Seeds of Arabidopsis plants expressing dominant-negative AtSKD1 under control of the GL2 promoter show atransparent testaphenotype and a mucilage defect
Copyright policy )Seeds of Arabidopsis plants expressing dominant-negative AtSKD1 under control of the GL2 promoter show atransparent testaphenotype and a mucilage defect
We have recently shown that overexpression of dominant-negative AtSKD1 versions under control of the trichome and non-root-hair-cell specific GL2 promoter (GL2pro) blocks trafficking of soluble cargo to the vacuole, resulting in its fragmentation and ultimately cell death. GL2pro is also active in the Arabidopsis seeds. When we inspected seeds of the dominant-negative AtSKD1 variants we found two phenotypes. The seeds display a transparent testa phenotype caused by a lack of proanthocyanidin (PA) and do not possess seed coat mucilage. Both phenotypes could be connected by cell death induced by the overexpression of dominant-negative AtSKD1.
- University of Cologne Germany
Adenosine Triphosphatases, Homeodomain Proteins, Phenotype, Arabidopsis Proteins, Adhesives, Seeds, Arabidopsis, Proanthocyanidins, Promoter Regions, Genetic, Genes, Dominant
Adenosine Triphosphatases, Homeodomain Proteins, Phenotype, Arabidopsis Proteins, Adhesives, Seeds, Arabidopsis, Proanthocyanidins, Promoter Regions, Genetic, Genes, Dominant
citations This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).10 popularity This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.Average influence This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).Average impulse This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.Average
Citations provided by BIP!Popularity provided by BIP!