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Mutants in paramecium tetraurelia defective in their axonemal response to calcium (1984)

Hinrichsen, Robert D. ; Saimi, Yoshiro ; Hennessey, Todd ; [et al.]

New York, NY : Wiley-Blackwell

Cell Motility and the Cytoskeleton 4 (1984), S. 283-295

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ISSN: 0886-1544

Keywords: axonemal mutants ; Ca++ response ; ciliary reversal ; electrophysiology ; models ; Life and Medical Sciences ; Cell & Developmental Biology

Source: Wiley InterScience Backfile Collection 1832-2000

Topics: Biology , Medicine

Notes: Six mutants of Paramecium tetraurelia, which display altered axonemal responses to Ca++, are described. The mutants, designated atalantas, are impaired in their ability to swim backward when stimulated by ions or heat; instead they spin very rapidly in one place. Three mutants, ataA1-3, are completely unable to swim backward. The three lines, however, can be distinguished from one another by their forward swimming velocities. The remaining three mutants are leaky. ataB swims backward briefly when stimulated, then stops and spins in place. ataC and ataD are extremely leaky and only display the spinning phenotype at elevated temperatures. An electrophysiological analysis reveals that all six mutants have normal membrane properties, including the Ca++ inward current under voltage clamp. When the membrane is disrupted so as to allow the axoneme free access to Ca++, wild-type cells swim backward, but the mutants do not. These data indicate the site(s) of lesion in the mutants is in the axoneme or in some step linking Ca++ influx and the axoneme, not within the ciliary membrane. These mutants may be useful in investigating the role of Ca++ in the regulation of axonemal motion.

Additional Material: 4 Ill.

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1002/cm.970040406

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Interactions between gene products involved in divalent cation transport in Saccharomyces cerevisiae (1994)

Conklin, Douglas S. ; Culbertson, Michael R. ; Kung, Ching

Springer

Molecular genetics and genomics 244 (1994), S. 303-311

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ISSN: 1617-4623

Keywords: Metal homeostasis ; Metal resistance ; Transport ; Yeast

Source: Springer Online Journal Archives 1860-2000

Topics: Biology

Notes: Abstract The COT1 and ZRC1 genes of Saccharomyces cerevisiae are structurally related dosage-dependent suppressors of metal toxicity. COT1 confers increased tolerance to high levels of cobalt; ZRC1 confers increased tolerance to high levels of zinc. The two genes are not linked and have been mapped; COT1 to chromosome XV and ZRC1 to chromosome XIII. Phenotypes related to metal homeostasis have been examined in strains with varied COT1 and ZRC1 gene doses. Overexpression of COT1 confers tolerance to moderately toxic levels of zinc and ZRC1 confers tolerance to moderately toxic levels of cobalt. Strains that carry null alleles at both loci are viable. The metal-hypersensitive phenotypes of mutations in either gene are largely unaffected by changes in dosage of the other. COT1 and ZRCI function independently in conferring tolerance to their respective metals, yet the uptake of cobalt ions by yeast cells is dependent on the gene dosage of ZRC1 as well as of COT1 Strains that overexpress ZRC1 have increased uptake of cobalt ions, while ZRCI null mutants exhibit decreased cobalt uptake. The defects in cobalt uptake due to mutations at COT1 and ZRC1 are additive, suggesting that the two genes are responsible for the majority of cobalt and zinc uptake in yeast cells. The function of either gene product seems to be more important in metal homeostasis than is the GRR1 gene product, which is also involved in metal metabolism. Mutations in the GRR1 gene have no effect on the cobalt-related phenotypes of strains that have altered gene dosage of either COT1 or ZRC1.