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The role of the MCM2-7 helicase complex during Arabidopsis seed development

The role of the MCM2-7 helicase complex during Arabidopsis seed development The MINICHROMOSOME MAINTENANCE 2-7 (MCM2-7) complex, a ring-shaped heterohexamer, unwinds the DNA double helix ahead of the other replication machinery. Although there is evidence that individual components might have other roles, the essential nature of the MCM2-7 complex in DNA replication has made it difficult to uncover these. Here, we present a detailed analysis of Arabidopsis thaliana mcm2-7 mutants and reveal phenotypic differences. The MCM2-7 genes are coordinately expressed during development, although MCM7 is expressed at a higher level in the egg cell. Consistent with a role in the egg cell, heterozygous mcm7 mutants resulted in frequent ovule abortion, a phenotype that does not occur in other mcm mutants. All mutants showed a maternal effect, whereby seeds inheriting a maternal mutant allele occasionally aborted later in seed development with defects in embryo patterning, endosperm nuclear size, and cellularization, a phenotype that is variable between subunit mutants. We provide evidence that this maternal effect is due to the necessity of a maternal store of MCM protein in the central cell that is sufficient for maintaining seed viability and size in the absence of de novo MCM transcription. Reducing MCM levels using endosperm-specific RNAi constructs resulted in the up-regulation of DNA repair transcripts, consistent with the current hypothesis that excess MCM2-7 complexes are loaded during G1 phase, and are required during S phase to overcome replicative stress or DNA damage. Overall, this study demonstrates the importance of the MCM2-7 subunits during seed development and suggests that there are functional differences between the subunits. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Plant Molecular Biology Springer Journals

The role of the MCM2-7 helicase complex during Arabidopsis seed development

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References (65)

Publisher
Springer Journals
Copyright
Copyright © 2014 by Springer Science+Business Media Dordrecht
Subject
Life Sciences; Plant Sciences; Biochemistry, general; Plant Pathology
ISSN
0167-4412
eISSN
1573-5028
DOI
10.1007/s11103-014-0213-x
pmid
24947836
Publisher site
See Article on Publisher Site

Abstract

The MINICHROMOSOME MAINTENANCE 2-7 (MCM2-7) complex, a ring-shaped heterohexamer, unwinds the DNA double helix ahead of the other replication machinery. Although there is evidence that individual components might have other roles, the essential nature of the MCM2-7 complex in DNA replication has made it difficult to uncover these. Here, we present a detailed analysis of Arabidopsis thaliana mcm2-7 mutants and reveal phenotypic differences. The MCM2-7 genes are coordinately expressed during development, although MCM7 is expressed at a higher level in the egg cell. Consistent with a role in the egg cell, heterozygous mcm7 mutants resulted in frequent ovule abortion, a phenotype that does not occur in other mcm mutants. All mutants showed a maternal effect, whereby seeds inheriting a maternal mutant allele occasionally aborted later in seed development with defects in embryo patterning, endosperm nuclear size, and cellularization, a phenotype that is variable between subunit mutants. We provide evidence that this maternal effect is due to the necessity of a maternal store of MCM protein in the central cell that is sufficient for maintaining seed viability and size in the absence of de novo MCM transcription. Reducing MCM levels using endosperm-specific RNAi constructs resulted in the up-regulation of DNA repair transcripts, consistent with the current hypothesis that excess MCM2-7 complexes are loaded during G1 phase, and are required during S phase to overcome replicative stress or DNA damage. Overall, this study demonstrates the importance of the MCM2-7 subunits during seed development and suggests that there are functional differences between the subunits.

Journal

Plant Molecular BiologySpringer Journals

Published: Jun 20, 2014

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