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作为引起水稻病害的主要病菌之一,稻瘟病菌是一种重要的模式生物,对于研究植物与病原菌之间的互作起着极其重要的作用。甘油激酶在体内可以催化甘油转化为甘油3-磷酸,对甘油的分解代谢起着重要的作用。在稻瘟病菌基因组中有两个编码甘油激酶的基因,分别为Mogly1和Mogly2。我们通过体内同源重组的基因敲除技术,获得两个基因的基因缺失突变体ΔMogly1和ΔMogly2,以及两个基因的双敲突变体ΔMogly1ΔMogly2。表型分析发现这些突变体在生长,产孢,致病性等方面相对于野生型均没有明显变化,但是ΔMogly1和ΔMogly1ΔMogly2在完全培养基上面的气生菌丝减少,菌落颜色变白。通过测量这些突变体在不同碳源培养基上的生长,发现ΔMogly1和ΔMogly1ΔMogly2在以山梨醇、葡萄糖、甘油和蔗糖为唯一碳源的培养基上生长速率均减慢。而在以甘油为唯一碳源的培养基上生长速度被抑制的最为显著。这说明Mogly1和Mogly2在碳源代谢中的作用是不同的,Mogly1基因可能在碳源代谢中扮演着重要的角色,而Mogly2可能是功能冗余的基因。
As one of the major pathogens causing rice diseases, Magnaporthe grisea is an important model organism and plays an extremely important role in studying the interaction between plants and pathogenic bacteria. Glycerol kinase can catalyze the conversion of glycerol to glycerol 3-phosphate in the body, which plays an important role in the catabolism of glycerol. There are two genes encoding glycerol kinase in the genome of Magnaporthe grisea, Mogly1 and Mogly2, respectively. We obtained the gene deletion mutants ΔMogly1 and ΔMogly2 of two genes and the knockout mutant ΔMogly1ΔMogly2 of the two genes by in vivo homologous recombination gene knockout technology. Phenotypic analysis revealed no significant changes in growth, sporulation, pathogenicity, etc. of these mutants relative to the wild type, but reduced aerophilic mycelium of ΔMogly1 and ΔMogly1ΔMogly2 on complete medium, and colony color became white. By measuring the growth of these mutants on different carbon source media, ΔMogly1 and ΔMogly1ΔMogly2 were found to slow down in medium with sorbitol, glucose, glycerol and sucrose as sole carbon source. In the glycerol as the only carbon source on the growth rate of the medium was the most significant inhibition. This suggests that Mogly1 and Mogly2 play different roles in carbon metabolism, Mogly1 may play an important role in carbon metabolism, and Mogly2 may be a functionally redundant gene.