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devoid of endosperm or embryo and develop only from ovules that are deficient of
MET1 in the sporophytic integuments but not from ovules from met1/+ plants,
50% of which are deficient of MET1 in the female gametophyte. We conclude
that autonomous growth of seed-like structures did not originate from the loss
of MET1 activity in the central cell or the egg cell. Rather, MET1 thus controls
seed size maternally through its action on cell proliferation and elongation in the
seed integuments. Double fertilization causes enhanced cell division followed by
elongation in the wild type [1]. Our results thus suggest that double-fertilization
releases MET1-inhibited controls. Hence we show that mechanisms acting in the
integuments in addition to the endosperm [23] and the embryo [3], [24] prevent
seed development in absence of fertilization.
Figure 3.
Maternal effects of met1/met1 on ovule integument.
(A) Wild-type
ovule at the mature stage shows four or five cell layers of integuments (int) surrounding the central
cell (cc). (B) A similar confocal section of a met1/met1 ovule. (C) Fruits from met1-3/met1-3 plants elongate in
absence of fertilization (10 Days After Emasculation, (DAE)) in comparison to wild-type fruits. (D) Wild-type
ovule with collapsed central cell at 8 DAE. (E) Seed-like structure in elongated fruits from met1-3/met1-3 plants
at 8 DAE. Scale bars represent 20 µm (A, B, D and E) and 1.5 mm (C).
