Expression of a truncated tobacco NtCBP4 channel in transgenic plants and disruption of the homologous Arabidopsis CNGC1 gene confer Pb 2+ tolerance

Abstract

Recently we reported on a plasma membrane tobacco protein (designated NtCBP4) that binds calmodulin. When overexpressed in transgenic plants, NtCBP4 confers Pb 2+ hypersensitivity associated with enhanced accumulation of this toxic metal. To further investigate possible modulation of Pb 2+ tolerance in plants, we prepared transgenic plants that express a truncated version of this protein (designated NtCBP4ΔC) 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 Pb 2+ , 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 Pb 2+ tolerance. We suggest that NtCBP4 and AtCNGC1 are components of a transport pathway responsible for Pb 2+ entry into plant cells.