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Abstract
The deposition of cellulose microfibrils plays an important role in shaping plant cells. It is believed that cortical microtubules regulate the orientation of microfibrils, but the mechanism remains unknown. A previous study showed that mutation of the microtubule motor protein Fragile Fiber1 (FRA1) alters the organization of microfibrils in Arabidopsis thaliana. Here, we found that overexpression of FRA1 reduced the thickness of fiber secondary walls and caused deformation of vessels. Furthermore, we isolated three putative FRA1 interacting proteins by yeast 2-hybrid: the FRA1 interacting protein1 (FIP1), the gibberellin-regulated protein, and the actin-related protein. Secondary cell wall biosynthesis is controlled by a transcriptional network, in which the secondary wall-associated NAC domain protein1 (SND1) and the NAC secondary wall thickening promoting factor1 (NST1) are master regulators and function redundantly. In this study, we demonstrated that expression of SND1 homologues in the snd1 nst1 mutant complemented the secondary wall defects in fiber cells, indicating that they are all functional homologues. Expression analysis revealed that one subgroup of SND1 homologues were expressed in stem vessels, another subgroup of SND1 homologues were expressed in stem fiber cells, while some others were mainly expressed in root caps. Overexpression of some of these SND1 homologues caused ectopic secondary cell wall deposition-like phenotypes in the wild-type. However, dominant repression of their functions did not result in obvious phenotypes. Therefore, we suggest that these SND1 homologues are minor regulators of secondary cell wall biosynthesis.