GPX3参与了H_2O_2对保卫细胞质膜钾通道的调控

GPX3 is Involved into the Progress of Regulating Potassium Channel on Guard Cell Membrane by H_2O_2

通过表皮条生物分析、失水率测定及膜片钳实验研究谷氨酸过氧化物酶3(GPX3)能够调节保卫细胞质膜钾通道活性,并因此来介导H2O2诱导的拟南芥气孔关闭过程.与野生型Col-0相比,gpx3缺失突变在气孔开度和细胞失水方面均有较大差异.全细胞膜片钳模式下,1mmol/L的H2O2处理使野生型保卫细胞质膜钾离子通道外向电流从50pA左右激增到240pA左右,而gpx3的电流则变化不大.单通道电流的进一步分析表明gpx3不能像野生型一样对1mmol/L的H2O2处理产生明显反应,野生型与突变体的单通道电流差距高达10倍以上.据此推断GPX3是通过特异地调节外向钾通道来介导H2O2的信号传递.

By the experiments of bioassay, water loss ratio and patch clamp, the authors found that glutathione peroxidase 3（GPX3） transduced hydrogen peroxide （H202） signal in stomatal closure by regulating the activity of potassium channel. Compared with Col-0, gpx3 showed differences in the aspects of stomataI aperture and water loss rate. Data from patch clamp under whole cell mode showed that the current of wild type guard cells increased seriously to 240 pA from 50 pA under the treatment of Hz 02 in lmmol/L, but mutant changed little of that. Single cell clamp showed that gpx3 mutant was actually insensitive to H202 , because gpx3 had no clear response when exposed to H2Oz in lmmol/L content, and the current of Col-0 was over 10 fold higher than that of mutant. So it seemed that GPX3 transduced signal of H2 02 by specially controlling outward potassium channel.