Characterization of Natural Antisense Transcript, Sclerotia Development and Secondary Metabolism by Strand-Specific RNA Sequencing of Aspergillus flavus
Characterization of Natural Antisense Transcript, Sclerotia Development and Secondary Metabolism by Strand-Specific RNA Sequencing of Aspergillus flavus
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通过黄曲霉链特异性 RNA 测序表征天然反义转录本、菌核发育和次生代谢
DOI:
10.1371/journal.pone.0097814
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发表时间:
2014-05
期刊:
影响因子:
3.7
通讯作者:
Wang, Bin
中科院分区:
文献类型:
--
作者:
Wu, Xinliang;Zhou, Bin;Yin, Chao;Guo, Yong;Lin, Ying;Pan, Li;Wang, Bin
Aspergillus flavus has received much attention owing to its severe impact on agriculture and fermented products induced by aflatoxin. Sclerotia morphogenesis is an important process related to A. flavus reproduction and aflatoxin biosynthesis. In order to obtain an extensive transcriptome profile of A. flavus and provide a comprehensive understanding of these physiological processes, the isolated mRNA of A. flavus CA43 cultures was subjected to high-throughput strand-specific RNA sequencing (ssRNA-seq). Our ssRNA-seq data profiled widespread transcription across the A. flavus genome, quantified vast transcripts (73% of total genes) and annotated precise transcript structures, including untranslated regions, upstream open reading frames (ORFs), alternative splicing variants and novel transcripts. We propose natural antisense transcripts in A. flavus might regulate gene expression mainly on the post-transcriptional level. This regulation might be relevant to tune biological processes such as aflatoxin biosynthesis and sclerotia development. Gene Ontology annotation of differentially expressed genes between the mycelia and sclerotia cultures indicated sclerotia development was related closely to A. flavus reproduction. Additionally, we have established the transcriptional profile of aflatoxin biosynthesis and its regulation model. We identified potential genes linking sclerotia development and aflatoxin biosynthesis. These genes could be used as targets for controlled regulation of aflatoxigenic strains of A. flavus.
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影响因子:
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