ABSTRACT
Recently we reported on a plasma membrane tobacco protein (designated NtCBP4) that binds calmodulin. When overexpressed in transgenic plants, NtCBP4 confers Pb2+ hypersensitivity associated with enhanced accumulation of this toxic metal. To further investigate possible modulation of Pb2+ tolerance in plants, we prepared transgenic plants that express a truncated version of this protein (designated NtCBP4DeltaC) from which its C-terminal, with the calmodulin-binding domain and part of the putative cyclic nucleotide-binding domain, was removed. In contrast to the phenotype of transgenic plants expressing the full-length gene, transgenic plants expressing the truncated gene showed improved tolerance to Pb2+, in addition to attenuated accumulation of this metal. Furthermore, disruption by T-DNA insertion mutagenesis of the Arabidopsis CNGC1 gene, which encodes a homologous protein, also conferred Pb2+ tolerance. We suggest that NtCBP4 and AtCNGC1 are components of a transport pathway responsible for Pb2+ entry into plant cells.
Subject(s)
Arabidopsis/genetics , Calmodulin-Binding Proteins/genetics , Ion Channels/genetics , Lead/toxicity , Nicotiana/genetics , Plant Proteins , Plants, Toxic , Adaptation, Physiological/genetics , Amino Acid Sequence , Arabidopsis/drug effects , Base Sequence , Calmodulin-Binding Proteins/metabolism , Cyclic Nucleotide-Gated Cation Channels , Dose-Response Relationship, Drug , Gene Expression Regulation, Plant , Immunoblotting , Lead/metabolism , Molecular Sequence Data , Mutation , Plant Development , Plants/drug effects , Plants/genetics , Plants, Genetically Modified , RNA, Messenger/genetics , RNA, Messenger/metabolism , Nicotiana/drug effects , Nicotiana/growth & developmentABSTRACT
This paper examines the sensitivity of endogenous bursters to a brief input pulse. The interneurons of the lobster cardiac ganglion were selected as a case study. Using a mathematical model specifically developed for the neurons in the cardiac ganglion of the lobster (Av-Ron et al., 1993), we show a tight link between burst characteristics and certain other parameters. We show that cells with different burst properties differ in their sensitivity to an input of a brief pulse. Irrespective of these differences, all cells display a bimodal response to a brief pulse applied during the quiescent period. During the first three-quarters of the quiescent period, they respond by producing a single spike at most. During the remaining one-quarter, the brief pulse can initiate the cells' intrinsic burst. Our predictions fit experimental results obtained by Tazaki and Cooke (1979). The results obtained herein are discussed with respect to fault tolerance considerations.
