phenotype of kob1-2 was stronger than that of kob1-1. The Kob1 phenotype is not a result of a brassinosteroid, auxin, or gibberellin deficiency, because none of these hormones added to the growth medium rescued the dwarf phenotype (data not shown). In addition, the Kob1 phenotype is not attributable to an overproduction of ethylene, because various concentrations of an inhibitor of ethylene perception (aminoethoxyvinylglycine) did not rescue the growth defect (data not shown).
Cellular Defects in kob1
The cellular phenotype also was investigated in roots using longitudinal optical root sections obtained by confocal microscopy (Figures 2C to 2F). The advantage of studying this organ is that all stages of cell development can be examined simultaneously. The root meristem is located at the root apex and includes a set of continuously dividing cells that produce the basic cell types and define their spatial organization. The elongation zone is delineated distally by the end of the mitotic zone, which in general coincides with the proximal end of the lateral root cap (Beemster and Baskin, 1998 ), and proximally by the differentiation zone, which is characterized by the appearance of root hairs. In mutant roots, the organization in cell files and division planes appeared unaltered (Figure 2E), suggesting that the mutation does not affect cytokinesis. The absence of a cytokinesis phenotype also was shown in mutant embryos using confocal microscopy. The homozygous plants being sterile, we studied 12 embryos from the progeny of a heterozygous plant; no differences compared with the wild type were observed in any of them (data not shown). By contrast, cell elongation was affected dramatically in kob1-1 roots. After cessation of mitosis, cells had barely elongated before entering the differentiation zone, as indicated by the premature appearance of root hairs. However, in contrast to hypocotyl cells, which showed a greatly increased diameter (Figures 2A and 2B), mature roots cells were significantly shorter but not wider than those of the wild type (Figures 2D and 2F). Mature root cortex cells of kob1-1 were at least two times shorter (wild type, 79.59 ± 11.19 µm [n = 30]; kob1-1, 37.10 ± 6.24 µm [n = 30]) but not wider (wild type, 28.71 ± 3.83 µm; kob1-1, 23.96 ± 3.67 µm) than those of the wild type.
Cell Wall Defects in kob1
Changes in Noncellulosic Polysaccharides
We also investigated the xyloglucan structure in kob1-1. To this end, xyloglucan fragments were released by an endo-1,4-  -glucanase treatment of cell wall material prepared from dark-grown wild-type and kob1-1 seedlings. This enzyme cleaves the xyloglucan backbone behind nonsubstituted Glc residues and releases heptasaccharide XXXG to decasaccharide XLFG fragments, according to the nomenclature reported by Fry et al. (1993).
Figures 3B and 3C show the matrix-assisted laser desorption ionization–time of flight mass spectra of the fragments produced from wild-type and kob1-1 cell walls. In both spectra, main ions were assigned to (M+Na)+ adducts of XXXG, XXLG, XXFG, and XLFG on the basis of their molecular masses and literature data (Zablackis et al., 1995
Ectopic Callose and Lignin
Cellulose Content and Cellulose Synthase Activity
We also compared the relative in vivo cellulose synthesis activity in mutant and wild-type cells. To this end, cell walls were prepared from dark-grown seedlings cultured for 4 days in the presence of 14C-Glc, and the incorporation of the label in the acetic acid:nitric acid–insoluble fraction was measured (Figure 3E). This acid-insoluble fraction is 97% crystalline cellulose (Peng et al., 2000
Cellulose Microfibril Orientation
In the meristematic zone, cellulose microfibrils were oriented transversely to the elongation axis, and no difference was observed between the wild type and kob1-1 (Figures 4D and 4E). In addition, the secondary wall thickening on the inner side of the xylem cell wall presented transversely orientated cellulose microfibrils in both kob1-1 (Figure 4K) and the wild type (data not shown). In the elongation zone of wild-type roots, microfibrils also showed a transverse orientation with respect to the elongation axis (Figure 4F). By contrast, no transverse microfibrils were observed in the elongation zone of kob1-1 (Figure 4G). Instead, an amorphous mass was visible. Given the increased pectin content in kob1-1 cell walls, we investigated whether this corresponded to pectic material. Indeed, treatment of the sections with pectolyase revealed a sparse network of randomly oriented microfibrils in the mutant (Figure 4I) compared with the dense microfibril arrays in the wild type (Figure 4H).
These observations are consistent with the idea that in kob1-1, cellulose synthesis is inhibited in elongating cells and the continuous supply of pectic polysaccharides in these cells would lead to the occlusion of the remaining microfibrils. It remains conceivable that the kob1 mutations affect cell elongation and that this results only indirectly in the observed changes in cellulose deposition. That this is unlikely was shown by the analysis of microfibril orientation in pompom1 (pom1), another root elongation mutant (Figure 4C) (Hauser et al., 1995
KOB1 Encodes a Novel Protein Specific for Plants
To confirm that the mutation in this gene is responsible for the mutant phenotype, the kob1-2 allele was sequenced. kob1-2 contains a G2795A transition that abolishes the splice acceptor site of the third intron. The effect of the kob1-2 mutation on the maturation of KOB1 mRNA was analyzed by reverse transcriptase–mediated (RT)–PCR using primers straddling the first three introns. A fragment of the expected size for a correctly spliced mRNA was observed in wild-type extracts. Interestingly, in kob1-2 heterozygous plants, three fragments were observed. Sequencing of these fragments showed that they represent three mRNA species: the largest fragment corresponds to a mRNA unspliced for the second intron; the middle fragment was a correctly spliced mRNA presumably derived from the wild-type allele; and the smallest fragment was a mRNA in which the splice acceptor site of the third intron was used instead, leading to a mRNA lacking the fourth exon (Figure 5B). For both incorrectly spliced mRNAs, conceptual translation produces a protein truncated at a premature stop codon (data not shown). Low levels of KOB1 mRNA were detected in all organs investigated, as shown by RNA gel blot analysis using specific probes as well as RT-PCR (data not shown). In addition, KOB1 mRNA levels were constitutive throughout seedling development both in the dark and in the light (data not shown). Comparison of the KOB1 cDNA and genomic sequences showed that the gene contains 11 exons. The cDNA carries an open reading frame of 1.6 kb encoding a predicted protein of 543 amino acids. The sequence did not match any protein of known function or any functional motifs in the public databases. The amino acid sequence shows four predicted N-glycosylation sites and a predicted transmembrane anchor at the N terminus. The protein is predicted to be a type II membrane protein with the N terminus exposed to the cytosol. Two additional KOB1 isoforms are encoded by genes in the Arabidopsis genome located on chromosomes 2 and 3, showing 70 and 66% amino acid sequence identity, respectively, with KOB1 (Figure 5C). Other sequences matching KOB1 were found in various plant species, including the dicotyledons cotton, tomato, and poplar and the monocotyledons rice and maize. KOB1 showed 65% identity with the protein predicted from the full-length rice sequence (Figure 5C). Interestingly, KOB1 ESTs also were detected in a library from 6-day-old elongating cotton fibers and in developing cambium cells of poplar (T. Teeri, personal communication). No database matches were found with sequences from nonplant species, including the completely sequenced genomes of various bacteria, yeast, Caenorhabditis elegans, and Drosophila melanogaster. In conclusion, KOB1 encodes a novel, highly conserved, plant-specific protein carrying a putative N-terminal membrane anchor.
KOB1 Is Localized in the Plasma Membrane but Not in All Cell Types The GFP-KOB1 localization was investigated by confocal analysis in the different cell types in roots of kob1-1 seedlings complemented by the construct. The GFP signal was observed at the cell surface of elongated epidermal or cortical cells (Figure 6A). The plasma membrane localization of GFP-KOB1 in these cells was demonstrated by the colocalization with the vital dye FM4-64, which stains specifically the phospholipids of the plasma membrane (Figures 6B and 6C). These results are consistent with the prediction from the amino acid sequence, which suggested that KOB1 is a type II membrane protein.
Interestingly, the plasma membrane localization of GFP-KOB1 was not observed in all cell types. Indeed, in cells within the meristem and the root cap, GFP fluorescence accumulated in the cytoplasm and in distinct punctate patches, which may correspond to an unidentified intracellular compartment (Figure 6D).
Mutations in KOB1 Cause the Cellulose-Deficient Dwarf Phenotype Two lines of evidence show that the observed growth defect and the cellulose deficiency are the results of mutations in KOB1. First, both independent alleles are cellulose-deficient dwarfs and carry mutations in the KOB1 gene; second, the mutant phenotype of kob1-1 was complemented by the expression of a KOB1 cDNA or a GFP-KOB1 fusion protein under the control of the duplicated 35S promoter of Cauliflower mosaic virus (data not shown). Both mutants may correspond to complete loss-of-function alleles, because they express aberrant transcripts that encode severely truncated fragments of KOB1. The possibility is not excluded, however, that low levels of correctly spliced wild-type transcripts persist in the mutants. In addition, it is not known whether the related KOB2 and KOB3 genes are partially redundant with KOB1, because RT-PCR experiments showed that all three KOB genes are at least expressed in light-grown seedlings (data not shown). To understand the function of KOB1, the causal relationship between the growth phenotype and the cellulose deficiency needs to be established. The following observations suggest that the cellulose deficiency is a primary defect of the kob1 mutations and not an indirect result of the cell elongation defect.
First, the dwarf phenotype with a radially expanded hypocotyl is very similar to that of other cellulose-deficient mutants (Arioli et al., 1998 We observed that both kob1 alleles clustered together inside a larger group containing exclusively cellulose-deficient mutants (rsw1, kor/rsw2, pom1, prc1) and wild-type plants treated with DCB or isoxaben. Other dwarfs, not deficient for cellulose, formed separate clusters (G. Mouille, unpublished results). In addition, the accumulation of ectopic lignin and callose as well as the presence of gapped walls in transverse hypocotyl sections also are characteristic of cellulose-deficient mutants.
Third, in cells within the cell elongation zone of kob1 roots, microfibrils were oriented randomly and occluded completely by pectic material at the cytoplasmic side of the wall. A reduced cellulose/pectin ratio in kob1 was confirmed by a chemical analysis of mutant and wild-type cell walls. Increased pectin content has been observed in other cellulose-deficient mutants (His et al., 2001
Why this randomization occurs is not understood, but it may indicate that a critical density of nascent microfibrils is required to coordinate the orientation of cellulose deposition. Alternatively, the disorganized microfibrils in the mutant may correspond to the deeper cell wall layers that are covered by the pectin-rich and cellulose-depleted superficial layers in the mutant. Indeed, microfibrils were shown to lose their characteristic transverse alignment in deeper layers of the cell walls of expanded cells (Sugimoto et al., 2000 Other observations also make it unlikely that the cellulose defect is an indirect result of the cell expansion defect in kob1. pom1 roots showed a reduction of the cell elongation zone comparable to that of kob1 but still contained normal transverse microfibrils in elongating cells. The same effect was observed for prc1 (G. Refrégier, unpublished data), which is mutated in CESA6. In addition, no evidence exists to date that reduced cell expansion can lead to changes in the ratio between cellulose and other wall polysaccharides. For instance, despite dramatic differences in the growth rate of dark-grown and light-grown hypocotyls and a much higher level of cell wall synthesis in light-grown seedlings, the ratio between cellulose and other cell wall polysaccharides remained constant (G. Refrégier, unpublished data). Together, these observations strongly suggest that the cellulose defect is a direct result of mutations in KOB1 and not an indirect result of the growth defect.
What Causes the Growth Defect in Cellulose-Deficient Mutants?
Therefore, the alternative possibility should be considered: that the inhibition of cellulose synthesis may lead to an active inhibition of cell elongation, suggesting that at least in these cases growth is linked to cellulose synthesis through feedback control mechanisms. Why different organs show differences in radial expansion behavior in the mutants remains to be determined (for a more detailed discussion, see Williamson et al., 2001
Potential Function of KOB1 The mutant phenotype also corroborated a role for KOB1 in elongating cells as opposed to meristematic cells. Indeed, cell division planes were unaltered in mutant root meristems and embryos, indicating that KOB1 is not essential for cytokinesis. Also, microfibrils in the meristematic zone of the mutant were indistinguishable from those of the wild type, suggesting that the absence of KOB1 becomes critical only in cells that have ceased dividing and that enter a rapid elongation phase. Together, these observations suggest that KOB1 has a specific role in cellulose synthesis in postmitotic cells and that its activity requires the presence of the protein in the plasma membrane. It is not clear from our data whether KOB1 also has a role in cellulose deposition in secondary walls. The observation that microfibrils appeared normal in the secondary wall thickenings of xylem cells suggests that normal cellulose deposition may resume in the mutant once growth has ceased. Preliminary FESEM data suggest that this also is the case for microfibrils in secondary walls of other cell types in kob1 roots (G. Refrégier, unpublished data). What could be the role of KOB1 in cellulose synthesis? From its plasma membrane localization, KOB1 may be part of the cellulose synthesis machinery or it may play a regulatory role. A functional specialization of the cellulose synthesis machinery in postmitotic cells may reflect specific constraints that are imposed on cellulose synthesis in rapidly growing cells. In addition, KOB may play a role in the coordination between cellulose synthesis and cell expansion. The molecular analysis of KOB1 will provide new insights in the role of this protein in any of these processes.
In Vitro Growth Conditions Arabidopsis thaliana seedlings were grown on medium as described by Estelle and Somerville (1987) without Suc at 25°C. Seeds were cold treated for 48 h to synchronize germination. For dark growth, seeds were exposed to fluorescent white light (200 µmol·m-2·s-1) for 4 h to induce germination, and the plates were wrapped in three layers of aluminum foil. The age of the seedlings was counted from the beginning of the light treatment.
Microscopy and Image Analysis Cells in living roots were stained with 0.1 µg/mL FM1-43 (Molecular Probes, Leiden, The Netherlands). The samples were washed twice after staining before observation with a TCSNT confocal microscope (Leica, Heidelberg, Germany) equipped with an argon/krypton laser (Omnichrome, Chino, CA) Length and width of root cells were measured using the image analysis software Optimas version 5 (Bioscan, Suresne, France).
Field emission scanning electron microscopy (FESEM) was performed as described by Sugimoto et al. (2000)
Preparation of Cell Wall Material and Sugar Composition For the analysis of cellulose content, cell walls were hydrolyzed for 2 h at 110°C with 800 µL of 2 M TFA containing 20 µg of inositol; after centrifugation, the supernatant was collected, neutralized, and lyophilized. The TFA-insoluble cellulosic material was washed with water and then dissolved in 30 µL of 72% H2SO4 at room temperature for 1 h. After dilution to 3% H2SO4 with water and the addition of 20 µg of inositol, the solution was heated at 110°C for 2 h. The sample then was neutralized with BaCO3 and centrifuged, and the supernatant was lyophilized. Sugar in both cellulosic fractions and the TFA-soluble fraction was quantified by gas chromatography using inositol as an internal standard. The percentage of cellulose was expressed as the ratio between the amount of Glc in the cellulosic fractions and the amount of total sugar in the TFA-soluble and TFA-insoluble fractions. For cellulose incorporation assays, heterozygous kob1 seeds were sown and germinated in the dark as described above, and homozygous seedlings were selected from the progeny and grown overnight in liquid medium. After liquid preincubation, they were washed three times with 15 mL of Glc-free growth medium before being resuspended in 1 mL of growth medium with 1.0 µCi/mL 14C-Glc (DuPont–New England Nuclear, Boston, MA). The seedlings then were incubated for 1 h in the dark at 15°C in glass tubes. After treatment, seedlings were washed three times with 6 mL of Glc-free growth medium. The seedlings were extracted with 5 mL of boiling absolute ethanol for 20 min. This step was repeated three times. Next, seedlings were resuspended in 3 mL of chloroform: methanol (1:1), extracted for 20 min at 45°C, and finally resuspended in 3 mL of acetone for 15 min at room temperature with gentle shaking.
The remaining material was resuspended in 500 µL of an acetic acid:nitric acid:water solution (8:1:2) as described by Updegraff (1969)
For the analysis of xyloglucan structure, xyloglucan fragments were generated by treating 500 µg of cell wall material with 5 units of endo-1,4-
RNA Gel Blot Analysis Upon request, all novel materials described in the article will be made available in a timely manner for noncommercial research purposes. No restrictions or conditions will be placed on the use of any materials described in this article that would limit their use for noncommercial research purposes.
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Estelle Aletti and Jocelyne Kronenberger are thanked for their skilled technical assistance, Olivier Grandjean for help with the confocal microscopy, and Guislaine Refrégier and Soizic Rochange for their help with the FESEM. Catherine Bellini and Thierry Desnos are thanked for the isolation of kob1-2. This work was financed in part by GENOPLANTE Grant 19990025 to H.H. and P.L., European Economic Community Framework 5 Grant GEMINI, a grant from the French Ministery of Science and Technology, and a grant from Centre de Coopération Internationale en Recherche Agronomique pour le Développement to S.P.
Article, publication date, and citation information can be found at www.plantcell.org/cgi/doi/10.1105/tpc.002873. Received March 13, 2002; accepted June 5, 2002.
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Zuo, J., Niu, Q.W., Nishizawa, N., Wu, Y., Kost, B., and Chua, N.H. (2000). KORRIGAN, an Arabidopsis endo-1,4- This article has been cited by other articles:
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Abstract
INTRODUCTION
-Glucosidase I is required for cellulose biosynthesis and morphogenesis in Arabidopsis. J. Cell Biol. 156, 1003–1013.
