Faculty of Biology, Institute of Genetics, Ludwig Maximilian University of Munich, Munich, Germany.
Molecular Plant Physiology, Department of Biology, University of Erlangen-Nürnberg, Erlangen, Germany.
Elife. 2017 Sep 21;6:e25012. doi: 10.7554/eLife.25012.
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.
真核生物的发育过程中，钙离子信号的协调控制至关重要。环核苷酸门控通道（CNGC）家族成员在植物中从细胞储存库中介导钙离子内流（Charpentier 等人，2016；Gao 等人，2016；Frietsch 等人，2007；Urquhart 等人，2007）。在这里，我们报道了一个数量获得性功能突变（）在 中导致泄漏四聚体通道的异常遗传行为。位于冗余编码亚基的簇中，这些亚基在组装和门控特性上类似于后生动物电压门控钾（Kv1-Kv4）通道。隐性单基因突变损害了根的发育和固氮根瘤菌的感染。等位基因表现出数量行为，因为需要过量表达簇亚基来抑制 表型。结果揭示了通道亚基之间用于四聚体组装的定量竞争如何影响突变携带者表型的机制。
