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Genetic evidence for interaction between eta- and beta-tubulins.

ABSTRACT: The thermosensitive allelic mutations sm19-1 and sm19-2 of Paramecium tetraurelia cause defective basal body duplication: growth at the nonpermissive temperature yields smaller and smaller cells with fewer and fewer basal bodies. Complementation cloning of the SM19 gene identified a new tubulin, eta-tubulin, showing low homology with each of the other five tubulins, alpha to epsilon, characterized in P. tetraurelia. In order to analyze eta-tubulin functions, we used a genetic approach to identify interacting molecules. Among a series of extragenic suppressors of the sm19-1 mutation, the su3-1 mutation was characterized as an E288K substitution in the beta-PT2 gene coding for a beta-tubulin, while the mutation nocr1 conferring nocodazole resistance and localized in another beta-tubulin gene, beta-PT3, was shown to enhance the mutant phenotype. The interaction between eta-tubulin and microtubules, revealed by genetic data, is supported by two further types of evidence: first, the mutant phenotype is rescued by taxol, which stabilizes microtubules; second, molecular modeling suggests that eta-tubulin, like gamma- and delta-tubulins, might be a microtubule minus-end capping molecule. The likely function of eta-tubulin as part of a complex specifically involved in basal body biogenesis is discussed.

SUBMITTER: Ruiz F

PROVIDER: S-EPMC329518 | biostudies-literature | 2004 Feb

REPOSITORIES: biostudies-literature

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Genetic evidence for interaction between eta- and beta-tubulins.

Ruiz F F Dupuis-Williams P P Klotz C C Forquignon F F Bergdoll M M Beisson J J Koll F F

Eukaryotic cell 20040201 1

The thermosensitive allelic mutations sm19-1 and sm19-2 of Paramecium tetraurelia cause defective basal body duplication: growth at the nonpermissive temperature yields smaller and smaller cells with fewer and fewer basal bodies. Complementation cloning of the SM19 gene identified a new tubulin, eta-tubulin, showing low homology with each of the other five tubulins, alpha to epsilon, characterized in P. tetraurelia. In order to analyze eta-tubulin functions, we used a genetic approach to identif ...[more]

PMID: 14871951

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Project description:Study hypothesis: CRC risk is affected by diet and by genetic polymorphisms leading to inter-individual variation in the metabolism of environmental carcinogens. Our first hypothesis is that these effects may combine to place certain individuals at greatly enhanced risk according to their diet. We shall examine how dietary factors known to affect CRC risk (including meats, fat, fruit and vegetables, cooking methods, dietary supplements and drugs) and genetic polymorphisms implicated in CRC (Glutathione S-transferase: GSTM1, GSTM3, GSTT1; N-acetyl transferase: NAT1, NAT2; and Cytochrome P450: CYP1A1, CYP2D6) combine to affect the prevalence of colorectal polyps, both adenomatous (the precursor lesion of CRC) and metaplastic. Our second hypothesis is that diets associated with increased risk (high red meat, low vegetable and low fibre consumption) may affect DNA damage markers which may be elevated in people with colorectal adenomas. We shall therefore examine the effect of diet on adduct rates (cross sectional) and adduct rates in people with and without colorectal adenomas. We shall examine malondialdehyde adduct rates in relation to anti-oxidant status and carboxymethyl adduct rates and k-ras mutation frequency in relation to meat consumption; and examine the effect of DNA repair enzyme (ATase) activity on any relationship found. In summary the aim of this population based study is to link dietary factors thought to be important in the genesis of colorectal polyps and cancer with genetic polymorphisms and DNA damage markers in rectal mucosa and in blood. Primary outcome(s): We shall perform cross-sectional and case-control analyses of the effect of diet and genetic polymorphisms on the prevalence of adenomatous and metaplastic polyps. Genetic polymorphisms will be examined in isolation and paired combinations and in groups stratified according to diet. We shall examine the effect of diet on MDA adduct rates (concentrating on foods relating to anti-oxidant status) and CBM adduct rates and k-ras mutations (concentrating on meat consumption and cooking methods) by categorical variables; and MDA and CBM adducts and k-ras mutation frequency in people with adenomatous polyps and polyp free controls (case-control). We shall examine the affect of ATase activity on any relationship found and ATase activity in people with adenomatous polyps and polyp free controls (case control). DNA will be stored for future analysis of as yet unrecognised polymorphisms which may be recognised as having a role in CRC. Samples taken from EPIC participants for adduct, ATase and k-ras measurement whose polyps are found to be metaplastic will be stored for possible future analysis: we shall investigate people with adenomatous polyps in the first instance as these are the precursors of colorectal cancer.

Dataset Information

Genetic evidence for interaction between eta- and beta-tubulins.

Publications

Genetic evidence for interaction between eta- and beta-tubulins.

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