Copper-handling by Polaris and the metallation-status of ETR1

林赛实验室(几年来)发现了短多肽(北极星)在植物发育控制中的作用，更具体地说，是在由乙烯触发的调节电路中发挥作用。他们(以及其他观察结果)证实，北极星多肽与乙烯受体ETR1共同定位于细胞内的膜室。重要的是，ETR1需要配位铜，以便与其气体信号分子形成重要的阳离子-pi相互作用。因为北极星有候选的铜配体，我们最近测试了它是否也可以配位铜，并且(到目前为止)已经确定它确实可以与铜离子形成络合物。巧合的是，林赛实验室也观察到铜或铜螯合(通过亚铜丙二磺酸)可以改变，在某些情况下，与北极星突变相关的表型。这创造了一个令人兴奋的机会来了解乙烯信号如何通过ETR1与铜的金属化来控制。此外，从人类的铜转运蛋白Menkes和Wilsons ATPase，植物和酵母菌的RAN1和CCC2转运蛋白，到军团菌等细菌的类似CopA的铜ATPase，铜是如何在运输到细胞内的膜室(或细菌的周质)后进行管理，从而能够在这些位置真正地传递到等待铜蛋白的位置，这仍然是一个谜：北极星-ETR1铜‘回路’可能成为一个通用的范例。

The Lindsey laboratory has (over several years) discovered a role for a short polypeptide (POLARIS) in the control of plant development and more specifically in regulatory circuits that are triggered by ethylene. They have (amongst other observations) established that the POLARIS peptide co-localises with the ethylene receptor ETR1 in intracellular membraneous compartments. Importantly, ETR1 is known to need to coordinate copper in order to form a vital cation-pi interaction with its gaseous signal molecule. Because POLARIS has candidate copper-ligands, we recently tested whether or not it may also coordinate copper and have (to date) already established that it can indeed form a complex with cuprous ions. Coincidentally, the Lindsey laboratory has also observed that copper or copper-chelation (by bathocuproinedisulphonic acid) can modify, and in some cases reverse, the phenotypes associated with POLARIS mutants. This has created an exciting opportunity to understand how ethylene signalling may be controlled via metallation of ETR1 with copper. Moreover, from the copper-transporting Menkes and Wilsons ATPases in humans, the RAN1 and CCC2 transporters of plants and yeast, to the CopA like copper-ATPases of bacteria such as Legionella, it remains a mystery how copper is managed after transport into intracellular membraneous compartments (or the periplasm of bacteria) to enable delivery to bona fide, awaiting cupro-proteins, in these locations: The POLARIS-ETR1 copper-'circuitry' could become a universal paradigm.