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Nucleic Acids Research, 1993, Vol. 21, No. 3 657-662
© 1993

MOLECULAR BIOLOGY

Fine mapping of mitochondrial RNAs derived from the mtDNA region containing a point mutation associated with MELAS

Yasutoshi Koga1, Mercy Davidson1, Eric A. Schon1,2 and Michael P. King1,*

1Departments of Neurology, Columbia University College of Physicians and Surgeons 630 West 168th Street, New York, NY 10032, USA 2Departments of Genetics and Development, Columbia University College of Physicians and Surgeons 630 West 168th Street, New York, NY 10032, USA

* To whom correspondence should be addressed

Received September 21, 1992. Revised December 30, 1992. Accepted December 30, 1992.

Mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) is a mitochondrial disorder associated with heteroplasmic point mutations in the mitochondrial tRNALeu(UUR) gene. While previous studies have shown that the MELAS mutation at nt-3243 results in impairments in mitochondrial protein synthesis and respiratory chain function, it was not clear whether these were associated with structural alterations in mature RNAs derived from transcription of the region containing the mutation. We have performed fine mapping and high-resolution Northern analysis of RNAS from cybrids derived from two MELAS patients harboring the nt-3243 mutation. No differences in the size or steady-state levels of transcripts from the 16S rRNA, tRNALeu(UUR), or ND 1 genes (which are contiguous in the mtDNA) were observed between cell lines containing mutated or wild-type mtDNAs. Therefore, it is not likely that the protein synthesis defects observed in cybrids with the MELAS-3243 mutation are directly caused by qualitative alterations in either transcription termination or processing of these mitochondrial RNAs.


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