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paternal allele of growth enhancers in the endosperm, which nurtures the em-
bryo. However, we find no evidence for a similar role of MET1 during female
gametogenesis. Rather, the reduction of MET1 dosage in the maternal somat-
ic tissues causes seed size increase. MET1 inhibits seed growth by restricting
cell division and elongation in the maternal integuments that surround the
seed. Our data demonstrate new controls of seed growth linked to the mode
of reproduction typical of flowering plants. We conclude that the regulation of
embryo growth by MET1 results from a combination of predominant mater-
nal controls, and that DNA methylation maintained by MET1 does not or-
chestrate a parental conflict.
Introduction
In flowering plants, meiosis is followed by the production of haploid structures,
the male pollen and the female embryo sac, each containing two gametes. After
double-fertilization, the female gametes, the egg cell and central cell, respectively
give rise to the embryo and its nurturing annex, the endosperm. The embryo and
the endosperm develop within the maternally derived seed integuments. Seed size
is controlled primarily by interactions between the endosperm and integuments
[1], [2] although the embryo also contributes [3].
The parental contributions to seed size were identified in crosses involving
diploid and tetraploid plants. Tetraploid mothers produced smaller seeds when
crossed to diploid fathers, however tetraploid fathers crossed to diploid mothers
produced larger seeds [4], [5]. Hence seed size is enhanced by an excess of pater-
nal genomes and restricted by an excess of maternal genomes. These phenomena
were linked to the DNA methyltransferase MET1, using a dominant antisense
construct, MET1a/s 6-9. Maternal inheritance of MET1a/s causes an increase
of seed size whereas paternal inheritance has an opposite effect. MET1 is a key
player in the control of parental genomic imprinting, which restricts gene expres-
sion from one of the two parental alleles [10]. In Arabidopsis, it was proposed that
MET1 controls the expression of two pools of imprinted genes: maternally ex-
pressed inhibitors and paternally expressed enhancers of endosperm growth [11].
In Arabidopsis two imprinted genes dependent on MET1 have been identified
[12]. MET1 silences the genes FWA and FERTILIZATION INDEPENDENT
SEED 2 (FIS2) in the male gametes [12]. FIS2 and FWA are expressed in the
female central cell [9], [13]. After fertilization FIS2 and FWA are expressed in the
endosperm from their maternal allele, while MET1 maintains silencing on the
paternal allele [12], [13]. The parental imbalance of expression thus defines FIS2
and FWA as imprinted genes.
