Seo Shigemi, Katou Shinpei, Seto Hideharu, Gomi Kenji, Ohashi Yuko
Plant-Microbe Interactions Research Unit, National Institute of Agrobiological Sciences, Tsukuba, Ibaraki, Japan.
Plant J. 2007 Mar;49(5):899-909. doi: 10.1111/j.1365-313X.2006.03003.x. Epub 2007 Jan 23.
In tobacco (Nicotiana tabacum), wounding causes rapid activation of two mitogen-activated protein kinases (MAPKs), wound-induced protein kinase (WIPK) and salicylic acid (SA)-induced protein kinase (SIPK), and the subsequent accumulation of jasmonic acid (JA). Our previous studies suggested that activation of WIPK is required for the production of wound-induced JA. However, the exact role of WIPK remains unresolved. We generated transgenic tobacco plants in which either WIPK or SIPK were silenced using RNA interference to define the roles of WIPK and SIPK in the wound response. In addition, transgenic tobacco plants were generated in which both WIPK and SIPK were silenced to examine the possibility that they have redundant roles. Wound-induced JA production was reduced compared with non-silenced plants in all of the WIPK-, SIPK- and WIPK/SIPK-silenced plants. Transgenic plants over-expressing NtMKP1, a gene encoding tobacco MAPK phosphatase, which inactivates WIPK and SIPK, also exhibited reduced JA production in response to wounding. In both WIPK/SIPK-silenced and NtMKP1-over-expressing plants, wounding resulted in an abnormal accumulation of both SA and transcripts for SA-responsive genes. These results suggest that WIPK and SIPK play an important role in JA production in response to wounding, and that they function cooperatively to control SA biosynthesis.
在烟草(Nicotiana tabacum)中,创伤会导致两种丝裂原活化蛋白激酶(MAPK)迅速激活,即创伤诱导蛋白激酶(WIPK)和水杨酸(SA)诱导蛋白激酶(SIPK),随后茉莉酸(JA)积累。我们之前的研究表明,创伤诱导的JA产生需要WIPK激活。然而,WIPK的确切作用仍未明确。我们利用RNA干扰技术构建了WIPK或SIPK沉默的转基因烟草植株,以确定WIPK和SIPK在创伤反应中的作用。此外,还构建了WIPK和SIPK均沉默的转基因烟草植株,以研究它们是否具有冗余作用。与未沉默的植株相比,所有WIPK、SIPK和WIPK/SIPK沉默的植株中,创伤诱导的JA产生均减少。过表达编码烟草MAPK磷酸酶的基因NtMKP1的转基因植株,该基因可使WIPK和SIPK失活,其创伤诱导的JA产生也减少。在WIPK/SIPK沉默和NtMKP1过表达的植株中,创伤均导致SA和SA响应基因转录本异常积累。这些结果表明,WIPK和SIPK在创伤诱导的JA产生中起重要作用,并且它们协同作用以控制SA生物合成。