2004 Fiscal Year Final Research Report Summary
Molecular genetic analyses of the plant shoot formation using Arabidopsis mutants.
| Project/Area Number |
15570027
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
植物生理・分子
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| Research Institution | OKAYAMA UNIVERSITY (2004)
Hokkaido University (2003) |
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Principal Investigator |
TAKAHASHI Taku Okayama University, Faculty of Science, Professor, 理学部, 教授 (20271710)
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| Project Period (FY) |
2003 – 2004
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| Keywords | Arabidopsis / polyamine / mutants / development / shoot formation |
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| Research Abstract |
In a previous study, loss-of-function mutations of the ACL5 gene, which encodes spermine synthase in Arabidopsis thaliana, have been shown to result in a severely dwarfed phenotype. To know further the function of polyamines in plants, mutants defective in the synthesis of spermidine and spermine were characterized. The Arabidopsis genome has two genes for spermidine synthase, SPDS1 and SPDS2, and two for spermine synthase, ACL5 and SPMS. spds1 spds2 double mutants were found to be embryonic lethal, suggesting that spermidine is essential for survival of plants, while acl5-1 spms-1 double mutants are fully as viable as the wild type and show no phenotype except for the reduced stem growth due to acl5-1. This suggests that ACL5 and SPMS function in different aspects of the plant growth.
To elucidate the molecular basis of the mode of actions of spermine in plant shoot development, Suppressor of acl5 (Sac) mutants were isolated from homozygous acl5 plants as mutants that suppress the dwarfed phenotype of acl5. So far, four mutations have been identified. Fine mapping experiments and DNA sequence determination revealed that the Sac51-1 allele contains a point mutation in an upstream ORF (uORF) of a gene encoding a putative transcription factor.
On the other hand, the short stem and midrib (ssm) mutants showing both semi-dwarf and wavy leaf phenotypes were isolated and characterized. Map-based cloning of the gene that is defective in ssm mutants has uncovered a small deletion in the 6th intron of a gene encoding a syntaxin, VAM3/SYP22, which has been implicated in vesicle transport to the vacuole.
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Research Products
(6 results)
