Gene Details:

Functional Descriptions:

  • Vegetative development is also affected in the APO1.
  • Leaves were formed rapidly throughout the vegetative phase, indicating that APO1 is also involved in temporal regulation of leaf production.
  • These phenotypes suggest that the APO1 plays an important role in the temporal regulation of both vegetative and reproductive development.
  • We previously reported that the ABERRANT PANICLE ORGANIZATION1 (APO1) gene, encoding an F-box-containing protein orthologous to Arabidopsis (Arabidopsis thaliana) UNUSUAL FLORAL ORGANS, suppresses precocious conversion of rachis branch meristems to spikelets to ensure generation of certain number of spikelets.
  • Positional cloning of the gene revealed that SCM2 was identical to ABERRANT PANICLE ORGANIZATION1 (APO1), a gene previously reported to control panicle structure.
  • Although SCM2 is a gain-of-function mutant of APO1, it does not have the negative effects reported for APO1 overexpression mutants, such as decreased panicle number and abnormal spikelet morphology.
  • In addition, APO1 is associated with the regulation of the plastchron, floral organ identity, and floral determinacy.
  • Phenotypic analyses of APO1 and floral homeotic double mutants demonstrate that APO1 positively regulates class-C floral homeotic genes, but not class-B genes.
  • Molecular studies revealed that APO1 encodes an F-box protein, an ortholog of Arabidopsis UNUSUAL FLORAL ORGAN (UFO), which is a positive regulator of class-B genes.
  • Further analysis indicated that APO2/RFL and APO1, the rice ortholog of Arabidopsis UNUSUAL FLORAL ORGANS, act cooperatively to control inflorescence and flower development.
  • ABERRANT PANICLE ORGANIZATION 2/RFL, the rice ortholog of Arabidopsis LEAFY, suppresses the transition from inflorescence meristem to floral meristem through interaction with APO1.
  • This alteration in growth rate is opposite to what is observed with the APO1 mutants that have a smaller inflorescence meristem.
  • However, in APO1, the main-axis meristem was converted to a spikelet meristem after producing a small number of branch primordia.
  • In addition, the branch meristems in APO1 became spikelet meristems earlier than in wild type.
  • Therefore, in the inflorescence, the APO1 mutation caused the precocious conversion of the meristem identity.
  • In the APO1 flower, lodicules were increased at the expense of stamens, and carpels were formed indeterminately by the loss of meristem determinacy.
  • Characterization of rice aberrant panicle organization 1 (APO1) mutants revealed that APO1 positively controls spikelet number by suppressing the precocious conversion of inflorescence meristems to spikelet meristems.
  • We report a recessive mutation of rice, aberrant panicle organization 1 (APO1), which severely affects inflorescence architecture, floral organ identity, and leaf production rate.
  • In the APO1-D dominant alleles, the inflorescence meristem starts to increase in size more vigorously than the wild type when switching to the reproductive development phase.
  • APO1 expression occurred not only in developing panicles but also in the developing vascular bundle systems.
  • It suggests that APO1 enhances the formation of vascular bundle systems which, consequently, promote carbohydrate translocation to panicles.
  • The HI1 allele is suggested to regulate the amount of APO1 expression, and thereby control the development of vascular bundle systems.
  • In this study, using chromosome segment substitution lines, we identified an effective quantitative trait loci (QTL) for culm strength, which was designated STRONG CULM2 (SCM2).
  • A near-isogenic line carrying SCM2 showed enhanced culm strength and increased spikelet number because of the pleiotropic effects of the gene.
  • Collectively, these results suggest that the level of APO1 activity regulates the inflorescence form through control of cell proliferation in the meristem.
  • As the mutant inflorescences and flowers differed considerably between APO1 and ufo, the functions of APO1 and UFO appear to have diverged during evolution.
  • Habataki-genotype segregated reciprocal recombinant lines for the APO1 locus increased both the number of PRB (12-13%) and the number of grains per panicle (9-12%), which increased the grain yield per plant (5-7%).
  • The PRB1 allele, which includes the APO1 open reading frame (ORF) and the proximal promoter region, controlled only the number of PRB but not the number of grains per panicle.
  • Here, we identified four dominant mutants producing an increased number of spikelets and found that they are gain-of-function alleles of APO1.
  • The APO1 expression levels are elevated in all four mutants, suggesting that an increase of APO1 activity caused the delay in the program shift to spikelet formation.
  • The resultant gene was ABERRANT PANICLE ORGANIZATION 1 (APO1).
  • Overexpression of APO1 caused an increase in inflorescence branches and spikelets.
  • These data indicate that ozone-induced grain yield loss in Habataki is caused by a reduction in the APO1 transcript level through an increase in the levels of phytohormones that reduce leaf damage.
  • The Habataki allele of the APO1 locus in a near-isogenic line also resulted in grain yield loss upon ozone exposure, suggesting APO1 involvement in ozone-induced yield loss.
  • Genetic analyses support that LARGE2 functions with APO1 and APO2 in a common pathway to regulate panicle size and grain number.

Literature:

Gene Resources:

Sequences:

cDNA Sequence
  • >LOC_Os06g45460.1
    ATGGACCCGCGCGTGTGGCGCCGGCTGCCGCAGCCGCTGGTGGACCGCATCCTGGCGTGCCTCCCGACGCCGTCGTTCCTCCGCCTCCGCGCCGCCTGCCGCCGCTTCTACCACCTCCTCTTCTCCTCCCCGTTCCTCCACTCCCACCTCCTCCTCTCCCCTCACCTCCCCTTCTTCGCCTTCGTCGTCCCCGCCGCCGGCCACCTCCTCCTCCTCGACCCCACCGCCACCGCCTCCTGGTCCCGCCTCCCGCTCCCGCTCCCGCCCGTCGCCGGCGGCCCCGCCGCGTTCTCGCCCGCGGCCGCGTCCGCCGGCCTGCTCGCGTTCCTGTCCGACGCGTCGGGGCACAAGACGCTGCTGCTCGCCAACCCGATCACCCGCCTCCTCGCCGCGCTCCCCATCTCCCCGACCCCGCGCCTCTCCCCCACCGTCGGCCTCGCCGCCGGCCCGACCTCCATCATCGCCGTCGTGGCCGGGGACGACCTCGTGTCCCCCTTCGCCGTCAAGAACATCTCCGCCGACACGTTCGTCGCCGACGCCGCCTCCGTCCCGCCCTCCGGCTTCTGGGCTCCCAGCTCCCTGCTCCCTCGCCTCTCCTCCCTCGATCCCCGCGCCGGCATGGCCTTCGCCTCCGGCAGGTTCTACTGCATGAGCTCGTCGCCGTTTGCGGTTCTGGTGTTCGACGTGGCGGAGAACGTATGGAGCAAGGTGCAGCCGCCGATGAGGCGGTTCCTGAGGTCGCCGGCGCTGGTGGAGCTCGGCGGCGGGAGGGAGGGAGCGGCGAGGGTGGCGCTGGTGTCGGCCGTCGAGAAGAGCCGTCTCAGCGTGCCCCGCAGCGTGCGCCTGTGGACGCTGCGCGGCGGCGGCGGCGGCGGCGGCGGTGGCGCGTGGACGGAGGTGGCGCGGATGCCGCCGGAGGTGCACGCGCAGTTCGCCGCGGCGGAGGGCGGGCGCGGGTTCGAGTGCGCGGCGCACGGCGACTACGTCGTGCTCGCGCCGCGCGGGCCCGTGGCGCAGGCGCCCACGAGCGCGCTCGTGTTCGACTCCCGCCGCGACGAGTGGCGGTGGGCGCCGCCGTGCCCGTACGTCGTCGTCGCGCACCACGGCGGCGCCGGCGCGGCGGGTTTCCGGGTGTTCGCGTACGAGCCCCGGCTGGCGACGCCGGCCATTGGCCTCCTCGACGCCACGGCGCCCGTCGCCTTGCATGGCATGCATGATGGTTAG
CDS Sequence
  • >LOC_Os06g45460.1
    ATGGACCCGCGCGTGTGGCGCCGGCTGCCGCAGCCGCTGGTGGACCGCATCCTGGCGTGCCTCCCGACGCCGTCGTTCCTCCGCCTCCGCGCCGCCTGCCGCCGCTTCTACCACCTCCTCTTCTCCTCCCCGTTCCTCCACTCCCACCTCCTCCTCTCCCCTCACCTCCCCTTCTTCGCCTTCGTCGTCCCCGCCGCCGGCCACCTCCTCCTCCTCGACCCCACCGCCACCGCCTCCTGGTCCCGCCTCCCGCTCCCGCTCCCGCCCGTCGCCGGCGGCCCCGCCGCGTTCTCGCCCGCGGCCGCGTCCGCCGGCCTGCTCGCGTTCCTGTCCGACGCGTCGGGGCACAAGACGCTGCTGCTCGCCAACCCGATCACCCGCCTCCTCGCCGCGCTCCCCATCTCCCCGACCCCGCGCCTCTCCCCCACCGTCGGCCTCGCCGCCGGCCCGACCTCCATCATCGCCGTCGTGGCCGGGGACGACCTCGTGTCCCCCTTCGCCGTCAAGAACATCTCCGCCGACACGTTCGTCGCCGACGCCGCCTCCGTCCCGCCCTCCGGCTTCTGGGCTCCCAGCTCCCTGCTCCCTCGCCTCTCCTCCCTCGATCCCCGCGCCGGCATGGCCTTCGCCTCCGGCAGGTTCTACTGCATGAGCTCGTCGCCGTTTGCGGTTCTGGTGTTCGACGTGGCGGAGAACGTATGGAGCAAGGTGCAGCCGCCGATGAGGCGGTTCCTGAGGTCGCCGGCGCTGGTGGAGCTCGGCGGCGGGAGGGAGGGAGCGGCGAGGGTGGCGCTGGTGTCGGCCGTCGAGAAGAGCCGTCTCAGCGTGCCCCGCAGCGTGCGCCTGTGGACGCTGCGCGGCGGCGGCGGCGGCGGCGGCGGTGGCGCGTGGACGGAGGTGGCGCGGATGCCGCCGGAGGTGCACGCGCAGTTCGCCGCGGCGGAGGGCGGGCGCGGGTTCGAGTGCGCGGCGCACGGCGACTACGTCGTGCTCGCGCCGCGCGGGCCCGTGGCGCAGGCGCCCACGAGCGCGCTCGTGTTCGACTCCCGCCGCGACGAGTGGCGGTGGGCGCCGCCGTGCCCGTACGTCGTCGTCGCGCACCACGGCGGCGCCGGCGCGGCGGGTTTCCGGGTGTTCGCGTACGAGCCCCGGCTGGCGACGCCGGCCATTGGCCTCCTCGACGCCACGGCGCCCGTCGCCTTGCATGGCATGCATGATGGTTAG
Protein Sequence
  • >LOC_Os06g45460.1
    MDPRVWRRLPQPLVDRILACLPTPSFLRLRAACRRFYHLLFSSPFLHSHLLLSPHLPFFAFVVPAAGHLLLLDPTATASWSRLPLPLPPVAGGPAAFSPAAASAGLLAFLSDASGHKTLLLANPITRLLAALPISPTPRLSPTVGLAAGPTSIIAVVAGDDLVSPFAVKNISADTFVADAASVPPSGFWAPSSLLPRLSSLDPRAGMAFASGRFYCMSSSPFAVLVFDVAENVWSKVQPPMRRFLRSPALVELGGGREGAARVALVSAVEKSRLSVPRSVRLWTLRGGGGGGGGGAWTEVARMPPEVHAQFAAAEGGRGFECAAHGDYVVLAPRGPVAQAPTSALVFDSRRDEWRWAPPCPYVVVAHHGGAGAAGFRVFAYEPRLATPAIGLLDATAPVALHGMHDG*