References and Notes Supporting Online Material Circadian Gating of the Cell Cycle Revealed in Single Cyanobacterial Cells-猫眼课题宝

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L. C. L. Palmer-L.-C.-L.-Palmer-2245994539;J. M. Cotton;Henley;Y Zheng;J. Mellem;P. J. Brockie;D. M. Madsen;Y Stern-Bach;S. Russo;M. Neuman;Christian Rosenmund;N Pilpel;N. Landeck;M. Klugmann;P. Seeburg;M. K. Schwarz;K M Partin;M. W. Fleck;M. L. Mayer;A Robert;N. Armstrong;J. Gouaux;J. R. Howe;M C Weston;C. Gertler;R. Hinz-Herkommer;I. Preugschat-Gumprecht;R. Zilberstein;Y. S. B. Sfb;Nationales Genomforschungsnetz;Max Planck Society;P. H. S. The;Qiong Yang;B. Pando;Guogang Dong;S. Golden;A. van Oudenaarden

同源基因2和3(2)，因为CKAMP44也减缓了AMPAR的失活，尽管方式不那么明显，并且，与TARPs类似，CKAMP44增加了谷氨酸伴侣的亲和力（3,12,13）。然而，CKAMP44在调节AMPAR脱敏方面与其他AMPAR辅助蛋白有很大不同。它通过增加脱敏、降低t des和减缓脱敏后的恢复来调节AMPAR功能，而TARPs和角状子则会减少和减缓脱敏（2,3,12）。CKAMP44对t - deact和t - des的影响值得注意，因为TARPs和cornichons都会增加t - deact和t - des（2,3,12）。在大多数影响二聚体界面稳定性的AMPAR突变中，也观察到t - deact和t - des的协同调节（两者的增加或减少）（14,15）。相反，影响闭裂构象稳定性的配体结合间隙中的AMPAR突变（D1和D2结构域之间的相互作用）对t - deact和t - des有相反的影响。破坏这些结构域之间相互作用的突变会降低t - deact，增加t - des。此外，这种突变会降低激动剂的亲和力，也会加速脱敏后的恢复（16）。相反，稳定闭裂构象的突变减慢了失活和脱敏后的恢复，并增加了激动剂的表观亲和力（17）。因此，CKAMP44对AMPAR性质的影响与CKAMP44稳定配体结合核的闭间隙构象是一致的。CKAMP44对脱敏的作用与TARPs相反，但不能用AMPAR复合体中TARPs的替代或消除来解释。根据我们的共免疫沉淀研究，CKAMP44似乎作用于与TARPs相关的ampar。此外，通过CA1和DG突触的比较以及CKAMP44的差异表达表明，AMPARs在这些突触上发生不同程度的调节。相比之下，锥体和tarp似乎是中枢神经系统中AMPAR复合体必不可少的辅助亚基。ckamp44介导的AMPAR脱敏增加通过降低成对脉冲促进作用影响EPSCs的短期可塑性。在大多数突触中，短期可塑性被认为反映了递质释放概率的变化。只有少数突触的AMPAR脱敏被证明会影响PPR（18-20）。脱敏恢复缓慢、谷氨酸明显溢出和高释放概率被认为是AMPAR脱敏影响PPR的原因。正如我们在这里所证明的，AMPAR脱敏可以降低CA1锥体和DG颗粒中的PPR。

cornichon homologs 2 and 3 (2), because CKAMP44 also slows AMPAR deactivation, although in a less pronounced manner, and, similarly to TARPs, CKAMP44 increases gluta-mate affinity (3, 12, 13). However, CKAMP44 differs considerably from other AMPAR auxiliary proteins in its modulation of AMPAR desensitization. It modulates AMPAR function by increasing desensitization, decreasing t des , and slowing the recovery from de-sensitization, whereas TARPs and cornichons reduce and slow desensitization (2, 3, 12). The influence of CKAMP44 on t deact and t des is noteworthy , as TARPs and cornichons increase both t deact and t des (2, 3, 12). Coregulation of t deact and t des (increase or decrease of both) was also observed for most AMPAR mutations that, for example, influence the dimer interface stability (14, 15). In contrast, AMPAR mutations in the ligand-binding cleft that affect the stability of the closed-cleft conformation (interaction between domains D1 and D2) have opposite effects on t deact and t des. Mutations that disrupt interactions between these domains decrease t deact and increase t des. In addition, such mutations decrease agonist affinity and also accelerate recovery from desen-sitization (16). Conversely, mutations that stabilize the closed-cleft conformation slow both deacti-vation and recovery from desensitization, and increase agonist apparent affinity (17). Therefore, the effects of CKAMP44 on AMPAR properties are consistent with CKAMP44 stabilizing the closed-cleft conformation of the ligand-binding core. The role that CKAMP44 exerts on de-sensitization is opposite to that of TARPs, but cannot be explained by the replacement or elimination of TARPs from the AMPAR complex. According to our coimmunoprecipitation studies, CKAMP44 appears to act on AMPARs associated with TARPs. Moreover, as demonstrated by the comparison of CA1 and DG synapses and the differential expression of CKAMP44, the modulation of AMPARs occurs to different extents at these synapses. By contrast, cornichons and TARPs seem to be essential auxiliary subunits of the AMPAR complex in the central nervous system. The CKAMP44-mediated increase in AMPAR desensitization influences short-term plasticity of EPSCs by reducing paired-pulse facilitation. In most synapses, short-term plasticity is thought to reflect changes in transmitter release probability. There are only a few synapses for which AMPAR desensitization has been shown to influence PPR (18–20). Slow recovery from desensitization, pronounced glutamate spillover, and high release probability are thought to enable AMPAR desensitization to influence PPR. As we have demonstrated here, AMPAR desensitization can reduce the PPR in CA1 pyramidal and DG granule …

References and Notes Supporting Online Material Circadian Gating of the Cell Cycle Revealed in Single Cyanobacterial Cells

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