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Abstract

The ability of date palm tree to survive under adverse abiotic conditions renders it as an important fruit tree growing in hot and dry regions. Nevertheless, the optimal conditions for date palm growth and production are also suitable for fungal growth leading to major diseases such as black scorch. The aim of this work was to develop a genetic control of date palm to Thielaviopsis punctulata, the causal agent of black scorch, through understanding molecular interactions between the plant host and the pathogen. Genomics and bioinformatics tools were used to sequence, assembly and annotate the whole genome of the pathogen and to decipher the molecular mechanisms of date palm resistance to the pathogen. The whole fungal genome was assembled and functionally annotated with an estimated size of 28.1 Mb containing 5,480 predicted genes. Some of the annotated genes belong to toxin-related genes such as necrosis inducing protein (NPP1) and Cerato-platanin, reflecting a potential functional role of fungal toxins in inducing disease symptoms. On the host side, real-time PCR and RNA-Seq approaches were used to quantify the fungal infection and profile the genome expression of date palm in response to the pathogen infection in two cultivars at 1, 2, 3 and 4 day post infection (dpi). Results from real-time PCR showed that the fungal infection started early at one dpi and the highest level of infection was detected at three dpi for both cultivars. Results also showed that Khalas cultivar is less infected by the pathogen compare to Kinzy cultivar reflecting a degree of resistance in Khalas cultivar. Data from RNA-Seq is being analyzed to identify regulatory genes involved in resistance to black scorch disease. Information from the current study will lead to further understanding of the molecular interactions between T. punctulata and date palm, assisting in deriving effective genetic control strategies for black scorch disease.

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/content/papers/10.5339/qfarc.2016.EEPP1164
2016-03-21
2019-08-23
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http://instance.metastore.ingenta.com/content/papers/10.5339/qfarc.2016.EEPP1164
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