Present address: School of Biological Sciences, University of Manchester, 3.614 Stopford Building, Oxford Road, Manchester M13 9PT, UK
Extensive developmental and metabolic alterations in cybrids Nicotiana tabacum (+ Hyoscyamus niger) are caused by complex nucleo-cytoplasmic incompatibility
Article first published online: 6 APR 2002
The Plant Journal
Volume 25, Issue 6, pages 627–639, March 2001
How to Cite
Zubko, M. K., Zubko, E. I., Ruban, A. V., Adler, K., Mock, H.-P., Misera, S., Gleba, Y. YU. and Grimm, B. (2001), Extensive developmental and metabolic alterations in cybrids Nicotiana tabacum (+ Hyoscyamus niger) are caused by complex nucleo-cytoplasmic incompatibility. The Plant Journal, 25: 627–639. doi: 10.1046/j.1365-313x.2001.00997.x
- Issue published online: 6 APR 2002
- Article first published online: 6 APR 2002
- Received 10 October 2000; revised 18 December 2000; accepted 2 January 2001.
- nucleo-cytoplasmic incompatibility;
- maternal inheritance;
- chloroplast biogenesis;
- cytoplasmic homeosis model
The genetic basis of multiple phenotypic alterations was studied in cell-engineered cybrids Nicotiana tabacum (+ Hyoscyamus niger) combining the nuclear genome of N. tabacum, plastome of H. niger and recombinant mitochondria. The plants possess a complex, maternally inheritable syndrome of nucleo-cytoplasmic incompatibility, severely affecting growth, metabolism and development. In vivo, the syndrome was manifested as: late germination of seeds; dramatic decrease of chlorophyll and carotenoids in cotyledons and leaves; altered morphology of cotyledons, leaves and flowers; and dwarfism. The leaf phenotype depended on light intensity. In ‘green flowers’ (an extreme phenotype), homeotic function B was downregulated. In vitro, the incompatibility syndrome was restricted to the pigment deficiency of cotyledons. Electron microscopy revealed perturbations in the differentiation of chloroplasts and palisade parenchyma cells in bleached leaves. The pigment deficiency accompanied by retarded growth is discussed as a result of plastome–genome incompatibility, whereas other features are likely to be due to nucleo-mitochondrial incompatibilities.