Samuilov V D, Lagunova E M, Gostimsky S A, Timofeev K N, Gusev M V
Department of Physiology of Microorganisms, School of Biology, Lomonosov Moscow State University, Moscow 119992, Russia.
Biochemistry (Mosc). 2003 Aug;68(8):912-7. doi: 10.1023/a:1025707200663.
Received Revision received We investigated the CN--induced apoptosis of guard cells in epidermal peels isolated from pea (Pisum sativum L.) leaves. This process was considerably stimulated by illumination and suppressed by the herbicides DCMU (an inhibitor of the electron transfer between quinones Q(A) and Q(B) in PS II) and methyl viologen (an electron acceptor from PS I). These data favor the conclusion drawn by us earlier that chloroplasts are involved in the apoptosis of guard cells. Pea mutants with impaired PS I (Chl-5), PS II (Chl-I), and PS II + PS I (Xa-17) were tested. Their lesions were confirmed by the ESR spectra of Signal I (oxidized PS I reaction centers) and Signal II (oxidized tyrosine residue Y(D) in PS II). Destruction of nuclei (a symptom of apoptosis) and their consecutive disappearance in guard cells were brought about by CN- in all the three mutants and in the normal pea plants. These results indicate that the light-induced enhancement of apoptosis of guard cells and its removal by DCMU are associated with PS II function. The effect of methyl viologen preventing CN--induced apoptosis in wild-type plants was removed or considerably decreased upon the impairment of the PS II and/or PS I activity.
收到 修订稿收到 我们研究了氰化物诱导豌豆（Pisum sativum L.）叶片表皮分离的保卫细胞凋亡。该过程受到光照的显著刺激，并被除草剂二氯苯基二甲基脲（DCMU，PS II中醌Q(A)和Q(B)之间电子传递的抑制剂）和甲基紫精（PS I的电子受体）抑制。这些数据支持我们之前得出的结论，即叶绿体参与保卫细胞的凋亡。对PS I（Chl-5）、PS II（Chl-I）和PS II + PS I（Xa-17）受损的豌豆突变体进行了测试。通过信号I（氧化的PS I反应中心）和信号II（PS II中氧化的酪氨酸残基Y(D)）的电子自旋共振光谱证实了它们的损伤。在所有三个突变体和正常豌豆植株中，氰化物导致保卫细胞核的破坏（凋亡的一个症状）及其随后的消失。这些结果表明，光照诱导的保卫细胞凋亡增强及其被DCMU消除与PS II功能有关。当PS II和/或PS I活性受损时，甲基紫精在野生型植物中阻止氰化物诱导凋亡的作用被消除或显著降低。
