Movement of plant viruses is delayed in a β-1,3-glucanase-deficient mutant showing a reduced plasmodesmatal size exclusion limit and enhanced callose deposition
Movement of plant viruses is delayed in a β-1,3-glucanase-deficient mutant showing a reduced plasmodesmatal size exclusion limit and enhanced callose deposition
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DOI：
10.1046/j.1365-313x.2000.00658.x
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发表时间：
2000-01-01
期刊：
影响因子：
7.2
通讯作者：
Meins, F
中科院分区：
文献类型：
--
作者：
Iglesias, VA;Meins, F
通过反义转化产生的烟草 I 类 β-1,3-葡聚糖酶 (GLU I) 缺陷突变体 (TAG4.4) 对病毒感染的敏感性降低。 TAG4.4表现出通过烟草病毒（烟草花叶病毒）、potexvirus（表达GFP的重组马铃薯病毒X）和黄瓜病毒（黄瓜花叶病毒）的运动蛋白（MP）3a的胞间连丝的延迟细胞间运输。通过新型生物射弹方法监测葡聚糖和肽的细胞间运动表明，TAG4.4 的胞间连丝尺寸排除极限 (SEL) 也从 1.0 nm 降低至 0.85 nm。因此，GLU I缺陷对胞间连丝运动具有广泛的影响，并不限于特定的病毒类型。 TAG4.4 中胼胝质（β-1,3-葡聚糖酶的底物）的沉积因 32°C 处理、真菌激发子木聚糖酶处理和创伤而增加，表明 GLU I 在调节胼胝质代谢中具有重要功能。人们认为胼胝质周转可调节胞间连丝 SEL。我们认为，针对感染的 GLU I 诱导可能有助于通过降解胼胝质来促进 MP 驱动的病毒传播。
Susceptibility to virus infection is decreased in a class I beta-1,3-glucanase (GLU I)-deficient mutant (TAG4.4) of tobacco generated by antisense transformation. TAG4.4 exhibited delayed intercellular trafficking via plasmodesmata of a tobamovirus (tobacco mosaic virus), of a potexvirus (recombinant potato virus X expressing GFP), and of the movement protein (MP) 3a of a cucumovirus (cucumber mosaic virus). Monitoring the cell-to-cell movement of dextrans and peptides by a novel biolistic method revealed that the plasmodesmatal size exclusion limit (SEL) of TAG4.4 was also reduced from 1.0 to 0.85 nm. Therefore, GLU I-deficiency has a broad effect on plasmodesmatal movement, which is not limited to a particular virus type. Deposition of callose, a substrate for beta-1,3-glucanases, was increased in TAG4.4 in response to 32 degrees C treatment, treatment with the fungal elicitor xylanase, and wounding, suggesting that GLU I has an important function in regulating callose metabolism. Callose turnover is thought to regulate plasmodesmatal SEL. We propose that GLU I induction in response to infection may help promote MP-driven virus spread by degrading callose.