Embryo and Endosperm Development Is Disrupted in the Female Gametophytic capulet Mutants of Arabidopsis

Embryo and Endosperm Development Is Disrupted in the Female Gametophytic capulet Mutants of... Paul E. Grini a , Gerd Jürgens a , and Martin Hülskamp a a ZMBP, Developmental Genetics Department, University of Tübingen, D-72076 Tübingen, Germany Corresponding author: Martin Hülskamp, University of Cologne, Gyrhofstr. 15, D-50931 Cologne, Germany., martin.huelskamp@uni-koeln.de (E-mail) Communicating editor: C. S. G ASSER The female gametophyte of higher plants gives rise, by double fertilization, to the diploid embryo and triploid endosperm, which develop in concert to produce the mature seed. What roles gametophytic maternal factors play in this process is not clear. The female-gametophytic effects on embryo and endosperm development in the Arabidopsis mea , fis , and fie mutants appear to be due to gametic imprinting that can be suppressed by METHYL TRANSFERASE1 antisense ( MET1 a/s ) transgene expression or by mutation of the DECREASE IN DNA METHYLATION1 ( DDM1 ) gene. Here we describe two novel gametophytic maternal-effect mutants, capulet1 ( cap1 ) and capulet2 ( cap2 ). In the cap1 mutant, both embryo and endosperm development are arrested at early stages. In the cap2 mutant, endosperm development is blocked at very early stages, whereas embryos can develop to the early heart stage. The cap mutant phenotypes were not rescued by wild-type pollen nor by pollen from tetraploid plants. Furthermore, removal of silencing barriers from the paternal genome by MET1 a/s transgene expression or by the ddm1 mutation also failed to restore seed development in the cap mutants. Neither cap1 nor cap2 displayed autonomous seed development, in contrast to mea , fis , and fie mutants. In addition, cap2 was epistatic to fis1 in both autonomous endosperm and sexual development. Finally, both cap1 and cap2 mutant endosperms, like wild-type endosperms, expressed the paternally inactive endosperm-specific FIS2 promoter GUS fusion transgene only when the transgene was introduced via the embryo sac, indicating that imprinting was not affected. Our results suggest that the CAP genes represent novel maternal functions supplied by the female gametophyte that are required for embryo and endosperm development. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Genetics Genetics Society of America

Embryo and Endosperm Development Is Disrupted in the Female Gametophytic capulet Mutants of Arabidopsis

Genetics, Volume 162 (4): 1911 – Dec 1, 2002

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Publisher
Genetics Society of America
Copyright
Copyright © 2002 by the Genetics Society of America
ISSN
0016-6731
eISSN
1943-2631
Publisher site
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Abstract

Paul E. Grini a , Gerd Jürgens a , and Martin Hülskamp a a ZMBP, Developmental Genetics Department, University of Tübingen, D-72076 Tübingen, Germany Corresponding author: Martin Hülskamp, University of Cologne, Gyrhofstr. 15, D-50931 Cologne, Germany., martin.huelskamp@uni-koeln.de (E-mail) Communicating editor: C. S. G ASSER The female gametophyte of higher plants gives rise, by double fertilization, to the diploid embryo and triploid endosperm, which develop in concert to produce the mature seed. What roles gametophytic maternal factors play in this process is not clear. The female-gametophytic effects on embryo and endosperm development in the Arabidopsis mea , fis , and fie mutants appear to be due to gametic imprinting that can be suppressed by METHYL TRANSFERASE1 antisense ( MET1 a/s ) transgene expression or by mutation of the DECREASE IN DNA METHYLATION1 ( DDM1 ) gene. Here we describe two novel gametophytic maternal-effect mutants, capulet1 ( cap1 ) and capulet2 ( cap2 ). In the cap1 mutant, both embryo and endosperm development are arrested at early stages. In the cap2 mutant, endosperm development is blocked at very early stages, whereas embryos can develop to the early heart stage. The cap mutant phenotypes were not rescued by wild-type pollen nor by pollen from tetraploid plants. Furthermore, removal of silencing barriers from the paternal genome by MET1 a/s transgene expression or by the ddm1 mutation also failed to restore seed development in the cap mutants. Neither cap1 nor cap2 displayed autonomous seed development, in contrast to mea , fis , and fie mutants. In addition, cap2 was epistatic to fis1 in both autonomous endosperm and sexual development. Finally, both cap1 and cap2 mutant endosperms, like wild-type endosperms, expressed the paternally inactive endosperm-specific FIS2 promoter GUS fusion transgene only when the transgene was introduced via the embryo sac, indicating that imprinting was not affected. Our results suggest that the CAP genes represent novel maternal functions supplied by the female gametophyte that are required for embryo and endosperm development.

Journal

GeneticsGenetics Society of America

Published: Dec 1, 2002

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