کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2787996 | 1154373 | 2009 | 10 صفحه PDF | دانلود رایگان |
![عکس صفحه اول مقاله: Cotton GhPOX1 encoding plant class III peroxidase may be responsible for the high level of reactive oxygen species production that is related to cotton fiber elongation Cotton GhPOX1 encoding plant class III peroxidase may be responsible for the high level of reactive oxygen species production that is related to cotton fiber elongation](/preview/png/2787996.png)
The accumulation of reactive oxygen species (ROS) is involved in plant cell development. In plant, class III peroxidases are heme-containing enzymes encoded by a large multi-gene family participated in the release or consumption of ROS. The specific function of each member of the family is still elusive. Here, we showed that ROS was significantly generated during cotton fiber initiation and elongation, whereas, application of NADPH oxidase inhibitor diphenyleneiodonium (DPI) and peroxidase inhibitor salicylhydroxamic acid (SHAM) to the wild-type cotton ovule culture significantly suppressed fiber growth, respectively. Their inhibitory effects were caused by the reduction of superoxide radical (O2−). Ten GhPOX genes (cDNAs) encoding cotton class III peroxidases were isolated, among them eight GhPOX genes were reported for the first time. Microarray analyses indicated that GhPOX1 was the mostly predominantly expressed in fast-elongating cotton fiber cells. Real-time quantitative PCR analysis revealed the transcript level of GhPOX1 was over 400-fold higher in growing fiber cells than in ovules, flowers, roots, stems and leaves. To reveal the role of GhPOX1 in plant development, its Arabidopsis orthologue atpox13 mutant was demonstrated to be defective in branch root development. Taken together, the data suggest that GhPOX1 plays an important role during fiber cell elongation possibly by mediating production of reactive oxygen species.
Journal: Journal of Genetics and Genomics - Volume 36, Issue 3, March 2009, Pages 141–150