CCS52 and DEL1 genes are key components of the endocycle in nematode-induced feeding sites

被引:74
作者
de Almeida Engler, Janice [1 ]
Kyndt, Tina [2 ]
Vieira, Paulo [1 ]
Van Cappelle, Elke [2 ]
Boudolf, Veronique [3 ,4 ]
Sanchez, Vanesa [1 ]
Escobar, Carolina [5 ]
De Veylder, Lieven [3 ,4 ]
Engler, Gilbert [1 ]
Abad, Pierre [1 ]
Gheysen, Godelieve [2 ]
机构
[1] Univ Nice Sophia Antipolis, Inst Natl Rech Agron, Ctr Natl Rech Sci, ISA,UMR 1355, Sophia Antipolis, France
[2] Univ Ghent, Dept Mol Biotechnol, B-9000 Ghent, Belgium
[3] Vlaams Inst Biotechnol, Dept Plant Syst Biol, B-9052 Ghent, Belgium
[4] Univ Ghent, Dept Plant Biotechnol & Bioinformat, B-9052 Ghent, Belgium
[5] Univ Autonoma Madrid, CSIC, Ctr Nacl Biotecnol, Unidad Genom, E-28049 Madrid, Spain
关键词
Arabidopsis; endocycle; cell cycle; root-knot nematode; cyst nematode; ANAPHASE-PROMOTING COMPLEX; DNA TOPOISOMERASE-VI; ROOT-KNOT; CELL-CYCLE; MEDICAGO-TRUNCATULA; PARASITIC NEMATODE; GIANT-CELLS; ENDOREDUPLICATION; INFECTION; EXPRESSION;
D O I
10.1111/j.1365-313X.2012.05054.x
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
The establishment of galls and syncytia as feeding sites induced by root-knot and cyst nematodes, respectively, involves a progressive increase in nuclear and cellular size. Here we describe the functional characterization of endocycle activators CCS52A, CCS52B and a repressor of the endocycle, DEL1, during two types of nematode feeding site development in Arabidopsis thaliana. In situ hybridization analysis showed that expression of CCS52A1 and CCS52B was strongly induced in galls and syncytia and DEL1 was stably but weakly expressed throughout feeding site development. Down-regulation and over-expression of CCS52 and DEL1 in Arabidopsis drastically affected giant cell and syncytium growth, resulting in restrained nematode development, illustrating the need for mitotic activity and endo-reduplication for feeding site maturation. Exploiting the mechanism of endo-reduplication may be envisaged as a strategy to control plant-parasitic nematodes.
引用
收藏
页码:185 / 198
页数:14
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