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

马铃薯和番茄的晚疫病是由卵霉菌疫霉引起的，它已重新成为世界范围内马铃薯最重要的病害。同时，这种病原体的世界种群在过去二十年中发生了巨大变化。新群体主要由US-8基因型组成，比旧的US-1基因型更具侵略性和成功性。然而，迄今为止，很少有研究涉及马铃薯与新菌株和旧菌株之间的差异相互作用。我实验室最近的研究表明，抑制植物防御基因是US-8菌株在感染部位抵消马铃薯防御机制的一种策略，而US-1菌株则没有。有趣的是，这种抑制作用适用于某些基因，而不适用于其他基因。多年来，人们一直怀疑这种病理系统中存在防御抑制，并且在病原菌中发现了葡聚糖性质的抑制因子。然而，这种抑制的机制及其作用尚不清楚。通过我的研究项目，我试图了解控制植物防御抑制的分子和生化机制，使目前主要的病原菌菌株能够克服马铃薯的防御。我将研究病原菌抑制防御基因表达的能力是否只是组成性的，或者它是否也在病原菌与宿主组织的相互作用中被诱导。然后，我将研究大肠杆菌葡聚糖与肽抑制因子在这种防御基因下调中的相对作用。在植物方面，我将研究是否其他同种异构体的积累，以牺牲抑制基因为代价，以响应病原菌抑制因子。最后，我将评估水杨酸（SA）、茉莉酸甲酯（MJ）、脱落酸（ABA）和乙烯（ET）对这些同工异构体的抑制/诱导作用。这项研究对于了解最具攻击性的病原菌是如何打败马铃薯的防御反应具有重要意义，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.