A quantitative hypermorphic <i>CNGC</i> allele confers ectopic calcium flux and impairs cellular development.

Abstract

The coordinated control of Ca²⁺ signaling is essential for development in eukaryotes. Cyclic nucleotide-gated channel (CNGC) family members mediate Ca²⁺ influx from cellular stores in plants (Charpentier et al., 2016; Gao et al., 2016; Frietsch et al., 2007; Urquhart et al., 2007). Here, we report the unusual genetic behavior of a quantitative gain-of-function <i>CNGC</i> mutation (<i>brush</i>) in <i>Lotus japonicus</i> resulting in a leaky tetrameric channel. <i>brush</i> resides in a cluster of redundant <i>CNGCs</i> encoding subunits which resemble metazoan voltage-gated potassium (Kv1-Kv4) channels in assembly and gating properties. The recessive mongenic <i>brush</i> mutation impaired root development and infection by nitrogen-fixing rhizobia. The <i>brush</i> allele exhibited quantitative behavior since overexpression of the cluster subunits was required to suppress the <i>brush</i> phenotype. The results reveal a mechanism by which quantitative competition between channel subunits for tetramer assembly can impact the phenotype of the mutation carrier.