Published April 1997 | Version Published
Journal Article Open

A Dominant Mutation in the Chlamydomonas reinhardtii Nuclear Gene SIM30 Suppresses Translational Defects Caused by Initiation Codon Mutations in Chloroplast Genes

Abstract

A suppressor of a translation initiation defect caused by an AUG to AUU mutation in the Chlamydomonas reinhardtii chloroplast petD gene was isolated, defining a nuclear locus that we have named SIM30. A dominant mutant allele at this locus, sim30-1d, was found to increase the translation initiation rate of the mutant petD mRNA. sim30-1d was also able to suppress the translational defect caused by an AUG to AUC mutation in the petD gene, and an AUG to AUU mutation in the chloroplast petA gene. We therefore suggest that the SIM30 gene may encode a general chloroplast translation factor. The ability of sim30-1d to suppress the petD AUG to AUU mutation is diminished in the presence of one or more antibiotic resistance markers located within the 16S and 23S rRNAs, suggesting that the activity of the sim30-1d gene product in translation initiation may involve interaction with ribosomal subunits.

Additional Information

© 1997 by the Genetics Society of America. Received October 17, 1996. Accepted January 13, 1997. We are grateful to Dr. ELIZABETH HARRIS of the Chlamydomonas Stock Center at Duke University for providing us with the strains CC1861 and CC1930 and the plasmid p-183, and to Dr. NANCY STURM for her efforts in the initial characterization of iniD2 suppressor strains. This work was supported by National Science Foundation grant DMB 9105652 to K.L.K. and D.B.S. X.C. was supported by a NSF/DOE/USDA Plant Science Center fellowship.

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Identifiers

PMCID
PMC1207898
Eprint ID
108376
Resolver ID
CaltechAUTHORS:20210310-072841505

Funding

NSF
DMB-9105652
Department of Energy (DOE)
United States Department of Agriculture (USDA)

Dates

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2021-03-10
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2021-03-10
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