Nutritional Control of Cellular Form in Trigonopsis variabilis

Sentheshanmuganathan, S.; Nickerson, Walter J.

doi:10.1099/00221287-27-3-437

Cited by 32 publications

(13 citation statements)

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“…For example, Ceratocystis ulmi cells grow as yeasts in the presence of proline but as hyphae in the presence of ammonia, arginine and most other nitrogen sources (Kulkarni & Nickerson, 1981). Trigonopsis variabilis cells grow as budding yeasts in the presence of ammonium sulfate and as triangles with methionine (Sentheshanmuganathan & Nickerson, 1962). …”

Section: Introductionmentioning

confidence: 99%

Dur3 is the major urea transporter in Candida albicans and is co-regulated with the urea amidolyase Dur1,2

et al. 2011

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Hemiascomycetes, including the pathogen Candida albicans, acquire nitrogen from urea using the urea amidolyase Dur1,2, whereas all other higher fungi use primarily the nickel-containing urease. Urea metabolism via Dur1,2 is important for resistance to innate host immunity in C. albicans infections. To further characterize urea metabolism in C. albicans we examined the function of seven putative urea transporters. Gene disruption established that Dur3, encoded by orf 19.781, is the predominant transporter. [14C]Urea uptake was energy-dependent and decreased approximately sevenfold in a dur3Δ mutant. DUR1,2 and DUR3 expression was strongly induced by urea, whereas the other putative transporter genes were induced less than twofold. Immediate induction of DUR3 by urea was independent of its metabolism via Dur1,2, but further slow induction of DUR3 required the Dur1,2 pathway. We investigated the role of the GATA transcription factors Gat1 and Gln3 in DUR1,2 and DUR3 expression. Urea induction of DUR1,2 was reduced in a gat1Δ mutant, strongly reduced in a gln3Δ mutant, and abolished in a gat1Δ gln3Δ double mutant. In contrast, DUR3 induction by urea was preserved in both single mutants but reduced in the double mutant, suggesting that additional signalling mechanisms regulate DUR3 expression. These results establish Dur3 as the major urea transporter in C. albicans and provide additional insights into the control of urea utilization by this pathogen.

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Section: Introductionmentioning

confidence: 99%

Dur3 is the major urea transporter in Candida albicans and is co-regulated with the urea amidolyase Dur1,2

et al. 2011

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“…For instance, the growth morphology of Ceratocystis ulmi and Trigonopsis variabilis could be modulated by the source of nitrogen. For C. ulmi , the cells grew as yeasts with proline and as hyphae with ammonia, arginine, and most other nitrogen sources (Kulkarni & Nickerson, 1981), while for T. variabilis , the cells grew as budding yeasts with ammonium sulfate and as triangles with methionine (Sentheshanmuganathan & Nickerson, 1962). One nitrogen source that has been understudied in Candida albicans is urea.…”

Section: Introductionmentioning

confidence: 99%

Evolutionary aspects of urea utilization by fungi

Navarathna

Harris

Roberts

et al. 2010

FEMS Yeast Research

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The higher fungi exhibit a dichotomy with regard to urea utilization. The hemiascomycetes use urea amidolyase (DUR1,2) whereas all other higher fungi use the nickel-containing urease. Urea amidolyase is an energy dependent biotin-containing enzyme. It likely arose prior to the Euascomycete/Hemiascomycete divergence ca. 350 million years ago by insertion of an unknown gene into one copy of a duplicated methylcrotonyl CoA carboxylase (MccA). The dichotomy between urease and urea amidolyase coincides precisely with that for the Ni/Co transporter (Nic1p) which is present in the higher fungi that use urease and absent in those that do not. We suggest that the selective advantage for urea amidolyase is that it allowed the hemiascomycetes to jettison all Ni 2+ and Co 2+ dependent metabolism and thus to have two fewer transition metals whose concentrations need to be regulated. Also, the absence of MccA in the hemiascomycetes coincides with and may explain their production of fusel alcohols.

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“…Numerous chemical and environmental parameters have been reported to shift the yeast-mycelium dimorphism. Among these have been temperature (18), pH (18), glucose levels (2,3,5,18), nitrogen source (12,22), carbon dioxide levels (2), and transition metals and chelating agents (3,8,17,18), as well as the inoculum size or cell density employed (3,12,19,24).…”

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Inoculum Size Effect in Dimorphic Fungi: Extracellular Control of Yeast-Mycelium Dimorphism in Ceratocystis ulmi

Hornby

Jacobitz-Kizzier

McNeel

et al. 2004

Appl Environ Microbiol

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We studied the inoculum size effect in Ceratocystis ulmi, the dimorphic fungus that causes Dutch elm disease. In a defined glucose-proline-salts medium, cells develop as budding yeasts when inoculated at >10 6 spores per ml and as mycelia when inoculated at <10 6 spores per ml. The inoculum size effect was not influenced by inoculum spore type, age of the spores, temperature, pH, oxygen availability, trace metals, sulfur source, phosphorous source, or the concentration of glucose or proline. Similarly, it was not influenced by added adenosine, reducing agents, methyl donors, amino sugars, fatty acids, or carbon dioxide. Instead, growing cells excreted an unknown quorum-sensing factor that caused a morphological shift from mycelia to budding yeasts. This yeast-promoting effect is abolished if it is extracted with an organic solvent such as ethyl acetate. The quorum-sensing activity acquired by the organic solvent could be added back to fresh medium in a dosedependent fashion. The quorum-sensing activity in C. ulmi spent medium was specific for C. ulmi and had no effect on the dimorphic fungus Candida albicans or the photomorphogenic fungus Penicillium isariaeforme. In addition, farnesol, the quorum-sensing molecule produced by C. albicans, did not inhibit mycelial development of C. ulmi when present at concentrations of up to 100 M. We conclude that the inoculum size effect is a manifestation of a quorum-sensing system that is mediated by an excreted extracellular molecule, and we suggest that quorum sensing is a general phenomenon in dimorphic fungi.Fungal dimorphism is defined (20) as an environmentally controlled reversible interconversion of the yeast and mycelial morphologies. Interest in this phenomenon derives from the prevalence of dimorphism among those fungi exhibiting pathogenicity towards plants and animals. Numerous chemical and environmental parameters have been reported to shift the yeast-mycelium dimorphism. Among these have been temperature (18), pH (18), glucose levels (2, 3, 5, 18), nitrogen source (12, 22), carbon dioxide levels (2), and transition metals and chelating agents (3,8,17,18), as well as the inoculum size or cell density employed (3,12,19,24).We have been studying quorum sensing in the regulation of yeast-mycelium dimorphism in fungi. In Candida albicans, we recently showed (9) that the inoculum size effect results from production of farnesol. Farnesol is continuously excreted by C. albicans during growth in amounts roughly proportional to the number of CFU per milliliter. At a sufficiently high level (1 to 5 M), farnesol prevents mycelial development during growth. It also blocks germ tube formation caused by three chemically distinct triggers: L-proline, N-acetylglucosamine, and serum. In all cases, the presence of farnesol at concentrations of up to 250 M prevents the yeast-to-mycelium conversion, resulting in actively budding yeasts without influencing cellular growth (9). Farnesol exhibits general cross-reactivity within C. albicans in that supernatants from strain A72 are act...

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Nutritional Control of Cellular Form in Trigonopsis variabilis

Cited by 32 publications

References 12 publications

Dur3 is the major urea transporter in Candida albicans and is co-regulated with the urea amidolyase Dur1,2

Dur3 is the major urea transporter in Candida albicans and is co-regulated with the urea amidolyase Dur1,2

Evolutionary aspects of urea utilization by fungi

Inoculum Size Effect in Dimorphic Fungi: Extracellular Control of Yeast-Mycelium Dimorphism in Ceratocystis ulmi

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