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Natural variation for seed dormancy in Arabidopsis is regulated by additive genetic and molecular pathways
aDepartment of Molecular Plant Physiology, Utrecht University, Utrecht, The Netherlands; Laboratory of Genetics, Wageningen University, Wageningen, The Netherlands.
Molecular Plant Physiology, Utrecht University, Utrecht, The Netherlands; Centre for BioSystems Genomics, Wageningen, The Netherlands.ORCID-id: 0000-0002-5605-7984
Wageningen, The Netherlands.
Wageningen, The Netherlands.
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2010 (engelsk)Inngår i: Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, E-ISSN 1091-6490, Vol. 107, nr 9, s. 4264-4269Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Timing of germination is presumably under strong natural selection as it determines the environmental conditions in which a plant germinates and initiates its postembryonic life cycle. To investigate how seed dormancy is controlled, quantitative trait loci (QTL) analyses has been performed in six Arabidopsis thaliana recombinant inbred line populations by analyzing them simultaneously using a mixed model QTL approach. The recombinant inbred line populations were derived from crosses between the reference accession Landsberg erecta (Ler) and accessions from different world regions. In total, 11 delay of germination (DOG) QTL have been identified, and nine of them have been confirmed by near isogenic lines (NILs). The absence of strong epistatic interactions between the different DOG loci suggests that they affect dormancy mainly by distinct genetic pathways. This was confirmed by analyzing the transcriptome of freshly harvested dry seeds of five different DOG NILs. All five DOG NILs showed discernible and different expression patterns compared with the expression of their genetic background Ler. The genes identified in the different DOG NILs represent largely different gene ontology profiles. It is proposed that natural variation for seed dormancy in Arabidopsis is mainly controlled by different additive genetic and molecular pathways rather than epistatic interactions, indicating the involvement of several independent pathways.

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PNAS , 2010. Vol. 107, nr 9, s. 4264-4269
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URN: urn:nbn:se:umu:diva-114423DOI: 10.1073/pnas.1000410107PubMedID: 20145108OAI: oai:DiVA.org:umu-114423DiVA, id: diva2:895325
Tilgjengelig fra: 2016-01-18 Laget: 2016-01-18 Sist oppdatert: 2018-06-07bibliografisk kontrollert

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