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.