Eldakak Moustafa, Das Aayudh, Zhuang Yongbin, Rohila Jai S, Glover Karl, Yen Yang
Department of Biology and Microbiology, South Dakota State University, Brookings, SD 57006, USA.
Genetics Department, College of Agriculture, Alexandria University, Alexandria 21526, Egypt.
Pathogens. 2018 Jun 22;7(3):58. doi: 10.3390/pathogens7030058.
Fusarium head blight (FHB) is a highly detrimental disease of wheat. A quantitative trait locus for FHB resistance, , is the most utilized source of resistance in wheat-breeding programs, but very little is known about its resistance mechanism. In this study, we elucidated a prospective FHB resistance mechanism by investigating the proteomic signatures of in a pair of contrasting wheat near-isogenic lines (NIL) after 24 h of inoculation of wheat florets by . Statistical comparisons of the abundances of protein spots on the 2D-DIGE gels of contrasting NILs (fhb1+ NIL = present; fhb1- NIL = absent) enabled us to select 80 high-ranking differentially accumulated protein (DAP) spots. An additional evaluation confirmed that the DAP spots were specific to the spikelet from fhb1- NIL (50 spots), and fhb1+ NIL (seven spots). The proteomic data also suggest that the absence of makes the fhb1- NIL vulnerable to attack by constitutively impairing several mechanisms including sucrose homeostasis by enhancing starch synthesis from sucrose. In the absence of , inoculations severely damaged photosynthetic machinery; altered the metabolism of carbohydrates, nitrogen and phenylpropanoids; disrupted the balance of proton gradients across relevant membranes; disturbed the homeostasis of many important signaling molecules induced the mobility of cellular repair; and reduced translational activities. These changes in the fhb1- NIL led to strong defense responses centered on the hypersensitive response (HSR), resulting in infected cells suicide and the consequent initiation of FHB development. Therefore, the results of this study suggest that largely functions to either alleviate HSR or to manipulate the host cells to not respond to infection.
赤霉病是小麦的一种极具危害性的病害。一个抗赤霉病的数量性状位点是小麦育种计划中使用最多的抗性来源，但对其抗性机制却知之甚少。在本研究中，我们通过调查一对对比小麦近等基因系（NIL）在接种小麦小花24小时后的蛋白质组特征，阐明了一种潜在的抗赤霉病机制。对对比NILs（fhb1 + NIL = 存在；fhb1 - NIL = 不存在）的二维差异凝胶电泳（2D - DIGE）凝胶上蛋白质斑点丰度的统计比较，使我们能够选择80个排名靠前的差异积累蛋白（DAP）斑点。进一步评估证实，这些DAP斑点分别特异于fhb1 - NIL（50个斑点）和fhb1 + NIL（7个斑点）的小穗。蛋白质组数据还表明，fhb1的缺失通过增强蔗糖向淀粉的合成，持续损害包括蔗糖稳态在内的多种机制，使fhb1 - NIL易受病原菌攻击。在没有fhb1的情况下，病原菌接种严重破坏了光合机制；改变了碳水化合物、氮和苯丙烷类化合物的代谢；破坏了相关膜上质子梯度的平衡；扰乱了许多重要信号分子的稳态，诱导了细胞修复的迁移；并降低了翻译活性。fhb1 - NIL中的这些变化导致了以过敏反应（HSR）为中心的强烈防御反应，导致受感染细胞自杀，从而引发赤霉病的发展。因此，本研究结果表明，fhb1主要起到减轻过敏反应或操纵宿主细胞对病原菌感染不产生反应的作用。
