RECOMBIO: Recombination mechanisms in higher plants and their use in plant biotechnology

• Unité de recherche: PCRD EU
• Numéro de projet: 96.0402-1
• Titre du projet anglais: RECOMBIO: Recombination mechanisms in higher plants and their use in plant biotechnology

Mots-clé (Anglais)

DNA repair; homologous recombination; Arabidopsis thaliana;SAMC protein

Autre Numéro de projet (Anglais)

EU project number: BIO4CT972028

Programme de recherche (Anglais)

EU-programme: 4. Frame Research Programme - 4.1 Biotechnology

Description succincte (Anglais)

See abstract

Autres indications (Anglais)

Full name of research-institution/enterprise:
Friedrich Miescher Institut
(Novartis Forschungsstiftung, Zweigniederlassung)

Partenaires et organisations internationales (Anglais)

Coordinator: Amica-Science-EEIG (UK)

Résumé des résultats (Abstract) (Anglais)

A T-DNA insertional mutant of Arabidopsis which is called mim was isolated and shows hypersensitivity to methyl methanesulfonate (MMS), irradiation, and mitomycin C (MMC), suggesting a defect in repair of DNA damage. The affected gene (MIM) encodes a protein with all structural features of a member of the SMC (Structure Maintenance of Chromosome) protein family. Evidence has been accumulating about the importance of SMCs in various chromosome activities (mitotic chromosome condensation, sister chromatid cohesion, recombinational repair and dosage compensation). The Arabidopsis SMC is most similar to RAD18 and RHC18 from Saccharomyces pombe and S. cerevisiae, respectively, which are involved in recombinational repair. We have performed intrachromosomal recombination (ICR) assays in somatic tissues of mim and wild type plants, using a transgenic recombination line with direct repeats of overlapping parts of a chimeric b-glucuronidase (GUS) gene. Our data suggest a deficiency in homologous recombination (HR) in the mutant, and its complemetation with MIM restored recombination properties to the wild type level. On the other hand, we have found that MIM is required for efficient DNA repair of double strand breaks caused by HR but is not critical for its induction. Furthermore, MIM does not seem to influence other repair pathways such as non-homologous end joining (NHEJ), since the T-DNA integration patterns in the mutant and wild type are comparable. It might be that MIM expression, after occurrence of DSB, influences the choice between HR and other repair pathways. This is supported by two Arabidopsis lines overexpressing the MIM gene: they show a two-fold increase of ICR frequency relative to the wild type. These data reinforce the hypothesis that MIM as an SMC-like protein may be involved in modification of chromatin structure allowing entry of the HR machinery but not of other repair complexes. Our results represent one step towards regulation of HR in plants using endogenous factors.

Références bases de données (Anglais)

Swiss Database: Euro-DB of the
State Secretariat for Education and Research
Hallwylstrasse 4
CH-3003 Berne, Switzerland
Tel. [phone]
Swiss Project-Number: 96.0402-1