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环磷酸腺苷依赖性蛋白激酶A催化亚基的失活导致炭疽菌附着胞形成延迟及致病性降低。

Inactivation of the catalytic subunit of cAMP-dependent protein kinase A causes delayed appressorium formation and reduced pathogenicity of Colletotrichum gloeosporioides.

作者信息

Priyatno Tri Puji, Abu Bakar Farah Diba, Kamaruddin Nurhaida, Mahadi Nor Muhammad, Abdul Murad Abdul Munir

机构信息

School of Biosciences and Biotechnology, Faculty of Science and Technology, Universiti Kebangsaan Malaysia, Selangor, 43600 Bangi, Malaysia.

出版信息

ScientificWorldJournal. 2012;2012:545784. doi: 10.1100/2012/545784. Epub 2012 May 1.

DOI:10.1100/2012/545784
PMID:22666136
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3361302/
Abstract

The cyclic AMP- (cAMP-) dependent protein kinase A signaling pathway is one of the major signaling pathways responsible for regulation of the morphogenesis and pathogenesis of several pathogenic fungi. To evaluate the role of this pathway in the plant pathogenic fungus, Colletotrichum gloeosporioides, the gene encoding the catalytic subunit of cAMP-dependent protein kinase A, CgPKAC, was cloned, inactivated, and the mutant was analyzed. Analysis of the Cgpkac mutant generated via gene replacement showed that the mutants were able to form appressoria; however, their formation was delayed compared to the wild type. In addition, the mutant conidia underwent bipolar germination after appressoria formation, but no appressoria were generated from the second germ tube. The mutants also showed reduced ability to adhere to a hydrophobic surface and to degrade lipids localized in the appressoria. Based on the number of lesions produced during a pathogenicity test, the mutant's ability to cause disease in healthy mango fruits was reduced, which may be due to failure to penetrate into the fruit. These findings indicate that cAMP-dependent protein kinase A has an important role in regulating morphogenesis and is required for pathogenicity of C. gloeosporioides.

摘要

环磷酸腺苷(cAMP)依赖性蛋白激酶A信号通路是负责调控多种致病真菌形态发生和致病机制的主要信号通路之一。为了评估该通路在植物致病真菌胶孢炭疽菌中的作用,编码cAMP依赖性蛋白激酶A催化亚基的基因CgPKAC被克隆、失活,并对突变体进行了分析。对通过基因替换产生的Cgpkac突变体的分析表明,突变体能够形成附着胞;然而,与野生型相比,其形成过程有所延迟。此外,突变体分生孢子在附着胞形成后进行双极萌发,但第二根芽管未产生附着胞。突变体还表现出附着于疏水表面以及降解附着胞中脂质的能力下降。根据致病性测试中产生的病斑数量,突变体在健康芒果果实中致病的能力降低,这可能是由于无法穿透果实所致。这些发现表明,cAMP依赖性蛋白激酶A在调控形态发生中具有重要作用,并且是胶孢炭疽菌致病性所必需的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/184d/3361302/87381f1c4b9e/TSWJ2012-545784.010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/184d/3361302/bf5cc7675c64/TSWJ2012-545784.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/184d/3361302/7011a09f5fcd/TSWJ2012-545784.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/184d/3361302/0df164e3115e/TSWJ2012-545784.003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/184d/3361302/b4d0b49d8ac6/TSWJ2012-545784.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/184d/3361302/97a2a02e028b/TSWJ2012-545784.008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/184d/3361302/3e3e82b1ebce/TSWJ2012-545784.009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/184d/3361302/87381f1c4b9e/TSWJ2012-545784.010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/184d/3361302/bf5cc7675c64/TSWJ2012-545784.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/184d/3361302/7011a09f5fcd/TSWJ2012-545784.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/184d/3361302/0df164e3115e/TSWJ2012-545784.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/184d/3361302/5ed1330d8a0e/TSWJ2012-545784.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/184d/3361302/c176bf6cc63e/TSWJ2012-545784.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/184d/3361302/8afde4c46458/TSWJ2012-545784.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/184d/3361302/b4d0b49d8ac6/TSWJ2012-545784.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/184d/3361302/97a2a02e028b/TSWJ2012-545784.008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/184d/3361302/3e3e82b1ebce/TSWJ2012-545784.009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/184d/3361302/87381f1c4b9e/TSWJ2012-545784.010.jpg

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