The regulation of inflorescence architecture in Arabidopsis.

Nobutoshi YAMAGUCHI; Yoshibumi KOMEDA

doi:10.5685/plmorphol.19and20.39

Nobutoshi YAMAGUCHI, Yoshibumi KOMEDA

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Keywords: Arabidopsis thaliana, auxin, CRM1/BIG gene, inflorescence development

JOURNAL FREE ACCESS

2008 Volume 19and20 Issue 1 Pages 39-44

DOI https://doi.org/10.5685/plmorphol.19and20.39

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Published: 2008 Received: - Available on J-STAGE: June 28, 2010 Accepted: - Advance online publication: - Revised: -
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Date of correction: June 28, 2010 Reason for correction: - Correction: PDF FILE Details: -

Date of correction: June 28, 2010 Reason for correction: - Correction: KEYWORD Details: Wrong : Key words:Arabidopsis thaliana, auxin, CRM1/BIG gene, inflorescence development
Right : Arabidopsis thaliana, auxin, CRM1/BIG gene, inflorescence development

Date of correction: June 28, 2010 Reason for correction: - Correction: CITATION Details: Wrong : E
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Abstract

The inflorescence architecture in Arabidopsis thaliana accession Columbia is a raceme with individualflowers developing acropetally. The accession Landsberg erecta(er)displays a corymb-like inflorescence. To understand the regulation of inflorescence architecture, we screened corymb-like inflorescence mutants, corymbosal(crm1)and crm2. We focused crm1 mutant and found that reduction of cell elongation in crml pedicels and stem internodes. crml is additive with er or crm2, suggesting CRM1, ER, and CRM2 control inflorescence development independently. Fine mapping and complementation test confirmed that crm1-1is a new allele of BIG, which is required for normal auxin transport. Histochemical analysis and in situ hybridization revealed that CRM1/BIG is highly expressed in inflorescence meristem, floral metistem and vasculature in pedicels and internodes. The decreased levels of auxin-responsive DRS and increased levels of PIN-FORMED1 (PIN1)were observed in crm1-1and wild type treated with auxin transport inhibitor. Furthermore, auxin transport inhibitor treatment also led to the elongation defects of pedicel cells, suggesting that the defect of CRM1/BIG-mediated auxin transport causes these changes. Expression analysis revealed that LEAFY(LFY)and CUP-SHAPED COTYLEDON2(CUC2) were increased in crm1-1mutant. These data strongly suggested the possibility that the cause of morphological change in crm1is not only due to the defect in auxin transport and requirement of examination of relationship between CRM1/BIG and these genes.

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