Induced expression of a temperature-sensitive leucine-rich repeat receptor-like protein kinase gene by hypersensitive cell death and wounding in tobacco plant carrying the N resistance gene.
Induced expression of a temperature-sensitive leucine-rich repeat receptor-like protein kinase gene by hypersensitive cell death and wounding in tobacco plant carrying the N resistance gene.
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在携带 N 抗性基因的烟草植物中，通过过敏性细胞死亡和损伤诱导温度敏感的富含亮氨酸重复受体样蛋白激酶基因的表达。
DOI：
10.1093/pcp/pcf031
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发表时间：
2002
影响因子：
4.9
通讯作者：
Y. Ohashi
中科院分区：
文献类型：
--
作者：
N. Ito;R. Takabatake;S. Seo;S. Hiraga;I. Mitsuhara;Y. Ohashi
分离到一个编码受体样蛋白激酶的基因，该基因在烟草叶片中N基因依赖的过敏性细胞死亡的早期被诱导。表达为谷胱甘肽S-转移酶融合蛋白的激酶结构域能够自磷酸化，表明该基因编码活性蛋白激酶。在携带N基因的烟草花叶病毒（TMV）接种的烟草叶片中，在坏死性病斑形成前转录本积累量较高，而在缺乏N基因的烟草品种中则较低。即使在健康的叶片中，在温度从30摄氏度变化到20摄氏度后1-2小时，也发现转录物的小但可重复的增加，这表明基因表达是温度敏感的。该基因被命名为WRK，即创伤诱导的受体样蛋白激酶，因为转录本在创伤后15-30分钟内增加到最大值。在悬浮培养的烟草细胞中，发现在转移到新的培养基后15分钟的转录增加，但它被抑制在高渗透压。伤口诱导的WRK积累增加放线菌酮处理，但不是由已知的防御信号化合物（水杨酸，茉莉酸，1-氨基环丙烷-1-羧酸和脱落酸）和一些植物激素。因此，WRK是一种创伤诱导的温度敏感性蛋白激酶基因，可能通过未知的信号通路在过敏性细胞死亡之前被诱导。
A gene encoding a receptor-like protein kinase was isolated as the gene induced in the early period of N gene-dependent hypersensitive cell death in tobacco leaves. The kinase domain expressed as a glutathione S-transferase fusion protein was capable of autophosphorylation, indicating that this gene encodes an active protein kinase. A high level of the transcript accumulated before necrotic lesion formation in tobacco mosaic virus (TMV)-inoculated tobacco leaves carrying the N gene but it was low in a tobacco cultivar lacking the N gene. A small but reproducible increase in the transcript was found 1-2 h after a temperature shift from 30 degrees C to 20 degrees C even in healthy leaves, suggesting the gene expression is temperature sensitive. The gene was named WRK for wound-induced receptor-like protein kinase, because the transcript increased to a maximum within 15-30 min of wounding. In suspension cultured tobacco cells, an increase in the transcript was found 15 min after transfer to a new medium, but it was suppressed under high osmotic pressures. The wound-induced WRK accumulation was enhanced by cycloheximide treatment, but not by known defense signal compounds (salicylic acid, jasmonic acid, 1-aminocyclopropan-1-carboxylic acid and abscisic acid) and some plant hormones. Thus, WRK is a wound-inducible and temperature-sensitive protein kinase gene induced before hypersensitive cell death probably through unknown signaling pathways.