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Calcium currents characterize the developing pollen tube in the small mustard plant Arabidopsis and correlate with growth at the tip of the pollen tube. 钙离子流在小芥属植物拟南芥中在花粉管发育的特征，也与花粉管尖端的生长相关。 This system constitutes a practical model for screening for Ca2+-signaling mechanisms in plants. 该系统构成了一个可用于研究植物中钙离子信号机制的试验模型。 Wudick et al. analyzed multiple variants of glutamate receptor–like (GLR) channels and discovered that some work alone and others work in pairs or trios. 伍迪克等分析了多种不同的谷氨酸受体样通路，发现有一些是独立工作的，而有一些是成对或者三者一起工作。 Subcellular localization of GLRs is a complex response to CORNICHON sorting proteins, which leave some GLRs at the plasma membrane and ferry others to internal calcium reservoirs. GLRs的细胞内分布是对CORNICHON分选蛋白的一种复杂反应，它在质膜上留下一些GLR，并将其他的GLR转运到内部的钙池中。 The calcium current at the tip of the growing pollen tube apparently integrates multiple intracellular currents. 生长的花粉管尖端的钙流明显也是各种细胞间钙流的一部分。 Compared to animals, evolution of plant calcium (Ca2+) physiology has led to a loss of proteins for influx and small ligand–operated control of cytosolic Ca2+, leaving many Ca2+mechanisms unaccounted for. 跟动物相比，植物钙离子生理的进化导致了内流蛋白的缺失和胞内钙离子的小配体控制，使得我们对很多的钙离子机制还知之甚少。 Here, researches show a mechanism for sorting and activation of glutamate receptor–like channels (GLRs) by CORNICHON HOMOLOG (CNIH) proteins. 在这里，研究显示了谷氨酸受体样通路通过酸黄瓜同族蛋白（CNIH）进行的的分选和活化机制。 Single mutants of pollen-expressed Arabidopsis thaliana GLRs (AtGLRs) showed growth and Ca2+flux phenotypes expected for plasma membrane Ca2+ channels. 单突变体拟南芥GLRs (AtGLRs)显示了质膜Ca2+通道的生长和Ca2+通量表型。 However, higher-order mutants of AtGLR3.3 revealed phenotypes contradicting this assumption. 然而，AtGLR3.3的高阶突变体显示了设想相矛盾的表型。 These discrepancies could be explained by subcellular AtGLR localization, and we explored the implication of AtCNIHs in this sorting. 这些差异可以用亚细胞AtGLR定位来解释，我们探讨了AtCNIHs在这一分类中的含义。 We found that AtGLRs interact with AtCNIH pairs, yielding specific intracellular localizations. 我们发现AtGLR和AtCNIH是成对反应的，从而产生特定的细胞内分布。 AtCNIHs further trigger AtGLR activity in mammalian cells without any ligand. 无需任何受体，AtCNIH可进一步引发AtGLR在哺乳动物细胞中的活化。 These results reveal a regulatory mechanism underlying Ca2+ homeostasis by sorting and activation of AtGLRs by AtCNIHs. 这些结果解释了钙离子自稳态背后的调节机制，即通AtCNIH来对AtGLR进行分选和激活。 感谢关注 跟amber一起看世界 |
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