Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
2011-7-7
pubmed:abstractText
Group II introns are found in bacteria and cell organelles (plastids, mitochondria) and are thought to represent the evolutionary ancestors of spliceosomal introns. It is generally believed that group II introns are selfish genetic elements that do not have any function. Here, we have scrutinized this assumption by analyzing two group II introns that interrupt a plastid gene (ycf3) involved in photosystem assembly. Using stable transformation of the plastid genome, we have generated mutant plants that lack either intron 1 or intron 2 or both. Interestingly, the deletion of intron 1 caused a strong mutant phenotype. We show that the mutants are deficient in photosystem I and that this deficiency is directly related to impaired ycf3 function. We further show that, upon deletion of intron 1, the splicing of intron 2 is strongly inhibited. Our data demonstrate that (i) the loss of a group II intron is not necessarily phenotypically neutral and (ii) the splicing of one intron can depend on the presence of another.
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/21357608-10481026, http://linkedlifedata.com/resource/pubmed/commentcorrection/21357608-11377794, http://linkedlifedata.com/resource/pubmed/commentcorrection/21357608-11563907, http://linkedlifedata.com/resource/pubmed/commentcorrection/21357608-11939782, http://linkedlifedata.com/resource/pubmed/commentcorrection/21357608-12073100, http://linkedlifedata.com/resource/pubmed/commentcorrection/21357608-12121445, http://linkedlifedata.com/resource/pubmed/commentcorrection/21357608-12172835, http://linkedlifedata.com/resource/pubmed/commentcorrection/21357608-12881426, http://linkedlifedata.com/resource/pubmed/commentcorrection/21357608-15563617, http://linkedlifedata.com/resource/pubmed/commentcorrection/21357608-15574835, http://linkedlifedata.com/resource/pubmed/commentcorrection/21357608-17041147, http://linkedlifedata.com/resource/pubmed/commentcorrection/21357608-1708111, http://linkedlifedata.com/resource/pubmed/commentcorrection/21357608-17114182, http://linkedlifedata.com/resource/pubmed/commentcorrection/21357608-17209805, http://linkedlifedata.com/resource/pubmed/commentcorrection/21357608-1723663, http://linkedlifedata.com/resource/pubmed/commentcorrection/21357608-17693527, http://linkedlifedata.com/resource/pubmed/commentcorrection/21357608-17965268, http://linkedlifedata.com/resource/pubmed/commentcorrection/21357608-18065687, http://linkedlifedata.com/resource/pubmed/commentcorrection/21357608-18424209, http://linkedlifedata.com/resource/pubmed/commentcorrection/21357608-18557832, http://linkedlifedata.com/resource/pubmed/commentcorrection/21357608-18757552, http://linkedlifedata.com/resource/pubmed/commentcorrection/21357608-1898872, http://linkedlifedata.com/resource/pubmed/commentcorrection/21357608-1915304, http://linkedlifedata.com/resource/pubmed/commentcorrection/21357608-19812182, http://linkedlifedata.com/resource/pubmed/commentcorrection/21357608-19920126, http://linkedlifedata.com/resource/pubmed/commentcorrection/21357608-20133623, http://linkedlifedata.com/resource/pubmed/commentcorrection/21357608-20351053, http://linkedlifedata.com/resource/pubmed/commentcorrection/21357608-20807881, http://linkedlifedata.com/resource/pubmed/commentcorrection/21357608-2125748, http://linkedlifedata.com/resource/pubmed/commentcorrection/21357608-2684776, http://linkedlifedata.com/resource/pubmed/commentcorrection/21357608-7490770, http://linkedlifedata.com/resource/pubmed/commentcorrection/21357608-7527587, http://linkedlifedata.com/resource/pubmed/commentcorrection/21357608-7574489, http://linkedlifedata.com/resource/pubmed/commentcorrection/21357608-7720718, http://linkedlifedata.com/resource/pubmed/commentcorrection/21357608-7838731, http://linkedlifedata.com/resource/pubmed/commentcorrection/21357608-7994178, http://linkedlifedata.com/resource/pubmed/commentcorrection/21357608-8108859, http://linkedlifedata.com/resource/pubmed/commentcorrection/21357608-8255751, http://linkedlifedata.com/resource/pubmed/commentcorrection/21357608-8381537, http://linkedlifedata.com/resource/pubmed/commentcorrection/21357608-8530436, http://linkedlifedata.com/resource/pubmed/commentcorrection/21357608-8744356, http://linkedlifedata.com/resource/pubmed/commentcorrection/21357608-9090875, http://linkedlifedata.com/resource/pubmed/commentcorrection/21357608-9121561, http://linkedlifedata.com/resource/pubmed/commentcorrection/21357608-9314531, http://linkedlifedata.com/resource/pubmed/commentcorrection/21357608-9362494
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
1362-4962
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
39
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
5181-92
pubmed:meshHeading
pubmed:year
2011
pubmed:articleTitle
Elimination of a group II intron from a plastid gene causes a mutant phenotype.
pubmed:affiliation
Max-Planck-Institut für Molekulare Pflanzenphysiologie, Am Mühlenberg 1, D-14476 Potsdam-Golm, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't