Molecular and biochemical mechanisms of potato defense suppression by P. infestans

晚疫病是由马铃薯和番茄中的卵菌致病疫霉（Phytophthora infestans）引起的，已重新成为世界范围内马铃薯上最重要的病害。同时，在过去的二十年里，这种病原体的世界人口发生了巨大变化。主要由US-8基因型组成的新种群比旧的US-1基因型更具攻击性和成功性。然而，到目前为止，很少有研究涉及马铃薯与新品系和旧品系的差异相互作用。我实验室最近的研究表明，US-8菌株在感染部位抑制马铃薯防御机制的策略之一是抑制植物防御基因，而US-1菌株则没有。有趣的是，这种抑制作用只适用于某些基因，而不适用于其他基因。多年来一直怀疑该病理系统中的防御抑制，并且已经在致病疫霉中鉴定出葡聚糖性质的抑制剂。然而，这种抑制的机制及其作用尚不清楚。通过我的研究计划，我试图了解控制植物防御抑制的分子和生化机制，使目前占主导地位的致病疫霉菌株能够克服马铃薯防御。我将研究致病疫霉抑制防御基因表达的能力是否只是组成型的，或者它是否也在这种病原体与宿主组织相互作用时被诱导。然后，我将研究致病疫霉葡聚糖与肽抑制剂在该防御基因下调中的相对参与。在植物方面，我将研究是否其他亚型积累的代价是抑制基因响应P. infestans抑制。最后，我将评估水杨酸（SA），茉莉酸甲酯（MJ），脱落酸（阿坝）和乙烯（ET）对这些异构体的抑制/诱导的影响。这项研究对于了解最具侵略性的致病疫霉菌株如何击败马铃薯防御反应非常重要，并有望为更有效的基于知识的疾病控制策略奠定基础。

Late blight, caused by the oomycete Phytophthora infestans in both potato and tomato, has re-emerged as the most important disease on potatoes worldwide. Concurrently, the world populations of this pathogen have drastically changed in the last two decades. The new populations, mainly composed of the US-8 genotype, are much more aggressive and successful than the old US-1 genotype. To date, however, very few studies have addressed potato differential interactions with the new versus the old strains. Recent studies in my lab suggested the suppression of plant defense genes as one strategy used by the US-8 strain to counteract potato defense mechanisms at the site of infection, while the US-1 strain did not. Interestingly, such suppression applied to some genes, but not to others. Defense suppression in this pathosystem has been suspected for many years, and suppressors of glucan nature have been identified in P. infestans. However, the mechanisms of such suppression and its role are not understood. Through my research program, I seek to understand the molecular and biochemical mechanisms governing the plant defense suppression that allows the currently predominant strain of P. infestans to overcome potato defenses. I will investigate whether P. infestans ability to inhibit the expression of defense genes is only constitutive or if it is also induced in this pathogen upon its interaction with the host tissues. Then, I will study the relative involvement of P. infestans glucan versus peptidic suppressors in this defense gene downregulation. On the plant side, I will investigate whether other isoforms accumulate at the expense of the suppressed gene in response to P. infestans suppressors. Finally, I will assess the effects of salicylic acid (SA), methyl jasmonate (MJ), abscissic acid (ABA) and ethylene (ET) on the suppression/induction of these isoforms. This research is important in order to understand how the most aggressive strains of P. infestans defeat potato defense reactions, and hopefully will lay the groundwork for more efficient knowledge-based disease control strategies.