Wang Hongyang, Sun Chunlian, Jiang Rui, He Qin, Yang Yu, Tian Zhejuan, Tian Zhendong, Xie Conghua
National Center for Vegetable Improvement (Central China), Key Laboratory of Horticultural Plant Biology, Ministry of Education, Huazhong Agricultural University, Wuhan 430070, People's Republic of China.
National Center for Vegetable Improvement (Central China), Key Laboratory of Horticultural Plant Biology, Ministry of Education, Huazhong Agricultural University, Wuhan 430070, People's Republic of China; Xinjiang Production and Construction Corps Key Laboratory of Protection and Utilization of Biological Resources, Tarim Basin 843300, People's Republic of China.
J Plant Physiol. 2014 Jul 1;171(11):907-14. doi: 10.1016/j.jplph.2014.02.011. Epub 2014 Mar 22.
Dihydrolipoyl acyltransferase (EC 2.3.1.12), a branched-chain α-ketoacid dehydrogenase E2 subunit (BCE2), catalyzes the transfer of the acyl group from the lipoyl moiety to coenzyme A. However, the role of BCE2 responding to biotic stress in plant is not clear. In this study, we cloned and characterized a BCE2 gene from potato, namely StBCE2, which was previously suggested to be involved in Phytophthora infestans-potato interaction. We found that the expression of StBCE2 was strongly induced by both P. infestans isolate HB09-14-2 and salicylic acid. Besides, when the homolog of StBCE2 in Nicotiana benthamiana named NbBCE2 was silenced, plants showed increased susceptibility to P. infestans and reduced accumulation of hydrogen peroxide (H2O2). Furthermore, we found that a marker gene NbrbohB involved in the production of reactive oxygen species, was also suppressed in NbBCE2-silenced plants. However, silencing of NbBCE2 had no significant effect on the hypersensitive responses trigged by INF1, R3a-AVR3a(KI) pair or Rpi-vnt1.1-AVR-vnt1.1 pair. Our results suggest that BCE2 is associated with the basal resistance to P. infestans by regulating H2O2 production.
二氢硫辛酰转酰基酶（EC 2.3.1.12），即支链α-酮酸脱氢酶E2亚基（BCE2），催化酰基从硫辛酰部分转移至辅酶A。然而，BCE2在植物应对生物胁迫中的作用尚不清楚。在本研究中，我们从马铃薯中克隆并鉴定了一个BCE2基因，即StBCE2，此前有研究表明它参与了致病疫霉与马铃薯的互作。我们发现，致病疫霉分离株HB09 - 14 - 2和水杨酸均能强烈诱导StBCE2的表达。此外，当本氏烟中StBCE2的同源基因NbBCE2被沉默时，植株对致病疫霉的易感性增加，过氧化氢（H2O2）的积累减少。此外，我们发现参与活性氧生成的一个标记基因NbrbohB在NbBCE2沉默的植株中也受到抑制。然而，沉默NbBCE2对由INF1、R3a - AVR3a(KI)对或Rpi - vnt1.1 - AVR - vnt1.1对引发的过敏反应没有显著影响。我们的结果表明，BCE2通过调节H2O2的产生与对致病疫霉的基础抗性相关。
