OsCD1 encodes a putative member of the cellulose synthase-like D sub-family and is essential for rice plant architecture and growth

Summary The cell wall plays important roles in plant architecture and morphogenesis. The cellulose synthase‐like super‐families were reported to contain glycosyltransferases motif and are required for the biosynthesis of cell wall polysaccharides. Here, we describe a curled leaf and dwarf mutant, cd...

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Veröffentlicht in:Plant biotechnology journal 2011-05, Vol.9 (4), p.513-524
Hauptverfasser: Luan, Weijiang, Liu, Yuqin, Zhang, Fengxia, Song, Yuanli, Wang, Zhengying, Peng, Yongkang, Sun, Zongxiu
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Sprache:eng
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Zusammenfassung:Summary The cell wall plays important roles in plant architecture and morphogenesis. The cellulose synthase‐like super‐families were reported to contain glycosyltransferases motif and are required for the biosynthesis of cell wall polysaccharides. Here, we describe a curled leaf and dwarf mutant, cd1, in rice, which exhibits multiple phenotypic traits such as the reduction of plant height and leaf width, curled leaf morphology and a decrease in the number of grains and in the panicle length. Map‐based cloning indicates that a member of the cellulose synthase‐like D (CSLD) group is a candidate for OsCD1. RNAi transgenic plants with the candidate CSLD gene display a similar phenotype to the cd1 mutant, suggesting that OsCD1 is a member of the CSLD sub‐family. Furthermore, sequence analysis indicates that OsCD1 contains the common D,D,D,QXXRW motif, which is a feature of the cellulose synthase‐like super‐family. Analysis of OsCD1 promoter with GUS fusion expression shows that OsCD1 exhibits higher expression in young meristem tissues such as fresh roots, young panicle and stem apical meristem. Cell wall composition analysis reveals that cellulose content and the level of xylose are significantly reduced in mature culm owing to loss of OsCD1 function. Take together, the work presented here is useful for expanding the understanding of cell wall biosynthesis.
ISSN:1467-7644
1467-7652
DOI:10.1111/j.1467-7652.2010.00570.x