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Isolation and analysis of the Neurospora crassa Cyt-21 gene. A nuclear gene encoding a mitochondrial ribosomal protein
The Neurospora crassa nuclear mutant cyt-21-1 (originally 297-24; Pittenger, T.H., and West, D.J. (1979) Genetics 93, 539-555) has a defect leading to gross deficiency of mitochondrial small ribosomal subunits. Here, we have cloned the cyt-21+ gene from a N. crassa genomic library, using the sib sel...
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Published in: | The Journal of biological chemistry 1988-02, Vol.263 (6), p.2840-2847 |
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Main Authors: | , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | The Neurospora crassa nuclear mutant cyt-21-1 (originally 297-24; Pittenger, T.H., and West, D.J. (1979) Genetics 93, 539-555) has a defect leading to gross deficiency of mitochondrial small ribosomal subunits. Here, we have cloned the cyt-21+ gene from a N. crassa genomic library, using the sib selection procedure (Akins, R. A., and Lambowitz, A. M. (1985) Mol. Cell Biol. 5, 2272-2278). The genomic clone contains a short split gene encoding a basic protein of 107 amino acid residues. This protein shows strong homology to Escherichia coli ribosomal protein S-16. Comparison of mutant and wild-type mitochondrial ribosomal proteins (Kuiper, M. T. R., Holtrop, M., Vennema, H., Lambowitz, A. M., and de Vries, H. (1988) J. Biol. Chem. 263, 2848-2852) indicates that the cyt-21 gene encodes N. crassa mitochondrial ribosomal protein S-24. The expression of the cyt-21+ gene is regulated such that the level of the putative cyt-21+ mRNA is increased about 5-fold when mitochondrial protein synthesis is inhibited. We suggest that this reflects part of a general mechanism for coordinately activating Neurospora nuclear genes that encode mitochondrial constituents in response to impaired mitochondrial function. This is the first report of the cloning and characterization of a mitochondrial ribosomal protein gene from N. crassa. |
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ISSN: | 0021-9258 1083-351X |
DOI: | 10.1016/s0021-9258(18)69145-8 |