PMID:15769737: Difference between revisions

From EcoliWiki
Jump to navigation Jump to search
← Older editNewer edit →
/Volumes/r3/t3/ul/working/touchTables/touch_all_tables.php
imported>Wikientrybot
change PMID template to TableEdit version
Line 1: Line 1:
{{RightTOC}}
{{RightTOC}}
<!--box uid=d41d8cd98f00b204e9800998ecf8427e.113781.I52238acee4363-->
<!--
******************************************************************************************
*
*  ** PLEASE DON'T EDIT THIS TABLE DIRECTLY.  Use the edit table link under the table. **
*
****************************************************************************************** -->
{|  id="I52238acee4363"  class=" tableEdit PMID_info_table" 


<span style = 'font-size: large'> '''Nagaike, T, Suzuki, T, Katoh, T and Ueda, T'''  (2005) Human mitochondrial mRNAs are stabilized with polyadenylation regulated by mitochondria-specific poly(A) polymerase and polynucleotide phosphorylase.''J. Biol. Chem.'' '''280''':19721-7</span>
{|{{Prettytable}} align = 'center' width= '70%'
|-
|-
|{{TableHeadingColor}} |'''Abstract''' || Mammalian mitochondrial (mt) mRNAs have short poly(A) tails at their 3' termini that are post-transcriptionally synthesized by mt poly(A) polymerase (PAP). The polyadenylation of mt mRNAs is known to be a key process needed to create UAA stop codons that are not encoded in mtDNA. In some cases, polyadenylation is required for the tRNA maturation by editing of its 3' terminus. However, little is known about the functional roles the poly(A) tail of mt mRNAs plays in mt translation and RNA turnover. Here we show human mt PAP (hmtPAP) and human polynucleotide phosphorylase (hPNPase) control poly(A) synthesis in human mitochondria. Partial inactivation of hmtPAP by RNA interference using small interfering RNA in HeLa cells resulted in shortened poly(A) tails and decreased steady state levels of some mt mRNAs as well as their translational products. Moreover, knocking down hmtPAP generated markedly defective mt membrane potentials and reduced oxygen consumption. In contrast, knocking down hPNPase showed significantly extended poly(A) tails of mt mRNAs. These results demonstrate that the poly(A) length of human mt mRNAs is controlled by polyadenylation by hmtPAP and deadenylation by hPNPase, and polyadenylation is required for the stability of mt mRNAs.
!align=left  |Citation
</noinclude>
||
'''No author listed''' (2005) Human mitochondrial mRNAs are stabilized with polyadenylation regulated by mitochondria-specific poly(A) polymerase and polynucleotide phosphorylase. ''J. Biol. Chem.'' '''280''':19721-7
|-
!align=left  |Abstract
||
Mammalian mitochondrial (mt) mRNAs have short poly(A) tails at their 3' termini that are post-transcriptionally synthesized by mt poly(A) polymerase (PAP). The polyadenylation of mt mRNAs is known to be a key process needed to create UAA stop codons that are not encoded in mtDNA. In some cases, polyadenylation is required for the tRNA maturation by editing of its 3' terminus. However, little is known about the functional roles the poly(A) tail of mt mRNAs plays in mt translation and RNA turnover. Here we show human mt PAP (hmtPAP) and human polynucleotide phosphorylase (hPNPase) control poly(A) synthesis in human mitochondria. Partial inactivation of hmtPAP by RNA interference using small interfering RNA in HeLa cells resulted in shortened poly(A) tails and decreased steady state levels of some mt mRNAs as well as their translational products. Moreover, knocking down hmtPAP generated markedly defective mt membrane potentials and reduced oxygen consumption. In contrast, knocking down hPNPase showed significantly extended poly(A) tails of mt mRNAs. These results demonstrate that the poly(A) length of human mt mRNAs is controlled by polyadenylation by hmtPAP and deadenylation by hPNPase, and polyadenylation is required for the stability of mt mRNAs.
|-
!align=left  |Links
||
[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15769737 PubMed]
Online version:[http://dx.doi.org/10.1074/jbc.M500804200 10.1074/jbc.M500804200]
|-
|-
|{{TableHeadingColor}} nowrap |'''Links''' ||  [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15769737 PubMed]
!align=left  |Keywords
||
Base Sequence; DNA, Complementary/genetics; HeLa Cells; Humans; Mitochondria/metabolism; Models, Molecular; Polynucleotide Adenylyltransferase/antagonists & inhibitors; Polynucleotide Adenylyltransferase/genetics; Polynucleotide Adenylyltransferase/metabolism; Polyribonucleotide Nucleotidyltransferase/metabolism; RNA/metabolism; RNA Processing, Post-Transcriptional; RNA Stability; RNA, Messenger/metabolism; RNA, Small Interfering/genetics; Recombinant Proteins/genetics; Recombinant Proteins/metabolism; Transfection
 
|- class="tableEdit_footer"
|<span class="tableEdit_editLink plainlinks">[{{SERVER}}{{SCRIPTPATH}}?title=Special:TableEdit&id=d41d8cd98f00b204e9800998ecf8427e.113781.I52238acee4363&page=113781&pagename={{FULLPAGENAMEE}}&type=1&template=PMID_info_table edit table]</span> ||
|}
|}
 
<!--box uid=d41d8cd98f00b204e9800998ecf8427e.113781.I52238acee4363-->
==Significance {{HelpIcon|Help:Literature}} ==
==Significance {{HelpIcon|Help:Literature}} ==
{{LitSignificance}}
{{LitSignificance}}

Revision as of 18:43, 1 September 2013

Citation

No author listed (2005) Human mitochondrial mRNAs are stabilized with polyadenylation regulated by mitochondria-specific poly(A) polymerase and polynucleotide phosphorylase. J. Biol. Chem. 280:19721-7

Abstract

Mammalian mitochondrial (mt) mRNAs have short poly(A) tails at their 3' termini that are post-transcriptionally synthesized by mt poly(A) polymerase (PAP). The polyadenylation of mt mRNAs is known to be a key process needed to create UAA stop codons that are not encoded in mtDNA. In some cases, polyadenylation is required for the tRNA maturation by editing of its 3' terminus. However, little is known about the functional roles the poly(A) tail of mt mRNAs plays in mt translation and RNA turnover. Here we show human mt PAP (hmtPAP) and human polynucleotide phosphorylase (hPNPase) control poly(A) synthesis in human mitochondria. Partial inactivation of hmtPAP by RNA interference using small interfering RNA in HeLa cells resulted in shortened poly(A) tails and decreased steady state levels of some mt mRNAs as well as their translational products. Moreover, knocking down hmtPAP generated markedly defective mt membrane potentials and reduced oxygen consumption. In contrast, knocking down hPNPase showed significantly extended poly(A) tails of mt mRNAs. These results demonstrate that the poly(A) length of human mt mRNAs is controlled by polyadenylation by hmtPAP and deadenylation by hPNPase, and polyadenylation is required for the stability of mt mRNAs.

Links

PubMed Online version:10.1074/jbc.M500804200

Keywords

Base Sequence; DNA, Complementary/genetics; HeLa Cells; Humans; Mitochondria/metabolism; Models, Molecular; Polynucleotide Adenylyltransferase/antagonists & inhibitors; Polynucleotide Adenylyltransferase/genetics; Polynucleotide Adenylyltransferase/metabolism; Polyribonucleotide Nucleotidyltransferase/metabolism; RNA/metabolism; RNA Processing, Post-Transcriptional; RNA Stability; RNA, Messenger/metabolism; RNA, Small Interfering/genetics; Recombinant Proteins/genetics; Recombinant Proteins/metabolism; Transfection

edit table

Significance

You can help EcoliWiki by summarizing why this paper is useful

Useful Materials and Methods

You can help Ecoliwiki by describing the useful materials (strains, plasmids, antibodies, etc) described in this paper.

Annotations

Gene product Qualifier GO ID GO term name Evidence Code with/from Aspect Notes Status
edit table

EcoliWiki Links

Add links to pages that link here (e.g. gene, product, method pages)

References

See Help:References for how to manage references in EcoliWiki.

Retrieved from "https://ecoliwiki.org/colipedia/index.php?title=PMID:15769737&oldid=1419832"