Characteristics of inositol phosphorylceramide synthase and effects of aureobasidin A on growth and pathogenicity of Botrytis cinerea.

Characteristics of inositol phosphorylceramide synthase and effects of aureobasidin A on growth and pathogenicity of Botrytis cinerea.
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DOI:
10.2323/jgam.61.108
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发表时间:
2015-08
期刊:
The Journal of general and applied microbiology
影响因子:
--
通讯作者:
Xin-hui Wang;Xingqi Guo;Hong-ye Li;Ping Gou
Xin-hui Wang;Xingqi Guo;Hong-ye Li;Ping Gou
中科院分区:
其他
文献类型:
--
作者:
Xin-hui Wang;Xingqi Guo;Hong-ye Li;Ping Gou

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肌醇磷酸神经酰胺合成酶(IPC)是真菌鞘脂生物合成的关键酶,具有高度保守的序列。抗生素金霉素A(阿坝)通过抑制IPC合酶活性诱导真菌死亡。真菌和原生动物中编码IPC合成酶的AUR 1基因的突变导致对阿坝的抗性。然而,阿坝甲酰胺耐药的机制仍不清楚。本文通过紫外线诱变,获得了灰葡萄孢(Botrytis cinerea)的两个抗ABA突变体BcAUR1a和BcAUR1b。BcAUR1a缺失一个内含子,BcAUR1b在AUR1基因中有三个氨基酸突变(L197P,F288S和T323A)。在野生型B中,阿坝强烈抑制IPC合酶的活性。灰霉病,这导致细胞形态的明显变化,包括分生孢子萌发延迟,芽管和菌丝体尖端附近的过度分枝,以及菌丝生长的抑制。此外,阿坝防止野生型B的感染。番茄果实中的灰霉病通过降低草酸的分泌以及纤维素酶和果胶酶的活性而起作用。相反,阿坝对两株突变体的生长和致病性均无影响。虽然这两个突变体表现出相似的阿坝抗性,但两个突变体之间的分子机制可能不同。
Inositol phosphorylceramide (IPC) synthase is the key enzyme with highly conserved sequences, which is involved in fungal sphingolipid biosynthesis. The antibiotic aureobasidin A (AbA) induces the death of fungi through inhibiting IPC synthase activity. The mutations of AUR1 gene coding IPC synthase in fungi and protozoa causes a resistance to AbA. However, the mechanism of AbA resistance is still elusive. In this paper, we generated two mutants of Botrytis cinerea with AbA-resistance, BcAUR1a and BcAUR1b, through UV irradiation. BcAUR1a lost an intron and BcAUR1b had three amino acid mutations (L197P, F288S and T323A) in the AUR1 gene. AbA strongly inhibits the activity of IPC synthase in wild-type B. cinerea, which leads to distinct changes in cell morphology, including the delay in conidial germination, excessive branching near the tip of the germ tube and mycelium, and the inhibition of the mycelium growth. Further, AbA prevents the infection of wild-type B. cinerea in tomato fruits via reducing oxalic acid secretion and the activity of cellulase and pectinase. On the contrary, AbA has no effect on the growth and pathogenicity of the two mutants. Although both mutants show a similar AbA resistance, the molecular mechanisms might be different between the two mutants.