Function of the ER located ATP carrier ER-ANT1

植物至少有两种类型的ATP转运蛋白，即存在于叶绿体中的核苷酸转运蛋白(NTT)，以及存在于线粒体内膜、质膜、质膜、过氧体膜和内质网(ER)膜上的线粒体载体家族(MCF)的几个同源成员。内质网定位的腺苷载体(ER-ANT1)催化ATP/ADP交换，而基因敲除突变体(ER-ANT1)惊人地表现出光呼吸表型。我们提出的证据表明，ER-ANT1植物处理光呼吸过程中释放的活性氧物种(ROS)的能力受到了损害。这一观察结果导致了这样的假设，即当生长在环境CO2下时，ROS是导致er-ANT1品系矮化表型的原因。借助ER-ANT1衍生的突变体显示出改善的ROS耐受性，我们希望证明这一假说。在Er-ANT1植株的基础上，我们启动了正向遗传方法，获得了几个EMS诱导的抑制系，在环境CO2下表现出更好的生长。我们认为，通过几个独立的细胞修饰清除这些抑制系中的ROS，可以抑制矮生表型。为了验证这一假设，将使用下一代测序(NGS)来确定责任基因座，并通过在er-ANT1背景中定向引入相应的变化来确认每个基因修改。到目前为止，ER-ANT1(位于ER膜内)在光呼吸(运行于ER外)中的确切参与尚不清楚。我们预计，对足够数量的EMS诱导的ER-ANT1抑制系的详细分子分析，今天提供了最好的(可能是唯一的)方法来澄清这个悬而未决的问题，即ER定位的过程和光呼吸之间令人惊讶的相互作用。

Plants possess at least two types of ATP transporters, namely the so called NTT (nucleotide transporters) residing in plastids, and several homologous members of the mitochondrial carrier family (MCF) residing in the inner mitochondrial membrane, the inner plastid-envelope membrane, the plasma membrane, the peroxisomal membrane and the Endoplasmic Reticulum (ER) membrane. The ER located adenylate carrier (ER-ANT1) catalyzes ATP/ADP exchange and knock-out mutants (er-ant1) surprisingly exhibit a photorespiratory phenotype. We raised evidence that er-ant1 plants show impaired ability to cope with reactive oxygen species (ROS) released during photorespiration. This observation led to the hypothesis that ROS are causative for the dwarf phenotype of er-ant1 lines when grown under ambient CO2. With help of er-ant1 derived mutants showing improved ROS tolerance we wish to prove this hypothesis. On basis of er-ant1 plants we initiated a forward genetic approach and generated several EMS induced suppressor lines, showing better growth under ambient CO2. We assume that repression of the dwarf phenotype is possible by several independent cellular modifications scavenging ROS in these suppressor lines. To proof this assumption the responsible loci will be identified by using Next Generation Sequencing (NGS) and each genetic modification will be confirmed by directed introduction of corresponding changes in the er-ant1 background. So far the exact involvement of ER-ANT1 (which is located in the ER membrane) in photorespiration (running outside ER) is fully obscure. We expect that detailed molecular analysis of a sufficient number of EMS induced er-ant1 suppressor lines provides today the best (maybe sole) way to clarify this open question on a surprising interaction between ER located processes and photorespiration.