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  • Title: Revealing the dominant long noncoding RNAs responding to the infection with Colletotrichum gloeosporioides in Hevea brasiliensis.
    Author: Yin H, Zhang X, Zhang B, Luo H, He C.
    Journal: Biol Direct; 2019 Apr 15; 14(1):7. PubMed ID: 30987641.
    Abstract:
    BACKGROUND: Rubber tree (Hevea brasiliensis) acts as an important tropic economic crop and rubber tree anthracnose, mainly caused by Colletotrichum gloeosporioides, is one of the most common fungal disease, which leads to serious loss of rubber production. Therefore, the investigation on disease resistance is of great worldwide significance. In the past decades, substantial progress has been made on coding gene families related with plant disease resistance. However, in rubber tree, whether the disease resistance mechanism involves noncoding RNAs, especially long noncoding RNAs (lncRNAs), still remains poorly understood. RESULTS: Here, we modeled the development of H. brasiliensis leaf samples inoculated with C. gloeosporioides at divergent stages, explored to identify the expressed ncRNAs by RNA-seq, and investigated the dominant lncRNAs responding to the infection, through constructing a co-expressed network systematically. On the dominant lncRNAs, we explored the potential functional role of lncRNA11254 recruiting the transcription factor, and that lncRNA11041 and lncRNA11205 probably stimulate the accumulation of corresponding disease responsive miRNAs, and further modulate the expressions of target genes, accompanying with experimental examination. CONCLUSIONS: Take together, computational analyses in silico and experimental evidences in our research collectively revealed the responsive roles of dominant lncRNAs to the pathogen. The results will provide new perspectives to unveil the plant disease resistance mechanisms, and will presumably provide a new theoretical basis and candidate prognostic markers for the optimization and innovation of genetic breeding for rubber tree. REVIEWERS: This article was reviewed by Ryan McGinty and Roland Huber.
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