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Genetics and Molecular Biology |
Section of Cell and Developmental Biology, Division of Biology, University of California at San Diego, 9500 Gilman Drive, La Jolla, California 92093-0116 USA
Received for publication May 24, 2001. Accepted for publication August 14, 2001.
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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Key Words: axillary meristem • barren stalk1 • ba1 • inflorescence • maize • spikelet • tillers
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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The shift from vegetative to reproductive development is a significant transition in the maize life cycle. During this transition, the SAM ceases to make leaves and transforms into an inflorescence meristem, which subsequently produces a number of specialized lateral meristems that ultimately lead to the formation of the tassel (male inflorescence) (Russell and Stuber, 1983
; Irish and Nelson, 1991
). The tassel is a branched inflorescence consisting of one central spike and several basal branches that together bear the spikelets and florets containing the floral organs. To initiate tassel formation, the inflorescence meristem gives rise to several files of branch meristems spanning its entire length. These branch meristems either elongate to form long lateral branches or become spikelet pair primordia, which branch again to form two spikelet meristems. Each spikelet meristem goes on to initiate a pair of floral meristems that give rise to the floral organs (Kiesselbach, 1949
; Cheng, Greyson, and Walden, 1983). In contrast to the tassel, ears (female inflorescences) develop from one or more axillary meristems on the main axis of the plant. The ear develops as a single thick rachis without basal branches (Kiesselbach, 1949
; Veit et al., 1993
; McSteen, Laudencia-Chingcuanco, and Colasanti, 2000
).
In maize, as well as in other plant species, a number of mutants have been described that possess defects in meristem fate, or identity, resulting in abnormal inflorescence development. For example, the tassel seed 4 (ts4) mutant of maize has highly branched inflorescences due to a reiteration of inflorescence branch meristems (Irish, 1997
). Like ts4, the branched silkless1 (bd1) mutant is also characterized by extra branching of the tassel and ear due primarily to reiterative branching of the spikelet meristems (Colombo et al., 1998
). There are several mutants that have opposite effects on branching. For example, the maize ramosa1 (ra1) mutant continues making long branches on the central spike of the tassel, whereas the unbranched 1 (ub1) mutant is completely devoid of tassel branches (Neuffer, Coe, and Wessler, 1997
). Other mutants of maize, such as teosinte branched1 (tb1) and tillered (tlr1), have normal inflorescence architecture but exhibit excessive vegetative branching (Doebley, Stec, and Hubbard, 1997
; Neuffer, Coe, and Wessler, 1997
). In Arabidopsis thaliana, the two mutants PINFORMED (PIN) and PINOID (PID), which encode a transmembrane auxin efflux carrier and a serine-threonine protein kinase, respectively, develop completely unbranched inflorescences (Bennet et al., 1995
; Gaelweiler et al., 1998
; Christensen et al., 2000
).
In this study, we characterize another inflorescence mutant of maize named barren stalk1 (ba1). ba1 is a recessive mutant first identified in 1928 (Hofmeyer, 1930
). In the original report, the ba1 mutant was described as having defective tassel branching and a central stalk devoid of any ears. Here, we present a detailed characterization of ba1 including scanning electron microscopy of developing inflorescences, in situ hybridization analysis with a meristem marker, and molecular mapping. We also show a genetic analysis of the relationship between ba1 and tb1 to determine the effect of the ba1 mutant on vegetative branching. Our study indicates that ba1 mutants are disrupted in the initiation of both vegetative and inflorescence axillary meristems. This defect manifests itself as a failure to produce vegetative branches (tillers), branches in the tassel, spikelets on the tassel's central spike, and ears.
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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). Due to the fact that ba1 mutants are frequently both male and female sterile, mutant stocks were maintained in heterozygous populations. Homozygous mutants used in scanning electron microscopy and in situ hybridization analyses were generated by self-pollination of heterozygous plants. All plants grown during the winter were in the greenhouse and supplemented with artificial light. During the summer, plants were grown in the field. Genotypes of plants in segregating populations were inferred from both developing and mature tassel morphology. Developing tassels were collected from both mutants and wild-type siblings 30–40 d after planting by manually removing all the enclosing leaves.
For scanning electron microscopy analyses, developing tassels were dissected and fixed in FAA (50% ethanol, 5% acetic acid, 3.7% formaldehyde) for 24 h at 4°C. Specimens were dehydrated through a graded ethanol series and then critical point dried with CO2. Coating was performed with gold and palladium. The specimens were examined with a Cambridge 360 scanning electron microscope at an accelerating voltage of 10 kV.
For Southern hybridizations, genomic DNA was extracted from leaf tissue of plants segregating for tb1 and ba1. DNA extractions were carried out in aqueous buffer (0.2 mol/L Tris HCl, 0.25 mol/L NaCl, 0.025 mol/L EDTA, 0.5% SDS, pH 8.0). For Southern blots DNA (5 µg per sample) was digested with ten units of restriction enzyme for 4 h at 37°C. Restriction fragments from the digest were separated on a 0.8% agarose gel, blotted to nylon membrane (Magna), and hybridized with 32P-labeled DNA probe. The probe was a 3.4 kilobase (kb) HindIII tb1 genomic fragment. Hybridization was performed in Church's buffer (7% SDS, 0.5 mol/L NaPO4, 1 mmol/L EDTA) at 65°C.
Sections for in situ hybridizations were prepared from immature tassels fixed in 4% para-formaldehyde in phosphate buffered saline (130 mmol/L NaCl, 7 mmol/L Na2HPO4, 3.5 mmol/L NaH2PO4) at 4°C for 36 h. Samples were then dehydrated at 4°C through a graded ethanol series containing 130 mmol/L NaCl. The tissue was then placed in a solution of 75 : 25 100% ethanol : Histoclear (National Diagnostics, Atlanta, Georgia, USA); 50 : 50, ethanol : Histoclear; 25 : 75, ethanol : Histoclear; and three times 100% Histoclear at room temperature for 1.5 h each. Histoclear was gradually replaced with molten paraplast, and tissue was poured into molds and sectioned on a microtome to 8 µm thickness. The treatment of the tissue prior to hybridization was as described by Freeling and Walbot (1994), except that the paraplast was removed with Histoclear. Hybridization, washes, antidigoxigenin antibody incubation, and detection were as previously described (Torres et al., 1995
), except that the tissue was not prehybridized and the antibody (antidigoxigenin alkaline phosphatase-conjugated Fab fragment) was obtained from Roche Diagnostics (Alameda, California, USA).
Linearized gene specific 3' Knotted-1 cDNA template including homeobox was used to synthesize the antisense probe (Jackson, Veit, and Hake, 1994
). The probe was labeled with the digoxigenin RNA labeling mix from Roche Diagnostics, and probes were resuspended in hybridization buffer. The kn1 probe was kindly provided by Sarah Hake (USDA, Plant Gene Expression Center, Albany, California, USA). The lg2 genomic clone used in molecular mapping was a gift from Mike Freeling (University of California at Berkeley, Berkeley, California, USA). Lines harboring the tb1 mutation were obtained from the MGCSC. A tb1 genomic clone was kindly provided by John Doebley (University of Wisconsin, Madison, Wisconsin, USA) for use in the genotyping of ba1/tb1 double mutants.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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). Like the main shoot, tillers eventually produce both male and female inflorescences.
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; Veit et al., 1993
). The axillary meristems that form the ear initially make several vegetative husk leaves that surround the developing inflorescence. Unlike the tassel, inflorescence branch meristems in the ear do not elongate before branching again to form spikelets and florets. A conspicuous aspect of the ba1 mutant phenotype is the lack of tillers, ears, tassel branches, and spikelets (Fig. 2). Although leaf number and morphology on ba1 mutants is normal, there is no detectable tiller or ear initiation on any node on the stalk (Fig. 3). The typical ba1 tassel (Fig. 5) is completely unbranched and devoid of any spikelets on the main tassel rachis. However, a few rare, malformed spikelets develop on some homozygous ba1 mutant tassels. The formation of these rare spikelets, which do shed small amounts of fertile pollen, is enhanced in some inbred backgrounds, such as A188 (P. McSteen and S. Hake, Plant Gene Expression Center, personal communication). In contrast, the wild-type tassel is a branched structure that sometimes contains 20 or more branches (Fig. 4). Ascending the main spike of a ba1 tassel are rows of small protrusions where basal tassel branches and spikelets are normally found (Fig. 6).
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Knotted-1 (kn1) expression in young ba1 tassels
In this study we have used kn1 as a meristem marker on developing ba1 tassels to help elucidate the nature and identity of the protruding tissue along the mutant tassels shown in Figs. 5, 6, and 9. kn1 is a maize homeobox gene that codes for a protein that localizes to the nuclei of cells of the SAM (Smith et al., 1992
; Jackson, Veit, and Hake, 1994
). In addition to being expressed in the SAM, kn1 is also expressed in all axillary meristems, in terminal and lateral inflorescence meristems, and in both male and female floral meristems (Kerstetter et al., 1997
). If the protruding structures along the axis of the developing ba1 tassel in Fig. 8 represent arrested lateral meristems, then one would predict that kn1 expression would be detected in these structures. Alternatively, if no kn1 expression is observed, this would suggest that these protrusions are not meristematic but determinate structures.
Figures 10, 11, and 12 are in situ hybridizations in developing male ba1 inflorescences using a kn1 antisense RNA probe. All three figures illustrate that kn1 expression is not maintained in the protruding tissue on the flanks of the young ba1 tassels. Strong kn1 expression can be observed in the inflorescence meristem as well as transient weak expression in what appears to be the location where the first lateral initiating meristems would be observed, just below the inflorescence meristem (Smith et al., 1992
). However, this expression is absent from the older, laterally initiated tissue swellings on ba1 tassels. Due to the fact that persistent kn1 expression is not observed in these structures as they develop, it is likely that these protrusions are determinate structures and not arrested SPP meristems.
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). The lg2 gene, a gene involved in ligule development, has recently been cloned (Walsh, Waters, and Freeling, 1998
). In an effort to carry out a detailed mapping of the ba1 locus, we have used an lg2 genomic clone as a restriction fragment length polymorphism marker to conduct a molecular mapping of the distance between the ba1 and lg2 loci.
A mapping population was generated by crossing ba1 plants, introgressed into the A188 inbred background, to the inbred line W23. Previous DNA blot analyses had established the existence of a polymorphism between these inbreds at the lg2 locus. The resulting heterozygous progeny were then backcrossed to heterozygous ba1 plants in the A188 background. The progeny from this cross, which segregated 1 : 4 for the ba1 phenotype, were scored and DNA was collected from homozygous ba1 individuals. DNA from these plants was probed with lg2 on Southern blots to score for recombinants that inherited the W23 polymorphism. Twelve of 197 homozygous ba1 were heterozygous for the A188 and W23 polymorphisms. Thus, in contrast to the previously reported genetic map distance of 1 cM, our molecular mapping places ba1 
6 cM from lg2.
The MADS box gene, ZMM16, has been reported to map at or near ba1 (Münster et al., 2001
) raising the possibility that they are one in the same locus. However, we know this is not the case as we have also cloned ZMM16 (designated Zea PISTILLATA or ZPI; C. M. Padilla and R. J. Schmidt, unpublished data) and mapped ZMM16/ZPI on the same A188/W23 mapping population used to map lg2 relative to ba1. Two plants that were recombinant for ba1 and lg2 were also recombinant at the ZMM16/ZPI locus (data not shown). This demonstrates unequivocally that they are distinct loci.
The barren stalk1 mutant is epistatic to teosinte branched1
In our studies of ba1 mutants, we observed a consistent lack of tillering. However, the absence of tillering among wild-type siblings, as well as in segregating populations, suggested the possibility that the genetic background did not support tillering. This trait is seen in several commercial maize inbred lines that have been bred to be nontillering (Kiesselbach, 1949
). Therefore, to establish whether the lack of tillering in ba1 mutants is an inherent characteristic of the mutant phenotype or merely an attribute of the genetic background, a double mutant was generated with ba1 and teosinte branched1 (tb1). teosinte branched1 is a recessive mutation that causes the plant to produce excess tillers and to elongate primary lateral branches terminated by tassels (Fig. 13) (Doebley, Stec, and Hubbard, 1997
).
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The tb1/ba1 double mutant is phenotypically indistinguishable from the ba1 single mutant (Fig. 14). Thus, it appears that ba1 is epistatic to tb1 and completely suppresses lateral branching in both vegetative and inflorescence meristems.
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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). The PIN protein, which shares homology with bacterial membrane transporters, functions as an auxin efflux carrier in the plant shoot (Gaelweiler et al., 1998
). The recently cloned PINOID (PID) gene, expressed predominantly in cells giving rise to lateral primordia, encodes a member of a plant-specific serine-threonine protein kinase family. Like pin, pid mutants also make an unbranched inflorescence, and the PID protein kinase has been shown to negatively regulate auxin signaling (Christensen et al., 2000
).
The similarities between phenotypes of the inflorescences of ba1 mutants and the aforementioned mutants of Arabidopsis are striking. ba1 mutants are characterized by blocked lateral organ growth, leading to the eventual formation of an unbranched, pin-like inflorescence structure (Fig. 5). In maize, like Arabidopsis, auxin participates in determining axillary meristem identity (Guilfoyle et al., 1998
). It is therefore enticing to speculate that, like these Arabidopsis mutants with similar phenotypes, ba1 plants could have a defect in some aspect of auxin signaling.
There are several other mutants of maize with similar phenotypes to that of ba1. Like ba1, barren-stalk 2 (ba2) and barren-stalk 3 (ba3) both exhibit an absence of tillers and ears (Pan and Peterson, 1992
; Neuffer, Coe, and Wessler, 1997
). However, unlike ba1, the tassel morphology of ba2 and ba3 mutants is largely wild type with well-developed tassel branches and spikelets. The barren-inflorescence genes (bif-1 and bif-2) also have defective tassel branching and ear development (Briggs and Johal, 1992
; Neuffer and Briggs, 1994
). Limited spikelet development due to a failure of initiation of inflorescence branch meristems is the principle defect of bif mutants (McSteen, Laudencia-Chingcuanco, and Colasanti, 2000
; McSteen and Hake, 2001). In comparison to ba1, the bif mutants make both a tassel and an ear on which a number of normal spikelets develop.
Recently, a detailed phenotypic characterization of the lax1 mutant of rice has been conducted (Komatsu et al., 2001
), and several aspects of the phenotype are similar to the maize ba1 mutant. With the most severe allele of the lax1 locus, the primary inflorescence meristem fails to initiate/maintain any axillary meristems in the rice panicle, leaving empty bract-like protrusions along the panicle axis. However, unlike ba1, lax1 mutants produce normal numbers of tillers, indicating that the formation of axillary vegetative meristems is unaffected by the lax1 mutation. This may indicate that ba1 and lax1 are not orthologous. Alternatively, they may represent the same gene, but rice may have evolved a distinct pathway for specifying vegetatively derived axillary meristems. ba1 may also represents a more severe allele than any that have yet been identified for the lax1 locus.
Studies in Arabidopsis have shown that flower-derived signals normally suppress bract development (Nilsson et al., 1998
), and secondary inflorescence branches and floral meristems develop in the axils of repressed bract leaves (Long and Barton, 2000
). With this evidence, one could extrapolate that during wild-type maize tassel development, inflorescence branches as well as SPP are initiated from the axils of suppressed bract leaves. In the tassel, the leaf that subtends the spikelet is rudimentary and appears in the form of a swelling at the base of the spikelets that has been called the glume cushion (Galinat, 1963
). Due to the formation of tassel branches and spikelets, these glume cushions, or suppressed bracts, would not be very conspicuous in wild-type tassels. However, in ba1 mutants, where tassel branches and spikelets are never formed, these suppressed bracts are still visible as small protuberances ascending the main tassel spike, as seen in Figs. 5, 6, and 9.
The maize homeobox gene kn1 can be used as a meristem marker. kn1 is expressed in the SAM, as well as in axillary and inflorescence meristems (Smith et al., 1992
). kn1 is not expressed in determinant products of meristems such as leaf primordia and floral organ primordia. It therefore follows that kn1 would not be expressed in bract leaves. Hence, the claim that the protrusions ascending both developing and mature ba1 inflorescences are suppressed bracts and not prematurely terminated meristems is supported by the fact that kn1 is not expressed in these structures (Figs. 10–12). Weak kn1 expression can be observed at the position from which laterally initiating meristems would normally form, but this expression is not maintained. Due to the fact that these axillary meristems fail to develop, the suppressed bracts subtending these meristems, which do not express kn1 during their development, become visible later as subtle glume cushions ascending the mature ba1 tassel. It is conceivable that one aspect of the ba1 mutant phenotype is the inability of these plants to maintain kn1 expression during their development. This pattern of kn1 expression was also observed in lax1 mutants of rice (Komatsu et al., 2001
). Using the kn1 orthologue, OSH1, as an in situ probe onto lax1–2 panicles, OSH1 mRNA accumulated only in the primary apical meristem of the mutant panicles and not in the axils of the bract-like structures that formed along the panicle axis.
The evolution of maize from teosinte, its probable ancestor, is marked by an increase in apical dominance. Apical dominance in maize manifests itself as a concentration of resources in the main stem of the plant, along with a corresponding suppression of axillary branching (Doebley, Stec, and Hubbard, 1997
). A major determinant in overall plant form is the degree to which axillary buds grow out into branches (Bell, 1991
; McSteen and Hake, 1998
). In maize, it has been proposed that increased vegetative branching draws energy and resources from the central stalk, thereby decreasing ear size and overall seed yield (Garnier, Mausrice, and Olivieri, 1993
). An increase in apical dominance has been a crucial determinant in the domestication of maize. In the U.S. cornbelt, maize has been bred to be unbranched, nontillering, single stalks adapted to the high-density growth conditions of modern day technological agriculture. Commercial varieties of dent corn make only one or two ears and rarely, if ever, tiller (Freeling and Walbot, 1994
).
In tb1 mutants (Fig. 13), the derepression of all axillary meristems produces a profusion of tillers. tb1 has been proposed to be a repressor of lateral organ growth (Doebley, Stec, and Hubbard, 1997
). ba1 is epistatic to tb1, (Fig. 14) and in contrast to tb1, appears to be required for the initiation of axillary branching. Down regulation of ba1 seems to promote severe apical dominance. A better understanding of ba1 and other mutants that affect the fate of axillary meristems could lead to biotechnological manipulations of apical dominance and plant architecture in agriculturally important crops such as maize.
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FOOTNOTES |
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2 Author for reprint requests (rschmidt{at}ucsd.edu
).
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LITERATURE CITED |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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Cheng P. C. R. I. Greyson D. B. Walden 1983 Organ initiation and the development of unisexual flowers in the tassel and ear of Zea mays. American Journal of Botany 70: 450-462[CrossRef][Web of Science]
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Colombo L. M. Giovanna S. Masiero P. Wittich R. J. Schmidt M. S. Gorla M. E. Pé 1998 BRANCHED SILKLESS mediates the transition from spikelet to floral meristem during Zea mays ear development. Plant Journal 16: 355-363[CrossRef][Web of Science]
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