Onyilo Francis, Tusiime Geoffrey, Chen Li-Hung, Falk Bryce, Stergiopoulos Ioannis, Tripathi Jaindra N, Tushemereirwe Wilberforce, Kubiriba Jerome, Changa Charles, Tripathi Leena
National Agricultural Research LaboratoriesKampala, Uganda.
Department of Agricultural Production, College of Agricultural and Environmental Sciences, Makerere UniversityKampala, Uganda.
Front Microbiol. 2017 May 16;8:830. doi: 10.3389/fmicb.2017.00830. eCollection 2017.
Black Sigatoka disease, caused by is a serious constraint to banana production worldwide. The disease continues to spread in new ecological niches and there is an urgent need to develop strategies for its control. The high osmolarity glycerol (HOG) pathway in is well known to respond to changes in external osmolarity. HOG pathway activation leads to phosphorylation, activation and nuclear transduction of the HOG1 mitogen-activated protein kinases (MAPKs). The activated HOG1 triggers several responses to osmotic stress, including up or down regulation of different genes, regulation of protein translation, adjustments to cell cycle progression and synthesis of osmolyte glycerol. This study investigated the role of the MAPK-encoding gene on osmotic stress adaptation and virulence of nsis. RNA interference-mediated gene silencing of significantly suppressed growth of on potato dextrose agar media supplemented with 1 M NaCl, indicating that regulates osmotic stress. In addition, virulence of the -silenced mutants of on banana was significantly reduced, as observed from the low rates of necrosis and disease development on the infected leaves. Staining with lacto phenol cotton blue further confirmed the impaired mycelial growth of the in the infected leaf tissues, which was further confirmed with quantification of the fungal biomass using absolute- quantitative PCR. Collectively, these findings demonstrate that plays a critical role in osmotic stress regulation and virulence of on its host banana. Thus, could be an interesting target for the control of black Sigatoka disease in banana.
黑叶斑病由[病原体名称未给出]引起,是全球香蕉生产的严重制约因素。该病继续在新的生态位中传播,迫切需要制定控制策略。[病原体名称未给出]中的高渗甘油(HOG)途径众所周知可响应外部渗透压的变化。HOG途径的激活导致HOG1丝裂原活化蛋白激酶(MAPK)的磷酸化、激活和核转导。激活的HOG1触发对渗透胁迫的几种反应,包括不同基因的上调或下调、蛋白质翻译的调节、细胞周期进程的调整以及渗透保护剂甘油的合成。本研究调查了编码MAPK的[基因名称未给出]基因在[病原体名称未给出]对渗透胁迫的适应性和毒力中的作用。RNA干扰介导的[基因名称未给出]基因沉默显著抑制了[病原体名称未给出]在补充有1 M NaCl的马铃薯葡萄糖琼脂培养基上的生长,表明[基因名称未给出]调节渗透胁迫。此外,从感染叶片上坏死和病害发展的低发生率可以看出,[基因名称未给出]沉默突变体在香蕉上的毒力显著降低。用乳酚棉蓝染色进一步证实了[病原体名称未给出]在感染叶片组织中的菌丝生长受损,使用绝对定量PCR对真菌生物量进行定量进一步证实了这一点。总的来说,这些发现表明[基因名称未给出]在渗透胁迫调节和[病原体名称未给出]对其寄主香蕉的毒力中起关键作用。因此,[基因名称未给出]可能是控制香蕉黑叶斑病的一个有趣靶点。