Finch-Boekweg Heather, Gardner John S, Allen Phil S, Geary Brad
First, third, and fourth authors: Brigham Young University, Department of Plant and Wildlife Sciences, Provo, UT 84602; and second author: Brigham Young University, Department of Biology, Provo, UT 84602.
Phytopathology. 2016 Mar;106(3):236-43. doi: 10.1094/PHYTO-09-15-0229-R. Epub 2016 Feb 8.
The Ascomycete fungus, Pyrenophora semeniperda, attacks a broad range of cool-season grasses. While leaf and predispersal infection of seeds (i.e., florets containing caryopses) have been previously characterized, little is known about the pathogenesis of mature seeds following dispersal. In this study, we examined infection and disease development of P. semeniperda on dormant seeds of Bromus tectorum. Inoculated seeds were hydrated at 20°C for up to 28 days. Disease development was characterized using scanning electron and light microscopy. P. semeniperda conidia germinated on the seed surface within 5 to 8 h. Hyphae grew on the seed surface and produced extracellular mucilage that eventually covered the seed. Appressoria formed on the ends of hyphae and penetrated through the lemma and palea, stomatal openings, and broken trichomes. The fungus then catabolized the endosperm, resulting in a visible cavity by 8 days. Pathogenesis of the embryo was associated with progressive loss of cell integrity and proliferation of mycelium. Beginning at approximately day 11, one to several stromata (approximately 150 μm in diameter and up to 4 mm in length) emerged through the lemma and palea. Degradation of embryo tissue was completed near 14 days. Conidiophores produced conidia between 21 and 28 days and often exhibited "Y-shaped" branching. This characterization of disease development corrects previous reports which concluded that P. semeniperda is only a weak seed pathogen with infection limited to the outermost seed tissues. In addition, the time required for disease development explains why infected dormant or slow-germinating seeds are most likely to experience mortality.
子囊菌真菌小麦根腐平脐蠕孢可侵染多种冷季型禾本科植物。虽然之前已经对叶片和种子（即含有颖果的小花）的预传播感染进行了描述，但对于传播后成熟种子的发病机制却知之甚少。在本研究中，我们检测了小麦根腐平脐蠕孢对休眠的雀麦种子的侵染及病害发展情况。将接种后的种子在20℃下吸水长达28天。利用扫描电子显微镜和光学显微镜对病害发展进行了表征。小麦根腐平脐蠕孢分生孢子在种子表面5至8小时内萌发。菌丝在种子表面生长并产生细胞外黏液，最终覆盖种子。附着胞在菌丝末端形成并穿透内外稃、气孔和断裂的毛状体。然后真菌分解胚乳，到8天时形成可见的空洞。胚的发病机制与细胞完整性的逐渐丧失和菌丝体的增殖有关。大约从第11天开始，一到几个子座（直径约150μm，长度可达4mm）从内外稃中穿出。胚组织的降解在14天左右完成。分生孢子梗在21至28天之间产生分生孢子，且常呈现“Y形”分支。这种病害发展的表征纠正了之前的报道，之前的报道认为小麦根腐平脐蠕孢只是一种弱种子病原菌，感染仅限于种子最外层组织。此外，病害发展所需的时间解释了为什么受感染的休眠或发芽缓慢的种子最有可能死亡。
