Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2002-11-27
pubmed:abstractText
We have previously shown that the activity of functional I retrotransposons (I factors) introduced into Drosophila devoid of such elements can be repressed by transgenes containing an internal fragment of the I factor itself and that this repressing effect presents the characteristic features of homology-dependent gene silencing or cosuppression. Here we show that the same transgenes can induce silencing of a nonhomologous reporter gene containing as the sole I-factor sequence its 100-bp promoter fragment. Silencing of the nonhomologous reporter gene shows strong similarities to I-factor cosuppression: It does not require any translation product from the regulating transgenes, sense and antisense constructs are equally potent, and the silencing effect is only maternally transmitted and fully reversible. A search for genomic I-like sequences containing domains with similarities to those of both the regulating and the reporter transgenes led to the identification of four such elements, which therefore could act as intermediates-or relays-in the cosuppression machinery. These results strongly suggest that ancestral transposition-defective I-related elements, which are naturally present in the Drosophila genome, may participate per se in the natural conditions of I-factor silencing.
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/12454066-10025394, http://linkedlifedata.com/resource/pubmed/commentcorrection/12454066-10069073, http://linkedlifedata.com/resource/pubmed/commentcorrection/12454066-10219236, http://linkedlifedata.com/resource/pubmed/commentcorrection/12454066-10520992, http://linkedlifedata.com/resource/pubmed/commentcorrection/12454066-10535732, http://linkedlifedata.com/resource/pubmed/commentcorrection/12454066-10542148, http://linkedlifedata.com/resource/pubmed/commentcorrection/12454066-10581283, http://linkedlifedata.com/resource/pubmed/commentcorrection/12454066-10731132, http://linkedlifedata.com/resource/pubmed/commentcorrection/12454066-10731138, http://linkedlifedata.com/resource/pubmed/commentcorrection/12454066-10749199, http://linkedlifedata.com/resource/pubmed/commentcorrection/12454066-10749214, http://linkedlifedata.com/resource/pubmed/commentcorrection/12454066-10753783, http://linkedlifedata.com/resource/pubmed/commentcorrection/12454066-10835392, http://linkedlifedata.com/resource/pubmed/commentcorrection/12454066-11013221, http://linkedlifedata.com/resource/pubmed/commentcorrection/12454066-11063690, http://linkedlifedata.com/resource/pubmed/commentcorrection/12454066-11102380, http://linkedlifedata.com/resource/pubmed/commentcorrection/12454066-11201747, http://linkedlifedata.com/resource/pubmed/commentcorrection/12454066-11250148, http://linkedlifedata.com/resource/pubmed/commentcorrection/12454066-11253050, http://linkedlifedata.com/resource/pubmed/commentcorrection/12454066-11485817, http://linkedlifedata.com/resource/pubmed/commentcorrection/12454066-11486075, http://linkedlifedata.com/resource/pubmed/commentcorrection/12454066-11719220, http://linkedlifedata.com/resource/pubmed/commentcorrection/12454066-11864605, http://linkedlifedata.com/resource/pubmed/commentcorrection/12454066-121289, http://linkedlifedata.com/resource/pubmed/commentcorrection/12454066-1647020, http://linkedlifedata.com/resource/pubmed/commentcorrection/12454066-1698618, http://linkedlifedata.com/resource/pubmed/commentcorrection/12454066-1710982, http://linkedlifedata.com/resource/pubmed/commentcorrection/12454066-1916244, http://linkedlifedata.com/resource/pubmed/commentcorrection/12454066-2158161, http://linkedlifedata.com/resource/pubmed/commentcorrection/12454066-2175814, http://linkedlifedata.com/resource/pubmed/commentcorrection/12454066-2430722, http://linkedlifedata.com/resource/pubmed/commentcorrection/12454066-2554335, http://linkedlifedata.com/resource/pubmed/commentcorrection/12454066-2845368, http://linkedlifedata.com/resource/pubmed/commentcorrection/12454066-6088060, http://linkedlifedata.com/resource/pubmed/commentcorrection/12454066-6319027, http://linkedlifedata.com/resource/pubmed/commentcorrection/12454066-7565601, http://linkedlifedata.com/resource/pubmed/commentcorrection/12454066-7984417, http://linkedlifedata.com/resource/pubmed/commentcorrection/12454066-8313476, http://linkedlifedata.com/resource/pubmed/commentcorrection/12454066-8670818, http://linkedlifedata.com/resource/pubmed/commentcorrection/12454066-9267028, http://linkedlifedata.com/resource/pubmed/commentcorrection/12454066-9315443, http://linkedlifedata.com/resource/pubmed/commentcorrection/12454066-9486653, http://linkedlifedata.com/resource/pubmed/commentcorrection/12454066-9617806, http://linkedlifedata.com/resource/pubmed/commentcorrection/12454066-9751742, http://linkedlifedata.com/resource/pubmed/commentcorrection/12454066-9841401
pubmed:language
eng
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:author
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1197-209
pubmed:dateRevised
2009-11-18
pubmed:articleTitle
Regulation of I-transposon activity in Drosophila: evidence for cosuppression of nonhomologous transgenes and possible role of ancestral I-related pericentromeric elements.
pubmed:affiliation
CNRS UMR 1573, Institut Gustave Roussy, 94805 Villejuif Cedex, France.