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Maternal Effects Linked to Loss-of-Function of MET1 in
Vegetative Tissues
In seeds derived from met1-3/+ fathers we expected that genetically wild-type
seeds would have a wild-type seed size. In contrast, both the seed area and width
of the BASTA sensitive wild type seeds derived from met1-3/+ fathers are signifi-
cantly larger than the wild-type controls pollinated after emasculation and grown
in the same conditions, even though these seeds are genetically identical (Table 2).
This effect on seed size likely originates from the reduced dosage of active MET1
in the heterozygous met1-3/+ vegetative tissues. Similarly the average seed size
of wild type seed produced from crosses between ovules from met1/+ plants and
wild type pollen were also larger than wild type ovules from controls emasculated
wild type plants crossed with wild type pollen (Table 2). Since we failed to detect a
gametophytic component in the genetic maternal control of seed size by met1-3/+
plants, we concluded that the size increase observed in met1/+×wt crosses origi-
nated from the effect of met1 in vegetative tissues. Thus, plants heterozygous for
met1-3 enhanced seed growth both maternally and paternally with no evidence
for antagonism between the two parents. In addition our results suggest that an
overall reduction of MET1 levels in met1-3/+ plants could lead to a reduced level
of DNA methylation activity prior to meiosis and promote seed size increase.
MET1 Controls Embryo Size Through Its Action on the
Maternal Tissues
The maternal inheritance of the dominant MET1a/s construct caused a dramatic
increase of seed size [7]. Similarly, seeds from crosses between ovules from met1-6
[15] or met1-3 homozygous crossed to wild type pollen are much larger than seeds
produced from met1/+ heterozygous mothers crossed to wild type pollen. The
range of phenotypes suggested that seed size and development were influenced
by MET1 dosage in the maternal sporophyte. All seeds were affected, indicating
that defects could originate from the maternal tissues responsible for supplying
maternal nutrients to the seed or the maternal seed integuments. Deregulation of
cell proliferation and cell elongation of integuments influences seed size [1], [21],
[22]. We thus investigated whether MET1 controls integuments development.
We observed that met1-3/met1-3 integuments contain 50% more cells than in
the wild type (Figures 3A and 3B and Table 3). We thus conclude that MET1
represses cell proliferation in the integuments. In addition, we observed that in
the absence of fertilization, the fruits of met1-3/met1-3 plants elongated (Figure
3C and Table 3), resulting in production of seed-like structures devoid of em-
bryo and endosperm (Figure 3, D and E and Table 3). Similar observations were
made with MET1a/s plants (Table 3). The autonomous seed-like structures are
