Linked Life Data

10070258

Source:http://linkedlifedata.com/resource/pubmed/id/10070258

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1999-4-7
pubmed:abstractText
In the vertebrates, programmed cell death or apoptosis frequently involves the relocalization of mitochondrial cytochrome c to the cytoplasm. This prominent role in the regulation of apoptosis is in addition to the primary function of cytochrome c in the mitochondrial electron transport chain. These seemingly divergent roles become plausible when considering the symbiotic origin of the mitochondrion. Symbiosis involves conflicts between levels of selection, in this case between the primitive host cell and the protomitochondria. In an aerobic environment, selection on the protomitochondria may have favored routine manipulations of the host cell's phenotype using products and by-products of oxidative phosphorylation, in particular reactive oxygen species (ROS). Blocking the mitochondrial electron transport chain by removing cytochrome c enhances the production of ROS; thus cytochrome c release by protomitochondria may have altered the host cell's phenotype via enhanced ROS production. Subsequently, this signaling pathway may have been refined by selection so that cytochrome c itself became the trigger for changes in the host's phenotype. A mechanism of apoptosis in metazoans may thus be a vestige of evolutionary conflicts within the eukaryotic cell.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0265-9247
pubmed:author
pubmed:issnType
Print
pubmed:volume
21
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
84-8
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
1999
pubmed:articleTitle
The evolution of a mechanism of cell suicide.
pubmed:affiliation
Department of Biological Sciences, Northern Illinois University, DeKalb 60115, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S., Review