Biology Reference
In-Depth Information
Table 3.
Morphometric measurements of autonomous fruits and seeds produced by plants deficient for
MET1.
Conclusions
MET1 independently controls both endosperm growth and cell division and
elongation of the integuments. Presumably MET1 silences maternal genes
in the integuments and restricts seed growth through this maternal sporo-
phytic control. In addition MET1 restricts the expression of imprinted genes
in endosperm to the maternal alleles, resulting eventually in a different type
of maternal control of endosperm growth. Our results also suggest that a
memory of the maternal epigenetic status prior to meiosis is recorded during
gametogenesis and influences seed size. Overall the epigenetic control of seed
size by MET1 appears to result primarily from maternal controls. These derive
directly from the action of MET1 on the sporophytic vegetative tissues and
indirectly from the restriction of expression of imprinted inhibitors of seed
size to their maternal allele by MET1 acting during male gametogenesis. This
conclusion does not support MET1-mediated antagonism between imprinted
loci expressed from the paternal or maternal genomes as originally predicted
by the parental conflict hypothesis. It is unlikely that CMT3 and DRM2
involved in global de novo DNA methylation control seed size since they do
not appear to impact the expression of imprinted genes [25], [26]. However
we do not exclude that other epigenetic controls such as histone methylation
by Polycomb group complexes [26]-[28] are responsible for an opposite ac-
tion of the expression between paternally and maternally expressed imprinted
genes. In mammals, the function and regulation of some imprinted genes
support the parental conflict theory [11], [12], [17], [29]. However some
results also suggest a predominant maternal control of placental and embryo
growth [30]-[32]. In conclusion, in plants and mammals a complex series of
maternal controls balance the unequal parental contributions to the offspring
and may mimic a parental conflict without involving symmetrical antagonis-
tic molecular controls.
