Global analysis of gene expression in flower buds of Ms-cd1Brassica oleracea conferring male sterility by using an Arabidopsis microarray View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2008-01

AUTHORS

Jungen Kang, Guoyu Zhang, Guusje Bonnema, Zhiyuan Fang, Xiaowu Wang

ABSTRACT

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. More... »

PAGES

177-192

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s11103-007-9261-9

DOI

http://dx.doi.org/10.1007/s11103-007-9261-9

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1042058204

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/18040866


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