| Suppression of mycelia formation by NO produced endogenously in Candida tropicalis. | |
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MedLine Citation:
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PMID: 10219571 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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In the experiments reported here we found that enzymatic NO synthesis in the yeast Candida tropicalis resembles the one in animal tissues with respect to the substrate arginine as well as its sensitivity to potential competitive inhibitors. Both, NO produced by the yeast's nitric oxide synthase and NO derived from an artificial donor, suppressed the formation of pseudomycelia. These results suggest to make use of NO as a tool in elucidating the mechanism controlling mycelia generation in this yeast. The apparent K(m) towards oxygen of the yeast's nitric oxide synthase (about 50 microM) was found to be high as compared to the apparent K(m) value of the yeast's respiratory chain (about 170 nM). From this observation it may be concluded that under conditions of little oxygen supply the nitric oxide synthase will unsuccessfully compete for oxygen with respiration. Therefore, the formation of mycelia spontaneously occurring in yeast cultures grown in sealed chambers can be attributed to a reduced internal NO level rather than limited respiratory activity. |
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Authors:
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M Wilken; B Huchzermeyer |
Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: European journal of cell biology Volume: 78 ISSN: 0171-9335 ISO Abbreviation: Eur. J. Cell Biol. Publication Date: 1999 Mar |
Date Detail:
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Created Date: 1999-07-29 Completed Date: 1999-07-29 Revised Date: 2000-12-18 |
Medline Journal Info:
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Nlm Unique ID: 7906240 Medline TA: Eur J Cell Biol Country: GERMANY |
Other Details:
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Languages: eng Pagination: 209-13 Citation Subset: IM |
Affiliation:
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ITZ, School of Veterinary Medicine Hannover, Germany. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Candida
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metabolism* Nitric Oxide / biosynthesis* Oxidation-Reduction Oxygen Consumption Oxyhemoglobins / metabolism |
| Chemical | |
Reg. No./Substance:
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0/Oxyhemoglobins; 10102-43-9/Nitric Oxide |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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