Open Access Highly Accessed Research article

Sequencing the genome of Marssonina brunnea reveals fungus-poplar co-evolution

Sheng Zhu1, You-Zhi Cao1, Cong Jiang1, Bi-Yue Tan1, Zhong Wang2, Sisi Feng2, Liang Zhang3, Xiao-Hua Su4, Brona Brejova5, Tomas Vinar5, Meng Xu1, Ming-Xiu Wang1, Shou-Gong Zhang4*, Min-Ren Huang1*, Rongling Wu12* and Yan Zhou36*

Author Affiliations

1 Jiangsu Key Laboratory for Poplar Germplasm Enhancement and Variety Improvement, Nanjing Forestry University, Nanjing, China

2 Center for Computational Biology, Beijing Forestry University, Beijing, China

3 Shanghai-MOST Key Laboratory of Health and Disease Genomics, Chinese National Human Genome Center at Shanghai, Shanghai, China

4 Research Institute of Forestry, Chinese Academy of Forestry, Beijing, China

5 Faculty of Mathematics, Physics, and Informatics, Comenius University, Mlynska Dolina, Bratislava, 84248, Slovakia

6 Department of Microbiology and Microbial Engineering, School of Life Sciences, Fudan University, Shanghai, China

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BMC Genomics 2012, 13:382  doi:10.1186/1471-2164-13-382

Published: 9 August 2012

Additional files

Additional file 1:

Table S1. Main features of M. brunnea genome assemblies.

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Additional file 2:

Figure S1. The structure of ITS (internal transcribed spacer) DNA sequence. ITS1 was located between the SSU (small subunit) RNA and 5.8 s RNA, and ITS2 was located between the 5.8 s RNA and LSU (large subunit) RNA.

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Additional file 3:

Figure S2. The taxonomic classification of three fungi including M. brunnea, B. cinerea and S. sclerotiorum.

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Additional file 4:

Figure S3. The distribution of protein families in M. brunnea.

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Additional file 5:

Table S3. Top 20 protein families in M. brunnea that are the most significantly different from those of other fungal genomes including B. cinerea, S. sclerotiorum, M. grisea, and F. graminearum.

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Additional file 6:

Figure S4. Pathogen protection mechanism during infection. Fungi have mechanisms to avoid induction of the host immunity systems and alleviate the defense responses. The fungal plant pathogen C. fulvum gene ECP6 encodes a small, secreted protein, which sequesters chitin oligosaccharides to prevent eliciting host defense responses. Pathogens have two methods of coping with the toxicity and antifungal compound secreted by the host. One is efflux by the ABC1-encoded protein. The other is to produce enzymes to degrade them: Gaeumannomyces graminis secrets saponin-degrading enzymes AVENACINASE to detoxify the triterpenoid oat root saponin avenacin A-1. As the pathogens can secret some substances that contribute to infection that are also harmful to the pathogen itself, pathogen should encode methods of mitigating self-harm. Fusarium sporotrichioides can produce the trichothecene mycotoxin deoxynivalenol (DON) to inhibit protein synthesis of the host. The fungi have a gene called TRI101 that encodes trichothecene 3-O acetyltransferase, which can reduce the damage to pathogen caused by trichothecene mycotoxin deoxynivalenol.

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Additional file 7:

Figure S5. The domain structure for the gene ABC3.

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Additional file 8:

Figure S6. Fungal toxin biosynthesis. Fungi produce toxins to destroy host cellular functions. They can be non-host specific or host specific. Fungi have many genes to control the biosynthesis, export, and regulation of the toxins. Cercosporin is a non-host specific toxin. A polyketide synthase gene, CTB1, plays a key role in cercosporin biosynthesis. CFP encodes a cercosporin Transporter exporting cercosporin, CZK3, which regulates cercosporin biosynthesis. Comparing to the non-host specific toxins, some toxins are active only toward hosts, i.e. host specific toxins, such as HC-toxin, AK-toxin, AM-toxin, and ACT-toxin. HTS1 encodes a multifunctional cyclic peptide synthetase involved in the biosynthesis of HC-toxin. Besides HTS1, ToxC and ToxF are also essential for toxin biosynthesis and pathogenicity. AKT1, which encodes a series of carboxyl-activating enzymes, and AKT2 are involved in the biosynthesis of the AK-toxin. The AMT gene is essential for the biosynthesis of the AM-toxin. ACTTS2 and ACTTS3 are essential genes for ACT-toxin biosynthesis.

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Additional file 9:

Text S1. Additional Description.

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Additional file 10:

Table S4. Six gene groups involved in pathogenesis.

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Additional file 11:

Table S5. The genes associated with mating and meiosis.

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Additional file 12:

Table S6. The number of RNA-seq reads mapped to the genome of Populus and M. brunnea.

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Additional file 13:

Table S7. Protein families with more than 10 genes that were up-regulated in M. brunnea.

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Additional file 14:

Figure S7. Multiple alignment of 28 putative proteins with highly similarity for M. brunnea. Multiple sequence alignment of the 28 putative proteins was performed using ClustalW.

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Additional file 15:

Table S8. Resistance genes (R) with differential expression in Populus.

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Additional file 16:

Table S9. The distribution of low complexity sequences for M. brunnea, B. cinerea, and S. sclerotiorum.

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Additional file 17:

Table S10. The distribution of simple repeat sequences for M. brunnea, B. cinerea, and S. sclerotiorum.

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Additional file 18:

Table S11. The number of putative secretory proteins among U. maydis, M. grisea, B. cinerea, S. sclerotiorum, and M. brunnea.

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Additional file 19:

Table S12. The secretory protein families with more than five members M. brunnea.

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Additional file 20:

Table S2. The GenBank accession no of ITS sequences used for phylogenetic tree analysis.

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