Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1997-5-29
pubmed:databankReference
pubmed:abstractText
The filamentous fungus Podospora anserina presents a degeneration syndrome called Senescence associated with mitochondrial DNA modifications. We show that mutations affecting the two different and interacting cytosolic ribosomal proteins (S7 and S19) systematically and specifically prevent the accumulation of senDNA alpha (a circular double-stranded DNA plasmid derived from the first intron of the mitochondrial cox1 gene or intron alpha) without abolishing Senescence nor affecting the accumulation of other usually observed mitochondrial DNA rearrangements. One of the mutant proteins is homologous to the Escherichia coli S4 and Saccharomyces cerevisiae S13 ribosomal proteins, known to be involved in accuracy control of cytosolic translation. The lack of accumulation of senDNA alpha seems to result from a nontrivial ribosomal alteration unrelated to accuracy control, indicating that S7 and S19 proteins have an additional function. The results strongly suggest that modified expression of nucleus-encoded proteins contributes to Senescence in P. anserina. These data do not fit well with some current models, which propose that intron alpha plays the role of the cytoplasmic and infectious Determinant of Senescence that was defined in early studies.
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/9055079-13107134, http://linkedlifedata.com/resource/pubmed/commentcorrection/9055079-1427034, http://linkedlifedata.com/resource/pubmed/commentcorrection/9055079-2041737, http://linkedlifedata.com/resource/pubmed/commentcorrection/9055079-3987896, http://linkedlifedata.com/resource/pubmed/commentcorrection/9055079-683172, http://linkedlifedata.com/resource/pubmed/commentcorrection/9055079-7078631, http://linkedlifedata.com/resource/pubmed/commentcorrection/9055079-7529208, http://linkedlifedata.com/resource/pubmed/commentcorrection/9055079-7621838, http://linkedlifedata.com/resource/pubmed/commentcorrection/9055079-7753635, http://linkedlifedata.com/resource/pubmed/commentcorrection/9055079-7772601, http://linkedlifedata.com/resource/pubmed/commentcorrection/9055079-7781070, http://linkedlifedata.com/resource/pubmed/commentcorrection/9055079-7840758, http://linkedlifedata.com/resource/pubmed/commentcorrection/9055079-7932720, http://linkedlifedata.com/resource/pubmed/commentcorrection/9055079-8087879, http://linkedlifedata.com/resource/pubmed/commentcorrection/9055079-8230190, http://linkedlifedata.com/resource/pubmed/commentcorrection/9055079-8232558, http://linkedlifedata.com/resource/pubmed/commentcorrection/9055079-8289244, http://linkedlifedata.com/resource/pubmed/commentcorrection/9055079-8622769, http://linkedlifedata.com/resource/pubmed/commentcorrection/9055079-887069
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0016-6731
pubmed:author
pubmed:issnType
Print
pubmed:volume
145
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
697-705
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
Cytosolic ribosomal mutations that abolish accumulation of circular intron in the mitochondria without preventing senescence of Podospora anserina.
pubmed:affiliation
Centre de Génétique Moléculaire du CNRS, Gif sur Yvette, France. silar@cgm.cnrs-gif.fr
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't