Durrant Wendy E, Wang Shui, Dong Xinnian
Developmental, Cell, and Molecular Biology Group, Department of Biology, Duke University, Box 91000, Durham, NC 27708, USA.
Proc Natl Acad Sci U S A. 2007 Mar 6;104(10):4223-7. doi: 10.1073/pnas.0609357104. Epub 2007 Feb 21.
The plant immune response known as systemic acquired resistance (SAR) is a general defense mechanism that confers long-lasting resistance against a broad spectrum of pathogens. SAR triggers many molecular changes including accumulation of antimicrobial pathogenesis-related (PR) proteins. Transcription of PR genes in Arabidopsis is regulated by the coactivator NPR1 and the repressor SNI1. Pathogen infection also triggers an increase in somatic DNA recombination, which results in transmission of changes to the offspring of infected plants. However, it is not known how the induction of homologous recombination during SAR is controlled. Here, we show that SNI1 and RAD51D regulate both gene expression and DNA recombination. In a genetic screen for suppressors of sni1, we discovered that RAD51D is required for NPR1-independent PR gene expression. As a result, the rad51d mutant has enhanced disease susceptibility. Besides altered PR gene expression, rad51d plants are hypersensitive to DNA-damaging agents and are impaired in homologous recombination. The dual role of RAD51D and SNI1 in PR gene transcription and DNA recombination suggests a mechanistic link between the short-term defense response and a long-term survival strategy.
被称为系统获得性抗性（SAR）的植物免疫反应是一种普遍的防御机制，可赋予植物对多种病原体的持久抗性。SAR引发许多分子变化，包括抗菌病程相关（PR）蛋白的积累。拟南芥中PR基因的转录受共激活因子NPR1和阻遏因子SNI1调控。病原体感染还会引发体细胞DNA重组增加，这会导致感染植物的后代发生变化并遗传下去。然而，尚不清楚在SAR过程中同源重组的诱导是如何被控制的。在这里，我们表明SNI1和RAD51D同时调节基因表达和DNA重组。在对sni1抑制子的遗传筛选中，我们发现RAD51D是不依赖NPR1的PR基因表达所必需的。因此，rad51d突变体对疾病的易感性增强。除了PR基因表达改变外，rad51d植物对DNA损伤剂高度敏感，并且在同源重组方面存在缺陷。RAD51D和SNI1在PR基因转录和DNA重组中的双重作用表明了短期防御反应与长期生存策略之间的机制联系。
