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

林赛实验室（经过几年）发现了短多肽（POLARIS）在控制植物发育中的作用，更具体地说，是在乙烯触发的调节回路中。他们（在其他观察中）确定了POLARIS肽与细胞内膜区室中的乙烯受体ETR1共定位。重要的是，已知ETR1需要协调铜，以便与其气体信号分子形成重要的阳离子- π相互作用。由于POLARIS有候选铜配体，我们最近测试了它是否也可以配铜，并且（到目前为止）已经确定它确实可以与铜离子形成配合物。巧合的是，Lindsey实验室也观察到铜或铜螯合（通过二磺酸）可以改变，并在某些情况下逆转与POLARIS突变体相关的表型。这创造了一个令人兴奋的机会来了解乙烯信号如何通过用铜金属化ETR1来控制。此外，从人类中运输铜的Menkes和Wilsons atp酶，植物和酵母的RAN1和CCC2转运体，到军团菌等细菌的CopA样铜atp酶，铜在运输到细胞内膜腔（或细菌的周质）后如何被管理，从而能够在这些位置传递到真正的铜蛋白，这仍然是一个谜：POLARIS-ETR1铜“电路”可能成为一个普遍的范例。

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.