|Title||Xyloglucan endo-transglycosylase (XET) functions in gelatinous layers of tension wood fibers in poplar - A glimpse into the mechanism of the balancing act of trees|
|Publication Type||Journal Article|
|Year of Publication||2007|
|Authors||Nishikubo, N, Awano, T, Banasiak, A, Bourquin, V, Ibatullin, F, Funada, R, Brumer, H, Teeri, TT, Hayashi, T, Sundberg, B, Mellerowicz, EJ|
|Journal||PLANT AND CELL PHYSIOLOGY|
|Type of Article||Article|
Tension wood is a specialized tissue of deciduous trees that functions in bending woody stems to optimize their position in space. Tension wood fibers that develop on one side of the stem have an increased potency to shrink compared with fibers on the opposite side, thus creating a bending moment. It is believed that the gelatinous (G) cell wall layer containing almost pure cellulose of tension wood fibers is pivotal to their shrinking. By analyzing saccharide composition and linkage in isolated G-layers of poplar, we found that they contain some matrix components in addition to cellulose, of which xyloglucan is the most abundant. Xyloglucan, xyloglucan endo-transglycosylase (XET) activity and xyloglucan endo-transglycosylase/hydrolase (XTH) gene products were detected in developing G-layers by labeling using CCRC-M1 monoclonal antibody, in situ incorporation of XXXG-SR and the polyclonal antibody to poplar PttXET16-34, respectively, indicating that xyloglucan is incorporated into the G-layer during its development. Moreover, several XTH transcripts were altered and were generally up-regulated in developing tension wood compared with normal wood. In mature G-fibers, XTH gene products were detected in the G-layers while the XET activity was evident in the adjacent S-2 wall layer. We propose that XET activity is essential for G-fiber shrinking by repairing xyloglucan cross-links between G- and S-2-layers and thus maintaining their contact. Surprisingly, XTH gene products and XET activity persisted in mature G-fibers for several years, suggesting that the enzyme functions after cell death repairing the cross-links as they are being broken during the shrinking process.