Os04g0396500 - Revision history

Liman: /* References */

2016-09-11T13:48:03Z

‎References

Liman: /* Mutation */

2016-09-11T13:47:11Z

‎Mutation

Liman: /* References */

2016-09-11T13:46:15Z

‎References

Liman: /* Mutation */

2016-09-11T13:45:10Z

‎Mutation

Liman at 13:40, 11 September 2016

2016-09-11T13:40:42Z

Liman: /* Expression */

2016-09-11T13:32:38Z

‎Expression

Liman at 13:30, 11 September 2016

2016-09-11T13:30:40Z

Liman: /* Mutation */

2016-09-11T13:24:56Z

‎Mutation

Liman: /* Mutation */

2016-09-11T13:19:38Z

‎Mutation

Liman: /* Mutation */

2016-09-11T13:14:33Z

‎Mutation

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 * <ref name="ref3">
 Komatsu, K., Maekawa, M., Ujiie, S., Satake, Y., Furutani, I., Okamoto, H., Shimamoto, K., and Kyozuka, J. (2003). LAX and SPA: Major regulators of shoot branching in rice. Proc. Natl. Acad. Sci. USA 100: 11765–11770.
 </ref>
 </references>

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 [[File:Os04g0396500-4.png|center|thumb|400px|'''Table 2. Quantification of the Double Mutants of lax1 and lax2''' '' <ref name="ref1" />.'']]
-* The researchers observed the expression of the OSH1 protein (a marker of the meristem) and the morphology of the AM in single and double mutants of lax2 and moc1. At the vegetative stage in a wild-type plant, a population of cells that expresses OSH1 can be detected at the axil of the second and third youngest leaf primordia (P2-P3) as a bulge (Steeves and Sussex, 1989), depending on the sampling stage within a plastochron (Figures 3A and 3E). Similar structures were observed in both lax2-2 and moc1-4 single and double mutants (Figures 3B to 3D). These bulges possibly include cells that give rise to an incipient AM. At the P4 leaf axil, the AM is formed and grows in wild-type plants and in lax2 and moc1 single mutants (Figures 3F to 3H and 3J). At the P5 leaf axil, the AM grows continuously and is covered by prophyll in wild-type plants and in lax2 and moc1 single mutants (Figure 3K to 3M and 3O). However, in the lax2 moc1 double mutant, the bulge with OSH1-expressing cells, although seen initially at the P2-P3 leaf axil, did not proliferate at the P4 leaf axil (Figure 3I) and was absent at the P5 leaf axil (Figure 3N). The lack of the AM in the lax2 moc1 double mutant was also observed by scanning electron microscopy analysis (Figures 3R and 3S). This phenotype is quite consistent because there is never a tiller in the lax2 moc1 double mutant. This observation negates the possibility that the initiation of the SAM is stochastically arrested in the mutant and indicates that the double mutant is defective in the maintenance of the AM. Thus, at the vegetative stage, both LAX2 and MOC1 are involved in the maintenance of the AM. At the reproductive stage, AM primordia that give rise to PBs formed normally in the lax2 mutant as in the wild type (Figures 3P and 3Q).
+* The researchers observed the expression of the OSH1 protein (a marker of the meristem) and the morphology of the AM in single and double mutants of lax2 and moc1. At the vegetative stage in a wild-type plant, a population of cells that expresses OSH1 can be detected at the axil of the second and third youngest leaf primordia (P2-P3) as a bulge <ref name="ref4" />, depending on the sampling stage within a plastochron (Figures 3A and 3E). Similar structures were observed in both lax2-2 and moc1-4 single and double mutants (Figures 3B to 3D). These bulges possibly include cells that give rise to an incipient AM. At the P4 leaf axil, the AM is formed and grows in wild-type plants and in lax2 and moc1 single mutants (Figures 3F to 3H and 3J). At the P5 leaf axil, the AM grows continuously and is covered by prophyll in wild-type plants and in lax2 and moc1 single mutants (Figure 3K to 3M and 3O). However, in the lax2 moc1 double mutant, the bulge with OSH1-expressing cells, although seen initially at the P2-P3 leaf axil, did not proliferate at the P4 leaf axil (Figure 3I) and was absent at the P5 leaf axil (Figure 3N). The lack of the AM in the lax2 moc1 double mutant was also observed by scanning electron microscopy analysis (Figures 3R and 3S). This phenotype is quite consistent because there is never a tiller in the lax2 moc1 double mutant. This observation negates the possibility that the initiation of the SAM is stochastically arrested in the mutant and indicates that the double mutant is defective in the maintenance of the AM. Thus, at the vegetative stage, both LAX2 and MOC1 are involved in the maintenance of the AM. At the reproductive stage, AM primordia that give rise to PBs formed normally in the lax2 mutant as in the wild type (Figures 3P and 3Q).
 [[File:Os04g0396500-5.png|center|thumb|400px|'''Figure 3. Anti-OSH1 Immunostaining of the Wild Type, lax2, moc1, and lax2 moc1 DoubleMutant and Scanning ElectronMicroscopy Image of theWild

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 </ref>
 * <ref name="ref2">
+Oikawa, T., and Kyozuka, J. (2009). Two-step regulation of LAX PANICLE1 protein accumulation in axillary meristem formation in rice. Plant Cell 21: 1095–1108.
 </ref>
 * <ref name="ref3">
+Komatsu, K., Maekawa, M., Ujiie, S., Satake, Y., Furutani, I., Okamoto, H., Shimamoto, K., and Kyozuka, J. (2003). LAX and SPA: Major regulators of shoot branching in rice. Proc. Natl. Acad. Sci. USA 100: 11765–11770.
 </ref>
 </references>

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 [[File:Os04g0396500-2.png|center|thumb|400px|'''Table 1. Phenotypic Characterization of lax2 Mutants and Their Respective Parental Wild Types in Rice''' '' <ref name="ref1" />.'']]
-* To clarify the genetic interactions of lax2 with other rice mutants that exhibit a defect in AM formation, the researchers made double mutants containing lax2 and either lax1 or moc1. lax1 had a sparse panicle with reduced SBs and spikelets, which was similar to the lax2 panicle, and lax1 had tillers with slightly reduced numbers at the vegetative stage (Figures 2A to 2C and 2G to 2I) (Oikawa and Kyozuka, 2009). The researchers made lax1 lax2 double mutants using null alleles of lax1, lax1-1, and lax1-6. lax1-1 is a deletion allele of lax1 (Komatsu et al., 2003), and lax1-6 has a single nucleotide deletion at the 59 end of the region encoding the conserved bHLH domain. The phenotype of the lax1 lax2 double mutant was more extreme than that of the single mutants. In the double mutant panicle, all SBs and spikelets except terminal spikelets were absent, whereas the number of PBs was not affected compared with the single mutants (Figure 2K, Table 2). At the vegetative stage, both single mutants shared the similar phenotype of a slightly reduced number of tillers (Figures 2B and 2C); however, there was a strong reduction in tiller branches in the double mutant (Figure 2E, Table 2). The allele of moc1 used in our analysis, moc1-4, also has a sparse panicle; however, the branching pattern of the moc1-4 panicle is different from that of the wild type, lax1, or lax2(Figure 2J,2G). The researchers used lax2-2 and moc1-4, both of which were derived from Nipponbare. The phenotype of the lax2-2 moc1-4 double mutant was more extreme than that of either single mutant. In the double mutant panicle, all PBs, SBs, and spikelets were absent (Figure 2L), and there were no tiller branches at the vegetative stage (Figure 2F).
+* To clarify the genetic interactions of lax2 with other rice mutants that exhibit a defect in AM formation, the researchers made double mutants containing lax2 and either lax1 or moc1. lax1 had a sparse panicle with reduced SBs and spikelets, which was similar to the lax2 panicle, and lax1 had tillers with slightly reduced numbers at the vegetative stage (Figures 2A to 2C and 2G to 2I)<ref name="ref2" />. The researchers made lax1 lax2 double mutants using null alleles of lax1, lax1-1, and lax1-6. lax1-1 is a deletion allele of lax1 <ref name="ref3" />, and lax1-6 has a single nucleotide deletion at the 59 end of the region encoding the conserved bHLH domain. The phenotype of the lax1 lax2 double mutant was more extreme than that of the single mutants. In the double mutant panicle, all SBs and spikelets except terminal spikelets were absent, whereas the number of PBs was not affected compared with the single mutants (Figure 2K, Table 2). At the vegetative stage, both single mutants shared the similar phenotype of a slightly reduced number of tillers (Figures 2B and 2C); however, there was a strong reduction in tiller branches in the double mutant (Figure 2E, Table 2). The allele of moc1 used in our analysis, moc1-4, also has a sparse panicle; however, the branching pattern of the moc1-4 panicle is different from that of the wild type, lax1, or lax2(Figure 2J,2G). The researchers used lax2-2 and moc1-4, both of which were derived from Nipponbare. The phenotype of the lax2-2 moc1-4 double mutant was more extreme than that of either single mutant. In the double mutant panicle, all PBs, SBs, and spikelets were absent (Figure 2L), and there were no tiller branches at the vegetative stage (Figure 2F).
 [[File:Os04g0396500-3.png|center|thumb|400px|'''Figure 2. Morphology of Double Mutants of lax2 with lax1 or moc1.

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 ===Function===
 * '''''LAX2''''' encodes a nuclear protein with a plant-specific conserved domain and that LAX2 physically interacts with LAX1 through a region containing this conserved domain. Thus, the rsearchers propose that '''''LAX2''''' is a novel genetic component that is required for the process of AM formation and acts together with '''''LAX1''''' in rice.
 ===Mutation===
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 ===Expression===
 *In the　vegetative shoots, LAX2 expression was observed at the axil of the P3 leaf, at the location where the AM is formed, as well as in　young leaves (Figures 5A, 5B, and 5G). In the reproductive stage, LAX2 expressionwas observed at all the AMsthat give rise toPBs, SBs, and spikelets (Figures 5C and 5D).
 ===Subcellular localization===

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 ===Expression===
 Please input expression information here.
 ===Evolution===