This Article Full Text Full Text (PDF) Supplemental material 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 Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Slomovic, S. Articles by Schuster, G. Search for Related Content PubMed PubMed Citation Articles by Slomovic, S. Articles by Schuster, G.

Polyadenylation and Degradation of Human Mitochondrial RNA: the Prokaryotic Past Leaves Its Mark

Departments of Biology,¹ Computer Science, Technion—Israel Institute of Technology, Haifa 32000, Israel²

Received 23 March 2005/ Returned for modification 18 April 2005/ Accepted 12 May 2005

RNA polyadenylation serves a purpose in bacteria and organelles opposite from the role it plays in nuclear systems. The majority of nucleus-encoded transcripts are characterized by stable poly(A) tails at their mature 3' ends, which are essential for stabilization and translation initiation. In contrast, in bacteria, chloroplasts, and plant mitochondria, polyadenylation is a transient feature which promotes RNA degradation. Surprisingly, in spite of their prokaryotic origin, human mitochondrial transcripts possess stable 3'-end poly(A) tails, akin to nucleus-encoded mRNAs. Here we asked whether human mitochondria retain truncated and transiently polyadenylated transcripts in addition to stable 3'-end poly(A) tails, which would be consistent with the preservation of the largely ubiquitous polyadenylation-dependent RNA degradation mechanisms of bacteria and organelles. To this end, using both molecular and bioinformatic methods, we sought and revealed numerous examples of such molecules, dispersed throughout the mitochondrial genome. The broad distribution but low abundance of these polyadenylated truncated transcripts strongly suggests that polyadenylation-dependent RNA degradation occurs in human mitochondria. The coexistence of this system with stable 3'-end polyadenylation, despite their seemingly opposite effects, is so far unprecedented in bacteria and other organelles.

Supplemental material for this article may be found at http://mcb.asm.org/.

This article has been cited by other articles:

• Slomovic, S., Schuster, G. (2008). Stable PNPase RNAi silencing: Its effect on the processing and adenylation of human mitochondrial RNA. RNA 14: 310-323 [Abstract] [Full Text]  
• Portnoy, V., Palnizky, G., Yehudai-Resheff, S., Glaser, F., Schuster, G. (2008). Analysis of the human polynucleotide phosphorylase (PNPase) reveals differences in RNA binding and response to phosphate compared to its bacterial and chloroplast counterparts. RNA 14: 297-309 [Abstract] [Full Text]  
• Wilusz, C. J., Wilusz, J. (2008). New ways to meet your (3') end oligouridylation as a step on the path to destruction. Genes Dev. 22: 1-7 [Full Text]  
• Portnoy, V., Schuster, G. (2006). RNA polyadenylation and degradation in different Archaea; roles of the exosome and RNase R. Nucleic Acids Res 34: 5923-5931 [Abstract] [Full Text]  
• Lung, B., Zemann, A., Madej, M. J., Schuelke, M., Techritz, S., Ruf, S., Bock, R., Huttenhofer, A. (2006). Identification of small non-coding RNAs from mitochondria and chloroplasts. Nucleic Acids Res 34: 3842-3852 [Abstract] [Full Text]  
• Slomovic, S., Laufer, D., Geiger, D., Schuster, G. (2006). Polyadenylation of ribosomal RNA in human cells. Nucleic Acids Res 34: 2966-2975 [Abstract] [Full Text]