- THIS ARTICLE
- Full Text (PDF)
- Alert me when this article is cited
- Alert me if a correction is posted
- SERVICES
- Similar articles in this journal
- Similar articles in PubMed
- Alert me to new issues of the journal
- Download to citation manager
- Reprints & Permissions
- CITING ARTICLES
- Citing Articles via HighWire
- Citing Articles via Google Scholar
- GOOGLE SCHOLAR
- Articles by Evans, T. C.
- Articles by Nelson, D. L.
- Search for Related Content
- PUBMED
- PubMed Citation
- Articles by Evans, T. C.
- Articles by Nelson, D. L.
Genetics, Vol 121, 491-500, Copyright © 1989
INVESTIGATIONS |
New Mutants of Paramecium tetraurelia Defective in a Calcium Control Mechanism: Genetic and Behavioral Characterizations
T. C. Evans and D. L. Nelson
Department of Biochemistry, College of Agricultural and Life Sciences, University of Wisconsin, Madison, Wisconsin 53706
The k-shy mutants of Paramecium tetraurelia are altered in several Ca(2+)-dependent functions which regulate ciliary motility. The isolation, genetics, and phenotypes of these mutants are described. Of six independent isolates, all contained recessive single-factor mutations and comprise two unlinked loci, ksA and ksB. All k-shy strains showed prolonged backward swimming responses to depolarizing stimuli, but gave infrequent responses to some stimuli. At least four k-shy strains displayed temperature sensitivity. Neither ksA nor ksB was allelic or linked to dancer, a mutation causing weak Ca(2+) current inactivation and prolonged backward swimming. Analysis of ks(+);Dn double mutants revealed synergism between the two mutations. The ksA mutant survived Ba(2+) solutions longer than wild type, but was more sensitive to K(+). Together with previous studies, these results are consistent with a defect in reducing intracellular Ca(2+) causing both prolonged ciliary reversal and reduced Ca(2+) channel activity due to more active Ca(2+)-dependent feedback mechanisms. The integration of the Ca(2+)-dependent stimulatory and inhibitory functions is therefore dependent on ks(+) gene functions. The ksA mutant was rescued by microinjection of wild-type cytoplasm, suggesting a possible behavioral assay for factors related to the ksA(+) gene product.
This article has been cited by other articles:
 |
|
 |
|
  J. A. Hammond and R. R. Preston Isolation and Characterization of Magbane, a Magnesium-Lethal Mutant of Paramecium Genetics, July 1, 2001; 158(3): 1061 - 1069. [Abstract] [Full Text] [PDF]
|
|