Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2000-11-3
pubmed:databankReference
pubmed:abstractText
Allopolyploid hybridization serves as a major pathway for plant evolution, but in its early stages it is associated with phenotypic and genomic instabilities that are poorly understood. We have investigated allopolyploidization between Arabidopsis thaliana (2n = 2x = 10; n, gametic chromosome number; x, haploid chromosome number) and Cardaminopsis arenosa (2n = 4x = 32). The variable phenotype of the allotetraploids could not be explained by cytological abnormalities. However, we found suppression of 20 of the 700 genes examined by amplified fragment length polymorphism of cDNA. Independent reverse transcription-polymerase chain reaction analyses of 10 of these 20 genes confirmed silencing in three of them, suggesting that approximately 0.4% of the genes in the allotetraploids are silenced. These three silenced genes were characterized. One, called K7, is repeated and similar to transposons. Another is RAP2.1, a member of the large APETALA2 (AP2) gene family, and has a repeated element upstream of its 5' end. The last, L6, is an unknown gene close to ALCOHOL DEHYDROGENASE on chromosome 1. CNG DNA methylation of K7 was less in the allotetraploids than in the parents, and the element varied in copy number. That K7 could be reactivated suggests epigenetic regulation. L6 was methylated in the C. arenosa genome. The present evidence that gene silencing accompanies allopolyploidization opens new avenues to this area of research.
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/11006331-10676818, http://linkedlifedata.com/resource/pubmed/commentcorrection/11006331-10999418, http://linkedlifedata.com/resource/pubmed/commentcorrection/11006331-15739260, http://linkedlifedata.com/resource/pubmed/commentcorrection/11006331-16593964, http://linkedlifedata.com/resource/pubmed/commentcorrection/11006331-1979162, http://linkedlifedata.com/resource/pubmed/commentcorrection/11006331-2231712, http://linkedlifedata.com/resource/pubmed/commentcorrection/11006331-2852134, http://linkedlifedata.com/resource/pubmed/commentcorrection/11006331-408210, http://linkedlifedata.com/resource/pubmed/commentcorrection/11006331-7644483, http://linkedlifedata.com/resource/pubmed/commentcorrection/11006331-7766876, http://linkedlifedata.com/resource/pubmed/commentcorrection/11006331-7851777, http://linkedlifedata.com/resource/pubmed/commentcorrection/11006331-797311, http://linkedlifedata.com/resource/pubmed/commentcorrection/11006331-8132503, http://linkedlifedata.com/resource/pubmed/commentcorrection/11006331-8188214, http://linkedlifedata.com/resource/pubmed/commentcorrection/11006331-8316832, http://linkedlifedata.com/resource/pubmed/commentcorrection/11006331-8441677, http://linkedlifedata.com/resource/pubmed/commentcorrection/11006331-8653120, http://linkedlifedata.com/resource/pubmed/commentcorrection/11006331-8692954, http://linkedlifedata.com/resource/pubmed/commentcorrection/11006331-8811101, http://linkedlifedata.com/resource/pubmed/commentcorrection/11006331-8846910, http://linkedlifedata.com/resource/pubmed/commentcorrection/11006331-9192694, http://linkedlifedata.com/resource/pubmed/commentcorrection/11006331-9260513, http://linkedlifedata.com/resource/pubmed/commentcorrection/11006331-9371740, http://linkedlifedata.com/resource/pubmed/commentcorrection/11006331-9383078, http://linkedlifedata.com/resource/pubmed/commentcorrection/11006331-9487390, http://linkedlifedata.com/resource/pubmed/commentcorrection/11006331-9582192, http://linkedlifedata.com/resource/pubmed/commentcorrection/11006331-9584105, http://linkedlifedata.com/resource/pubmed/commentcorrection/11006331-9590167, http://linkedlifedata.com/resource/pubmed/commentcorrection/11006331-9590690, http://linkedlifedata.com/resource/pubmed/commentcorrection/11006331-9693137, http://linkedlifedata.com/resource/pubmed/commentcorrection/11006331-9843986
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1040-4651
pubmed:author
pubmed:issnType
Print
pubmed:volume
12
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1551-68
pubmed:dateRevised
2010-9-14
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
Phenotypic instability and rapid gene silencing in newly formed arabidopsis allotetraploids.
pubmed:affiliation
Department of Botany, Box 355325, University of Washington, Seattle, Washington 98195, USA. comai@u.washington.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S.