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We have identified sequences at the telomeres of the yeast Candida albicans and have found that they are composed of tandem copies of a 23-bp sequence. Through the cloning of native telomeric ends and the characterization and cloning of a "healed" end, we demonstrate that these repeated sequences are sufficient to function as a telomere. All copies of the 23-bp repeat that have been sequenced from a number of C. albicans strains are identical. In contrast, adjacent subtelomeric sequences are variable both between strains and within the WO-1 strain. In the WO-1 strain, the lengths of the telomeres are dependent upon growth temperature and are substantially longer at higher temperatures. Telomere growth is accompanied by increases in the number of the 23-bp repeats present on the telomeric fragments. These results suggest that either telomerase-maintained telomeres can be more complex in structure than was previously imagined or that Candida telomeres are maintained via a telomerase-independent mechanism. 相似文献
3.
Dosage of the smallest chromosome affects both the yeast-hyphal transition and the white-opaque transition of Candida albicans WO-1. 总被引:6,自引:2,他引:4
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The WO-1 strain of Candida albicans is capable of alternating between two highly distinct yeast cell types termed white and opaque (E. H. A. Rikkerrink, B. B. Magee, and P. T. Magee, J. Bacteriol. 170:895-899, 1988; B. Slutsky, M. Staebell, J. Anderson, L. Risen, M. Pfaller, and D. R. Soll, J. Bacteriol. 169:189-197, 1987). We have isolated WO-1 mutants that show a marked deficiency at being able to switch from the white form to the opaque form under conditions normally favorable for this transition. Pulsed-field electrophoresis demonstrated that one of the initial two spontaneous nonswitching mutants lacked the smallest chromosome that is normally present in WO-1. The availability of a WO-1 derivative whose only functional ADE2 gene is located on this small chromosome made possible, through the induction of chromosome nondisjunction, the isolation of numerous new mutants missing this chromosome as well as mutants containing two copies of the chromosome. Mutants missing the smallest chromosome showed a greatly diminished ability to produce opaque sectors and to produce germ tubes in the presence of human serum. Mutants containing two copies of the small chromosome showed an increased ability to produce germ tubes. These results indicate that this small chromosome carries one or more genes involved in both the white-opaque switch and the yeast-hyphal switch. 相似文献
4.
D. S. McEachern 《CMAJ》1945,53(5):421-425
5.
Katherine E. Horn Stephen D. Glasgow Delphine Gobert Sarah-Jane Bull Tamarah Luk Jacklyn Girgis Marie-Eve Tremblay Danielle McEachern Jean-François Bouchard Michael Haber Edith Hamel Paul Krimpenfort Keith K. Murai Anton Berns Guy Doucet C. Andrew Chapman Edward S. Ruthazer Timothy E. Kennedy 《Cell reports》2013,3(1):173-185
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6.
BACKGROUND: In patients with impalpable testes,laparoscopy or open surgery is considered conclusive in establishing the absence of testicular tissue. METHODS: Retrospective chart review. RESULTS: Over a 22-year period, 4 out of 82 patients with a diagnosis of bilateral anorchia by laparoscopy or laparotomy had persistent testicular tissue suggested by endocrine evaluations. The clue to the presence of testicular tissue was: (1) a pubertal rise in plasma testosterone (2 patients); (2) the presence of possible Müllerian structures and of a detectable plasma anti-Müllerian hormone (1 patient), and (3) the fact that one of the gonads had not been seen at surgery (1 patient who still had a testosterone response to hCG postoperatively). Testes were localized by venography (3 patients) and laparotomy (1 patient). CONCLUSION: A surgical diagnosis of bilateral anorchia needs to be confirmed by hCG stimulation, gonadotropin levels, or other markers of testicular function. 相似文献
7.
We report that recombination rates specifically increase by up to 10(3) near shortened telomeres in K. lactis cells. This occurs in cells lacking telomerase that undergo growth senescence as well as in cells with stably shortened telomeres that cause little effect on cell growth. The high rates of gene conversion allowed a subtelomeric marker, initially present at a single telomere, to efficiently spread to most or all other telomeres in the cell. We propose that short telomeres in K. lactis are not fully competent at capping chromosome ends and hence are occasionally processed by proteins that normally act to repair broken DNA ends through recombination. This helps explain how recombination can be frequent enough to permit maintenance of telomeres in yeast cells lacking telomerase. 相似文献
8.
McEachern G Kassovska-Bratinova S Raha S Tarnopolsky MA Turnbull J Bourgeois J Robinson B 《Biochemical and biophysical research communications》2000,273(1):359-363
The most frequent genetic causes of amyotrophic lateral sclerosis (ALS) determined so far are mutations occurring in the gene for copper/zinc superoxide dismutase (CuZnSOD). The mechanism may involve inappropriate formation of hyroxyl radicals, peroxynitrite or malfunctioning of the SOD protein. We hypothesized that undiscovered genetic causes of sporadically occurring amyotrophic lateral sclerosis might be found in the mechanisms that create and destroy oxygen free radicals within the cell. After determining that there were no CuZnSOD mutations present, we measured superoxide production from mitochondria and manganese superoxide dismutase (MnSOD), glutathione peroxidase, NFkappaB, Bcl-2 and Bax by immunoblot. Of the ten sporadic patients we tested we found three patients with significantly increased concentrations of MnSOD. These patients also had lower levels of superoxide production from mitochondria and decreased expression of Bcl-2. No mutations were found in the cDNA sequence of either MnSOD in any of the sporadic patients. A patient with a CuZnSOD mutation (G82R) used as a positive control showed none of these abnormalities. The patients displaying the MnSOD aberrations showed no specific distinguishing features. This result suggests that the cause of ALS in a subgroup of ALS patients (30%) is genetic in origin and can be identified by these markers. The alteration in MnSOD and Bcl-2 are likely epiphenomena resulting from the primary genetic defect. It suggests also that the oxygen free radicals are part of the cause in this subgroup and that dysregulation of MnSOD or increased endogenous superoxide production might be responsible. 相似文献
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Annemarie MM Vlaar Angela EP Bouwmans Marinus JPG van Kroonenburgh Werner H Mess Selma C Tromp Piet GWM Wuisman Alfons GH Kessels Ania Winogrodzka Wim EJ Weber 《BMC neurology》2007,7(1):28