Global analysis of gene expression in flower buds of Ms-cd1 Brassica oleracea conferring male sterility by using an Arabidopsis microarray

被引:37
作者
Kang, Jungen [2 ]
Zhang, Guoyu [2 ]
Bonnema, Guusje [1 ]
Fang, Zhiyuan [2 ]
Wang, Xiaowu [2 ]
机构
[1] Univ Wageningen & Res Ctr, Lab Plant Breeding, NL-6709 PD Wageningen, Netherlands
[2] Chinese Acad Agr Sci, Inst Vegetables & Flowers, Beijing 100081, Peoples R China
关键词
Brassica oleracea; bud; gene expression; male sterility; microarray;
D O I
10.1007/s11103-007-9261-9
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The dominant male sterility gene Ms-cd1 is identified in Brassica oleracea. Electron microscopical observations revealed that abortion of pollen development starts after tetrad formation. This important male sterility phenotype is characterized by lack of degradation of the primary pollen mother cell (PMC) wall and delayed degradation of callose surrounding the tetrads and thus arrest of microspore release. Gene expression of the male sterile and fertile buds was analyzed by heterologous hybridization of Brassica oleracea cRNA onto an Arabidopsis whole genome oligonucleotide microarray. A total of 277 suppressed genes including 40 kinase-, 32 cell wall modification and 29 transport related genes were found to be significantly down regulated >3-fold in the male sterile mutant. The vast majority of the differentially expressed transcripts are found to present late pollen stage specific genes. Kinase genes, cell wall modification genes and ion transport genes were greatly over-represented when compared to their percentage of all flower bud expressed genes and represent 36.5% of the genes suppressed by Ms-cd1. Our results also suggest that Ms-cd1 may blocks an anther developmental pathway with a small number of genes suppressed in tapetum cells which prevent the degradation of callose and PMC wall, which further leads to the suppression of a large number of genes involved in signaling pathways, cell wall modification and ion transport in pollen grains.
引用
收藏
页码:177 / 192
页数:16
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