Michael Weber
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Michael Weber has a total of 6 co-authors. Here are the top co-authors by number of shared publications:
- Benedikt Brors
Division of Applied Bioinformatics, The German Cancer Research Center (DKFZ), Heidelberg, Germany
1 shared publication - Ina N. Talke
Max Planck Institute of Molecular Plant Physiology, Am Mühlenberg 1, Potsdam, 14476, Germany
1 shared publication - Roland Eils
Digital Health Center, Berlin Institute of Health (BIH) and Charité University Medicine, Berlin, Germany
1 shared publication - Stephan Clemens
Plant Physiology, Bayreuth Center for Ecology and Environmental Research (BayCEER) University of Bayreuth Bayreuth Germany
1 shared publication - Ute Krämer
Ruhr University Bochum
1 shared publication - Vasantika Suryawanshi
La Jolla Institute for Immunology
1 shared publication
Latest Publications
- Open Access
- 22 December 2016
- Published by Springer Nature in BMC Genomics
- Vol. 17 (S13) , 43-64
Between-species differences in gene copy number are enriched among functions critical for adaptive evolution in Arabidopsis halleri
Gene copy number divergence between species is a form of genetic polymorphism that contributes significantly to both genome size and phenotypic variation. In plants, copy number expansions of single genes were implicated in cultivar- or species-specific tolerance of high levels of soil boron, aluminium or calamine-type heavy metals, respectively. Arabidopsis halleri is a zinc- and cadmium-hyperaccumulating extremophile species capable of growing on heavy-metal contaminated, toxic soils. In contrast, its non-accumulating sister species A. lyrata and the closely related reference model species A. thaliana exhibit merely basal metal tolerance. For a genome-wide assessment of the role of copy number divergence (CND) in lineage-specific environmental adaptation, we conducted cross-species array comparative genome hybridizations of three plant species and developed a global signal scaling procedure to adjust for sequence divergence. In A. halleri, transition metal homeostasis functions are enriched twofold among the genes detected as copy number expanded. Moreover, biotic stress functions including mostly disease Resistance (R) gene-related genes are enriched twofold among genes detected as copy number reduced, when compared to the abundance of these functions among all genes. Our results provide genome-wide support for a link between evolutionary adaptation and CND in A. halleri as shown previously for Heavy metal ATPase4. Moreover our results support the hypothesis that elemental defences, which result from the hyperaccumulation of toxic metals, allow the reduction of classical defences against biotic stress as a trade-off.
- 22 December 2016
- Published by Springer Nature in BMC Genomics
- Vol. 17 (S13) , 43-64
Open AccessBetween-species differences in gene copy number are enriched among functions critical for adaptive evolution in Arabidopsis halleri
Gene copy number divergence between species is a form of genetic polymorphism that contributes significantly to both genome size and phenotypic variation. In plants, copy number expansions of single genes were implicated in cultivar- or species-specific tolerance of high levels of soil boron, aluminium or calamine-type heavy metals, respectively. Arabidopsis halleri is a zinc- and cadmium-hyperaccumulating extremophile species capable of growing on heavy-metal contaminated, toxic soils. In contrast, its non-accumulating sister species A. lyrata and the closely related reference model species A. thaliana exhibit merely basal metal tolerance. For a genome-wide assessment of the role of copy number divergence (CND) in lineage-specific environmental adaptation, we conducted cross-species array comparative genome hybridizations of three plant species and developed a global signal scaling procedure to adjust for sequence divergence. In A. halleri, transition metal homeostasis functions are enriched twofold among the genes detected as copy number expanded. Moreover, biotic stress functions including mostly disease Resistance (R) gene-related genes are enriched twofold among genes detected as copy number reduced, when compared to the abundance of these functions among all genes. Our results provide genome-wide support for a link between evolutionary adaptation and CND in A. halleri as shown previously for Heavy metal ATPase4. Moreover our results support the hypothesis that elemental defences, which result from the hyperaccumulation of toxic metals, allow the reduction of classical defences against biotic stress as a trade-off.