Magnaporthe grisea avirulence gene ACE1 belongs to an infection-specific gene cluster involved in secondary metabolism

Magnaporthe grisea avirulence gene ACE1 belongs to an infection-specific gene cluster involved in secondary metabolism
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DOI:
10.1111/j.1469-8137.2008.02459.x
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发表时间:
2008-01-01
期刊:
影响因子:
9.4
通讯作者:
Boehnert, Heidi U.
Boehnert, Heidi U.
中科院分区:
生物学1区
文献类型:
--
作者:
Collemare, Jerome;Pianfetti, Mikael;Boehnert, Heidi U.

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稻瘟病菌(Magnaporthe grisea)的无毒基因ACE 1编码一个与非核糖体肽合成酶(NRPS)融合的聚酮合酶(PKS),该酶可能参与抗Pi 33水稻品种识别的次生代谢物的生物合成。从稻瘟病菌基因组中发现ACE 1位于15个基因簇中,其中14个可能参与次生代谢,因为它们编码酶,如第二个PKS-NRPS(SYN 2),两个烯酰还原酶(RAP 1和RAP 2)和推定的Zn(II)(2)Cys(6)转录因子(BC 2)。这15个基因在侵入宿主植物期间特异性表达,定义感染特异性基因簇。pORF 3-GFP转录融合显示来自ACE 1簇的高表达ORF 3基因仅在附着胞中表达,ACE 1也是如此。SYN 2和RAP 2的缺失或破坏突变体的表型分析表明,它们不需要在Pi 33水稻品种无毒,不像ACE 1。其他基因的失活是不成功的,因为有针对性的基因替换和破坏是低效的,在这个locus.Overall,ACE 1基因簇显示感染特异性的表达模式限制在渗透阶段,这可能是在转录水平控制,并反映了特定的早期感染阶段的监管网络。
The avirulence gene ACE1 from the rice blast fungus Magnaporthe grisea encodes a polyketide synthase (PKS) fused to a nonribosomal peptide synthetase (NRPS) probably involved in the biosynthesis of a secondary metabolite recognized by Pi33 resistant rice (Oryza sativa) cultivars.Analysis of the M. grisea genome revealed that ACE1 is located in a cluster of 15 genes, of which 14 are potentially involved in secondary metabolism as they encode enzymes such as a second PKS-NRPS (SYN2), two enoyl reductases (RAP1 and RAP2) and a putative Zn(II)(2)Cys(6) transcription factor (BC2).These 15 genes are specifically expressed during penetration into the host plant, defining an infection-specific gene cluster. A pORF3-GFP transcriptional fusion showed that the highly expressed ORF3 gene from the ACE1 cluster is only expressed in appressoria, as is ACE1. Phenotypic analysis of deletion or disruption mutants of SYN2 and RAP2 showed that they are not required for avirulence in Pi33 rice cultivars, unlike ACE1. Inactivation of other genes was unsuccessful because targeted gene replacement and disruption were inefficient at this locus.Overall, the ACE1 gene cluster displays an infection-specific expression pattern restricted to the penetration stage which is probably controlled at the transcriptional level and reflects regulatory networks specific to early stages of infection.