- 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 Sebastiano, M.
- Articles by Bazzicalupo, P.
- Search for Related Content
- PUBMED
- PubMed Citation
- Articles by Sebastiano, M.
- Articles by Bazzicalupo, P.
ß-GLUCURONIDASE MUTANTS OF THE NEMATODE CAENORHABDITIS ELEGANS
Marisa Sebastiano 1, Marina D'Alessio 1, and Paolo Bazzicalupo 1
1 International Institute of Genetics and Biophysics, Consiglio
Nazionale delle Ricerche, via G. Marconi 10, 80125 Napoli, Italy
Using a screening procedure that is based on a histochemical stain for the enzyme ß-glucuronidase, we have isolated several mutants of the nematode Caenorhabditis elegans affected in ß-glucuronidase activity. All of the mutations fall into one complementation group and identify a new gene, gus-1, which has been mapped on the right arm of linkage group I (LG I), 1.1 map units to the left of unc-54. The mutants have no visible phenotype, and their viabilities and fertilities are unaffected. Linked revertants of two of the mutations have been isolated. They restore enzyme activity to almost wild-type levels; the ß-glucuronidase that one of the revertants produces differs from that of the wild type. We propose that gus-1 is the structural locus for ß-glucuronidase.
Submitted on June 17, 1985Accepted on October 28, 1985
This article has been cited by other articles:
![]() |
J. J. Welch and D. Waxman Nonequivalent Loci and the Distribution of Mutant Effects Genetics, June 1, 2002; 161(2): 897 - 904. [Abstract] [Full Text] [PDF] |
||||
![]() |
N. Szewczyk, J. Hartman, S. Barmada, and L. Jacobson Genetic defects in acetylcholine signalling promote protein degradation in muscle cells of Caenorhabditis elegans J. Cell Sci., January 6, 2000; 113(11): 2003 - 2010. [Abstract] [PDF] |
||||

