Host barriers and responses to Uncinula necator in developing grape berries
Host barriers and responses to Uncinula necator in developing grape berries
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DOI：
10.1094/phyto.2004.94.5.438
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发表时间：
2004-05-01
期刊：
影响因子：
3.2
通讯作者：
Dry, IB
中科院分区：
文献类型：
--
作者：
Ficke, A;Gadoury, DM;Dry, IB
葡萄浆果在开花后1周对白粉病高度敏感，但在2-3周后获得个体抗性。我们最近证明，葡萄白粉病病原菌(Uncinula Necator)的萌发分生孢子在角质层穿透较老的抗性浆果之前停止发育。在那个特定阶段阻止U-Necator的机制尚不清楚。以前的几项研究调查了浆果和叶片对白粉病的潜在寄主屏障或细胞反应，但没有一项研究包括观察这些因素对病原菌发育的直接影响。我们发现，角质层厚度随着浆果年龄的增加而增加，但病原菌的侵入在形成可见的渗透孔之前就停止了。在浆果从高度敏感到几乎免疫的这段时间里，细胞壁厚度在开花后的前4周保持不变。在高度敏感的浆果上，自发荧光多酚化合物在附着部下积累的频率高于在高度抗性的浆果上；在敏感浆果上，细胞变色表明上述酚类化合物的氧化频率显著高于敏感浆果。在所有萌发的分生孢子的第一次形成附着体的下面。乳突在2至5天的浆果上的出现频率显著高于30至31天的水果。在老浆果上观察到的乳突相对较少，大多数情况下(82.8-97.3%)是在不产生次生菌丝的分生孢子附着体下发现的。与此形成对比的是，年轻浆果上产生的乳突更丰富，只有35.4%~41.0%的乳突位于不产生次生菌丝的分生孢子附着体的下方。致病相关基因(VvPR-1)在感病浆果中的诱导比在抗病浆果中高得多。相反，抗性浆果在接种16h内就表达了类Germin蛋白(VvGLP3)，而在感病浆果中则没有表达。我们的结果表明，几种可能的感染屏障，即角质层和细胞壁厚度，抗菌酚，以及之前描述的两种与病程相关的蛋白质，并不是阻止病原菌进入个体发育抗性浆果的主要原因，而是通过以下一种或多种方式阻止感染：(I)在角质层表面附近预先形成的物理或生化屏障，或(Ii)在感染过程的最初几个小时内，老浆果中抗真菌化合物的快速合成。
Grape berries are highly susceptible to powdery mildew 1 week after bloom but acquire ontogenic resistance 2 to 3 weeks later. We recently demonstrated that germinating conidia of the grape powdery mildew pathogen (Uncinula necator) cease development before penetration of the cuticle on older resistant berries. The mechanism that halts U. necator at that particular stage was not known. Several previous studies investigated potential host barriers or cell responses to powdery mildew in berries and leaves, but none included observation of the direct effect of these factors on pathogen development. We found that cuticle thickness increased with berry age, but that ingress by the pathogen halted before formation of a visible penetration pore. Cell wall thickness remained unchanged over the first 4 weeks after bloom, the time during which berries progressed from highly susceptible to nearly immune. Autofluorescent polyphenolic compound, accumulated at a higher frequency beneath appressoria on highly susceptible berries than on highly resistant berries; and oxidation of the above phenolics, indicated by cell discoloration, developed at a significantly higher frequency on susceptible berries. Beneath the first-formed appressoria of all germinated conidia. papillae occurred at a significantly higher frequency on 2- to 5-day-old berries than on 30- to 31-day-old fruit. The relatively few papillae observed on older berries were, in most cases (82.8 to 97.3%), found beneath appressoria of conidia that had failed to produce secondary hyphae. This contrasted with the more abundantly produced papillae on younger berries, where only 35.4 to 41.0% were located beneath appressoria of conidia that had failed to produce secondary hyphae. A pathogenesis-related gene (VvPR-1) was much more highly induced in susceptible berries than in resistant berries after inoculation with U. necator. In contrast, a germin-like protein (VvGLP3) was expressed within 16 h of inoculation in resistant, but not in susceptible berries. Our results suggest that several putative barriers to infection, i.e., cuticle and cell wall thickness, antimicrobial phenolics, and two previously described pathogenesis-related proteins, are not principal causes in halting pathogen ingress on ontogenically resistant berries, but rather that infection is halted by one or more of the following: (i) a preformed physical or biochemical barrier near the cuticle surface, or (ii) the rapid synthesis of an antifungal compound in older berries during the first few hours of the infection process.