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Chiasson, David M. ORCID: 0000-0002-0770-2684; Haage, Kristina; Sollweck, Katharina; Brachmann, Andreas ORCID: 0000-0001-7980-8173; Dietrich, Petra ORCID: 0000-0002-9209-8089; Parniske, Martin ORCID: 0000-0001-8561-747X (21. September 2017): A quantitative hypermorphic CNGC allele confers ectopic calcium flux and impairs cellular development. In: Elife, Vol. 6, e25012: pp. 1-15
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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 CNGC mutation (brush) in Lotus japonicus resulting in a leaky tetrameric channel. brush resides in a cluster of redundant CNGCs encoding subunits which resemble metazoan voltage-gated potassium (Kv1-Kv4) channels in assembly and gating properties. The recessive mongenic brush mutation impaired root development and infection by nitrogen-fixing rhizobia. The brush allele exhibited quantitative behavior since overexpression of the cluster subunits was required to suppress the brush phenotype. The results reveal a mechanism by which quantitative competition between channel subunits for tetramer assembly can impact the phenotype of the mutation carrier.