The coordinated control of Ca signaling is essential for development in eukaryotes. Cyclic nucleotide-gated channel (CNGC) family members mediate Ca 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 mutation () in resulting in a leaky tetrameric channel. resides in a cluster of redundant encoding subunits which resemble metazoan voltage-gated potassium (Kv1-Kv4) channels in assembly and gating properties. The recessive mongenic mutation impaired root development and infection by nitrogen-fixing rhizobia. The allele exhibited quantitative behavior since overexpression of the cluster subunits was required to suppress the phenotype. The results reveal a mechanism by which quantitative competition between channel subunits for tetramer assembly can impact the phenotype of the mutation carrier.
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| http://dx.doi.org/10.7554/eLife.25012 | DOI Listing |
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