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CglCUT1 gene required for cutinase activity and pathogenicity of Colletotrichum gloeosporioides causing anthracnose of Camellia oleifera

Colletotrichum gloeosporioides is the causal agent of Camellia oleifera anthracnose, mainly infecting fruits and leaves. The fungus secretes degrading enzymes to destroy the cuticle of aerial plant parts and help infect the host successfully. To validate whether a cutinase gene ( CglCUT1 ) was requi...

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Bibliographic Details
Published in:European journal of plant pathology 2017-01, Vol.147 (1), p.103-114
Main Authors: Wang, Yixun, Chen, Jingyuan, Li, De-Wei, Zheng, Lu, Huang, Junbin
Format: Article
Language:English
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Summary:Colletotrichum gloeosporioides is the causal agent of Camellia oleifera anthracnose, mainly infecting fruits and leaves. The fungus secretes degrading enzymes to destroy the cuticle of aerial plant parts and help infect the host successfully. To validate whether a cutinase gene ( CglCUT1 ) was required for cutinase activity and pathogenicity of C. gloeosporioides , the CglCUT1 gene was cloned and analyzed. The characterization of CglCUT1 predicted protein suggests that the cloned DNA encoded a cutinase in C. gloeosporioides affecting C. oleifera . The CglCUT1 showed a high homology to those from C. gloeosporioides causing papaya anthracnose and C. capsici causing pepper anthracnose, as well as those of other ascomycetes. The whole CglCUT1 gene was knocked-out and the knockout mutant (∆ CglCUT 39) was subsequently complemented using Agrobacterium tumefaciens mediated transformation. The knockout transformants exhibited significant decreases in cutinase activity and virulence compared with the wild-type strain. The complemented transformants of the disrupted transformant ∆ CglCUT 39 showed a significant increase in cutinase activity and virulence compared with the disrupted transformant ∆ CglCUT 39. This study suggests that the CglCUT1 gene has a positive effect on fungal virulence of the hemibiotrophic C. gloeosporioides on C. oleifera .
ISSN:0929-1873
1573-8469
DOI:10.1007/s10658-016-0983-x