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Updated: May 10, 2025

A Mouse Model for Pathogen-induced Chronic Inflammation at Local and Systemic Sites
Published on: August 8, 2014
Study on Pathogenesis of Cytospora pyri in Korla Fragrant Pear Trees (Pyrus sinkiangensis)
Yiwen Zhang1,2,3, Zhe Wang1,2,3, Zhen Zhang1,2,3
1College of Life Science and Technology, Tarim University, Alar 843300, China.
Abstract:
Pear Valsa cankers were found in various Korla fragrant pear orchards in Alaer, Xinjiang. Disease samples underwent tissue isolation, resulting in six isolates. Pathogenicity tests revealed that the XLFL-6 isolate was the most virulent, demonstrating typical Valsa canker symptoms. Research on its biological characteristics indicated that the optimal growth conditions for XLFL-6 were a temperature of 28 °C and a pH of five. Under these conditions, the colonies of XLFL-6 exhibited the largest growth diameter, and adding glucose and peptone separately to the Czapek medium was most conducive to the growth of its mycelium. Based on morphological observations and multigene sequence analyses (ITS+TEF+TUB), the pathogenic fungus was identified as C. pyri. The infection process of C. pyri was elucidated through tissue observations using both light and electron microscopy. The conidia displayed a similar germination pattern on both wounded and intact twigs. However, the infection process was delayed in the case of intact bark. By 8 h post-inoculation, the conidia achieved a germination rate of 15%. Although germination had occurred, the infection process had not yet commenced. In contrast, for wounded bark tissue, it was observed that 24 h post-inoculation, the fungal hyphae from the conidia directly invaded the wounded tissue. These hyphae penetrate the cell walls, proliferate within the host tissue, and spread throughout the phloem and xylem. After 20 d, numerous pycnidia had breached the bark surface, and yellow waxy gums filled with conidia flowed abundantly from the pycnidia ostioles, with the host tissue being nearly totally disintegrated. Regarding enzyme activity, the polygalacturonase (PG) activity, the primary cell wall-degrading enzyme in the treatment group, was seven times greater than that of the control group. The carboxymethyl cellulose (Cx) activity within the treatment group continued to increase. Xylanase activity rose swiftly to its peak between days 1 and 4, then decreased from days 5 to 10, although it remained higher than that of the control group. Overall, this study is the first to provide a detailed report on the characteristics and proliferation of C. pyri and further elucidates its modes and pathways of invasion.
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